AntiTum Cancer Research Results

AntiTum, AntiTumor: Click to Expand ⟱

Source:

Type:

AntiTumor

Scientific Papers found: Click to Expand⟱

5269-

3BP,

The anti-metabolite KAT/3BP has in vitro and in vivo anti-tumor activity in lymphoma models.

in-vitro,

HCC,

toxicity↑, 3-Bromopyruvate (3BP), a small alkylating agent, acts as an anti-metabolite to vital substrates in cancer metabolism and exhibits antitumor activity across various cancer types, but the unformulated 3BP can cause high toxicity
eff↝, This study explores the efficacy of the 3BP clinical derivative KAT/3BP, currently in phase 1 for patients with hepatocellular carcinoma, in lymphoma models.
eff↑, AT/3BP exhibited synergistic activity when combined with lymphoma therapies, including bendamustine and R-CHOP.
Glycolysis↓, At acidic extracellular pH, 3BP enters cancer cells via monocarboxylic acid-1 (MCT-1) and inhibits glycolysis through hexokinase II (HK-2) covalent modification
HK2↓, with HK-2 inhibition and dissociation from mitochondria, apoptosis-inducing factor (AIF) release, and apoptosis induction (9).
AIF↑,
Apoptosis↑,
NK cell↑, In the latter, tumor growth was in vivo reversed, with an increase in the number of circulating CD4+, CD8+, and NK- cells
toxicity↑, unformulated 3BP administrations are associated with severe toxicities, including deaths (22,23)
toxicity↓, However, improvements have been made in developing novel 3BP formulations based on liposomes, polyethylene glycol (PEG), PEGylated liposomes (stealth liposomes), perillyl alcohol formulations, and others (12,22,24
Dose↝, KAT-101 and KAT-201 are two clinical 3BP derivatives formulated for oral or intratumoral (IT) administration, respectively (National Cancer Institute Thesaurus Codes C193479 and C193479), now entering the early clinical evaluation of patients with h
AntiTum↑, KAT/3BP has in vivo antitumor activity in a syngeneic mouse model.

5314-

acetaz,

Carbonic Anhydrase Inhibitors Targeting Metabolism and Tumor Microenvironment

Review,

Var,

AntiTum↑, such as CA IX and XII, actively participate in these processes and were validated as antitumor/antimetastatic drug targets.
CA↓, Indeed, primary sulfonamides [56,57,58] such as acetazolamide were known for decades to potently inhibit CAs

5462-

AF,

Repurposing Auranofin for Oncology and Beyond: A Brief Overview of Clinical Trials as Mono- and Combination Therapy

Review,

Var,

AntiTum↑, Over the last twenty years, AF has also been repurposed as an antitumor, antiviral, and antibacterial drug.
Bacteria↓,
TrxR↓, ability to inhibit thioredoxin reductase (TrxR) and disrupt redox homeostasis, leading to selective cytotoxicity in cancer cells.
ChemoSen↑, synergistic effects observed when AF is combined with chemotherapeutics, targeted therapies, or immune modulators.
Dose↝, Patients received AF orally twice daily on days 1–28. atients received AF orally, 6 mg in the morning and 6 mg in the evening.
ROS↑, AF induces oxidative stress and apoptosis in cancer cells by disrupting redox homeostasis, while sirolimus inhibits mTOR signaling.
Apoptosis↑,
mTOR↓,

5471-

AF,

Anti-Tumoral Treatment with Thioredoxin Reductase 1 Inhibitor Auranofin Fosters Regulatory T Cell and B16F10 Expansion in Mice

vitro+vivo,

Melanoma,

B16-F10

TrxR1↓, Auranofin, an FDA-approved antirheumatic drug and thioredoxin reductase 1 (TXNRD1) inhibitor, has demonstrated anti-tumoral properties
AntiTum↑,
ROS↑, TXNRD1 Inhibitors Elevated ROS Levels, Activate NRF2, and Kill B16F10 Cells In Vitro
NRF2↑,
TumCD↑,

1295-

AG,

Cisplatin,

Chemosensitizing Effect of Astragalus Polysaccharides on Nasopharyngeal Carcinoma Cells by Inducing Apoptosis and Modulating Expression of Bax/Bcl-2 Ratio and Caspases

in-vivo,

Laryn,

mice

AntiTum↑,
Apoptosis↑,
Bcl-2↓,
BAX↑,
Casp3↑,
Casp9↑,
Bax:Bcl2↑, ratio of Bax to Bcl-2 was significantly enhanced by the APS to cisplatin

5444-

AG,

A Systematic Review of Phytochemistry, Pharmacology and Pharmacokinetics on Astragali Radix: Implications for Astragali Radix as a Personalized Medicine

Review,

Var,

*Imm↑, AR possesses various biological functions, including potent immunomodulation, antioxidant, anti-inflammation and antitumor activities.
*antiOx↑,
*Inflam↓,
AntiTum↑,
eff↑, characteristics of increasing curative effect and reducing the toxicity of chemotherapeutic drugs [11 , 118].
chemoP↑,
Dose↝, main bioactive compounds responsible for the anti-cancer effects of AR mainly include formononetin, AS-IV and APS. S
TumCMig↓, AS-IV could inhibit the migration and proliferation of non-small cell lung cancer (NSCLC
TumCP↓,
Akt↓, h via inhibition of the Akt/GSK-3β/β-catenin signaling axis.
GSK‐3β↓,
MMP2↓, downregulating the expression of matrix metalloproteases (MMP)-2 and -9
MMP9↓,
EMT↓, AS-IV could inhibit TGF-B1 induced EMT through inhibition of PI3K/AKT/NF-KB
PI3K↓,
Akt↓,
NF-kB↓,
Inflam↓,
TGF-β1↓,
TNF-α↓,
IL6↓,
Fas↓, reduced FAS/FasL
FasL↓,
NOTCH1↓, decressing notch1
JNK↓, inactivating JNK pathway [145]
TumCG↓, The results showed that the AR water extract could inhibit the growth of colorectal cancer in vivo without apparent toxicity and side effect, which suggests that AR is a potential therapeutic drug for colorectal cancer

5431-

AG,

Advances in research on the anti-tumor mechanism of Astragalus polysaccharides

Review,

Var,

AntiTum↑, APS has been increasingly used in cancer therapy owing to its anti-tumor ability as it prevents the progression of prostate, liver, cervical, ovarian, and non-small-cell lung cancer by suppressing tumor cell growth and invasion and enhancing apoptosi
TumCG↓,
TumCI↓,
Apoptosis↑, after APS treatment, the apoptosis of HepG2 cells is accelerated (57).
Imm↑, APS enhances the sensitivity of tumors to antineoplastic agents and improves the body’s immunity
Bcl-2↓, Huang et al. proposed that APS induces H22 (a hepatocellular cancer [HCC] cell line) apoptosis by downregulating Bcl-2 and upregulating Bax expression (56).
BAX↑,
Wnt↓, downregulating the Wnt/β-catenin signaling pathway.
β-catenin/ZEB1↓,
TumCG↓, APS effectively inhibited the growth of MDA-MB-231 (a human breast cancer [BC] cell line) graft tumor (58)
miR-133a-3p↑, apoptosis rate of human osteosarcoma MG63 cells increased owing to the upregulation of miR-133a and inactivation of the JNK signaling pathways (71).
JNK↓,
Fas↑, Li and Shen found that APS can induce apoptosis by activating the Fas death receptor pathway.
P53↑, Zhang et al. showed that APS could activate p53 and p21 and inhibit the expression of Notch1 and Notch3 in vitro, ultimately inhibiting cell proliferation and promoting their apoptosis
P21↑,
NOTCH1↓,
NOTCH3↓,
TumCP↓,
TumCCA↑, Liu et al. found that APS induced the cell cycle of bladder cancer UM-UC-3 to stop in the G0/G1 phase, thus inhibiting its proliferation
GPx4↓, APS was found to reduce GPX4 expression, inhibit the activity of the light chain subunit SLC7A11 (xCT), and promote the formation of BECN1-xCT complex by activating AMPK/BECN1 signaling.
xCT↓,
AMPK↑,
Beclin-1↑,
NF-kB↓, APS could control the proliferation of lung cancer cells (A549 and NCI-H358 cells) by inhibiting the NF-κB signaling pathway (97)
EMT↓, APS treatment led to reduced EMT markers (vimentin, AXL) and MIF levels in cells.
Vim↓,
TumMeta↓, APS inhibits Lewis lung cancer growth and metastasis in mice by significantly reducing VEGF and EGFR expression in cancerous tissues
VEGF↓,
EGFR↓,
eff↑, Nano-drug delivery systems can increase efficiency and reduce toxicity
eff↑, Jiao et al. developed selenium nanoparticles modified with macromolecular weight APS and observed positive results in hepatoma treatment
MMP↓, Subsequent investigations revealed that APS can decrease the ΔΨm values and Bcl-2, p-PI3K, P-gp, and p-AKT levels while elevating Bax expression.
P-gp↓,
MMP9↓, downregulation of MMP-9 expression,
ChemoSen↑, Li et al. observed that APS could enhance the sensitivity of SKOV3 ovarian cancer cells to CDDP treatment by activating the mitochondrial apoptosis pathway and JNK1/2 signaling pathway
SIRT1↓, APS significantly suppressed SIRT1 and SREBP1 expression, decreased cholesterol and triglyceride levels in PC3 and DU145, and attenuated cell proliferation.
SREBP1↓,
TumAuto↑, APS can induce autophagy in colorectal cancer cells by inhibiting the PI3K/AKT/mTOR axis and the development of cancer cells.
PI3K↓,
mTOR↓,
Casp3↑, Shen found that APS elevated caspase-9, caspase-3, and Bax protein levels, decreased Bcl-2 protein expression, and inhibited CD133 and CD44 co-positive colon cancer stem cell proliferation time
Casp9↑,
CD133↓,
CD44↓,
CSCs↓,
QoL↑, QOL was significantly improved as indicated by the reduction in pain and improvement in appetite

4394-

AgNPs,

Silver nanoparticles provoke apoptosis of Dalton's ascites lymphoma in vivo by mitochondria dependent and independent pathways

in-vivo,

lymphoma,

OS↑, Results indicate that the AgNPs were efficient in prolongation of life span, reduction of tumor volume and body weight in tumor animals.
TumVol↓,
Weight↑,
AntiTum↑, AgNPs are potent in antitumor activity and the molecular mechanism is by the induction of apoptosis through the mitochondrial dependent and independent pathways.
Apoptosis↑,
mtDam↑,

4364-

AgNPs,

Selective cytotoxicity of green synthesized silver nanoparticles against the MCF-7 tumor cell line and their enhanced antioxidant and antimicrobial properties

in-vitro,

BC,

MCF-7

31.4 nm with a Zeta potential of −33.8 mV,

TumCD↑, AgNPs and the extract exhibited 70% and 40% cytotoxicity against MCF-7 cancerous cells, respectively, while CSN caused 56% cell death (at the concentration of 60 µg/mL)
selectivity↑, It was observed that AgNPs were much less cytotoxic when tested against a noncancerous cell line (L-929)
*antiOx↑, These include antioxidant, antifungal, anti-inflammatory, antiviral, anti-angiogenesis, and antimicrobial effects
*Inflam↓,
AntiTum↑, antitumor properties of AgNPs
ROS↑, AgNPs interact with mitochondria and disrupt the cellular electron transfer chain function leading to an increase in the ROS level. oxidative stress generated by ROS could be considered as a main toxicity mechanism of AgNPs against cells

4378-

AgNPs,

Exploring silver nanoparticles for cancer therapy and diagnosis

Review,

Var,

AntiTum↑, AgNPs show great promise for cancer therapy due to their antitumoral effects demonstrated by several in vitro and in vivo studies (Table 1)
ROS↑, well known that their toxicity relies on the generation of reactive oxygen species (ROS)
eff↑, synergic combination of AgNPs and chemotherapy drugs
RadioS↑, in vitro studies have highlighted the ability of AgNPs to enhance cell/tissue sensitivity to radiotherapy (RT).

4383-

AgNPs,

Exploring the Potentials of Silver Nanoparticles in Overcoming Cisplatin Resistance in Lung Adenocarcinoma: Insights from Proteomic and Xenograft Mice Studies

in-vitro,

Lung,

A549

AgNPs was 23.45 nm, with zeta potentials lying on −20.33 mV.

in-vivo,

Lung,

A549

A549 and A549/DDP-bearing mice

Apoptosis↑, Silver nanoparticles (AgNPs) have shown great potential as therapeutic agents due to their ability to cause apoptotic cell death in cancer cells.
VEGF↓, suppressing the VEGF signaling pathway, repressing p53-mediated pathways, promoting cell cycle arrest,
P53↓,
TumCCA↑,
ROS↑, we found that AgNPs induced ROS generation
AntiTum↑, AgNPs exhibit similar antitumoral effects on both A549 and A549/DDP-bearing mice.
eff↑, AgNPs are internalized by cells far more effectively than free Ag+ under identical exposure conditions
ATP↓, AgNPs exposure also decreased basal respiration (52.3 ± 4.6 pmol/min/106 cells), maximal respiration (109.2 ± 12.2 pmol/min/106 cells), ATP production (
eff↑, These results explain why AgNPs remain effective against cisplatin-resistant A549 cells.
CTR1↑, recent studies have shown that AgNPs treatment significantly upregulates CTR1

4546-

AgNPs,

Chapter 2 - Silver nanoparticles in cancer therapy

Study,

Var,

AntiTum↑, In recent years, numerous studies have claimed that silver nanoparticles can be successfully used as antitumor agents due to their antiproliferative and apoptosis-inducing properties.
Apoptosis↑,

5352-

AL,

Anticancer potential of allicin: A review

Review,

Var,

*cardioP↑, Allicin has many health-promoting properties, such as cardioprotective, antimicrobic, cholesterol-lowering, anti-inflammatory, and antitumor.
*Bacteria↓,
*Inflam↓,
AntiTum↑,
*DNAdam↓, DNA damage protection, induction of cell death, inhibition of cell proliferation, and block of angiogenesis and metastasis formation.
TumCP↓,
angioG↓,
TumMeta↓,

2657-

AL,

Allicin pharmacology: Common molecular mechanisms against neuroinflammation and cardiovascular diseases

Review,

CardioV,

Review,

AD,

*Inflam↓, allicin integrate a broad spectrum of properties (e.g., anti-inflammatory, immunomodulatory, antibiotic, antifungal, antiparasitic, antioxidant, nephroprotective, neuroprotective, cardioprotective, and anti-tumoral activities, among others).
*antiOx↑, improving the antioxidant system
*neuroP↑,
*cardioP↑,
*AntiTum↑,
*mtDam↑, Indeed, the current evidence suggests that allicin improves mitochondrial function by enhancing the expression of HSP70 and NRF2, decreasing RAAS activation, and promoting mitochondrial fusion processes.
*HSP70/HSPA5↑, llicin improves mitochondrial function by enhancing the expression of HSP70 and decreasing RAAS activation
*NRF2↑,
*RAAS↓,
*cognitive↑, Allicin enhances the cognitive function of APP (amyloid precursor protein)/PS1 (presenilin 1) double transgenic mice by decreasing the expression levels of Aβ, oxidative stress, and improving mitochondrial function.
*SOD↑, positive effects on cognition in an AD mouse model by administrating a preventive dose of allicin. These effects might be mediated by an increase of SOD and reduction of ROS
*ROS↓,
*NRF2↑, Chronic treatment with allicin increased the expression of NRF2 and targeted downstream of NRF2, such as NADPH, quinone oxidoreductase 1 (NQO1), and Î³-glutamyl cysteine synthetase (Î³-GCS), in the hippocampus of aged mice
*ER Stress↓, protective effects of 16 weeks of allicin treatment in a rat model of endoplasmic reticulum stress-related cognitive deficits.
*neuroP↑, allicin was able to ameliorate depressive-like behaviors by decreasing neuroinflammation, oxidative stress iron aberrant accumulation,
*memory↑, allicin improved lead acetate-caused learning and memory deficits and decreased the ROS level
*TBARS↓, Oral administration of allicin was able to reduce thiobarbituric reactive substances (TBARS) and myeloperoxidase (MPO) levels, and concurrently increased (SOD) activity, glutathione S-transferase (GST) and glutathione (GSH) levels in a rat model of
*MPO↓,
*SOD↑,
*GSH↑,
*iNOS↓, decreasing the expression of iNOS and increased the phosphorylation of endothelial NOS (eNOS)
*p‑eNOS↑,
*HO-1↑, OSCs upregulate the endogenous antioxidant NRF2 and heme oxygenase-1 (HO-1)

2593-

Api,

Apigenin promotes apoptosis of 4T1 cells through PI3K/AKT/Nrf2 pathway and improves tumor immune microenvironment in vivo

in-vivo,

BC,

4T1

4T1 xenograft tumor mouse model

TumCP↓, API suppresses 4T1 cells proliferation
TumCMig↓, API restraints 4T1 cells migration and invasion
TumCI↓,
Apoptosis↑, API triggers 4T1 apoptosis and modulates the expression levels of apoptotic-associated proteins in 4T1 cells
MMP↑, API triggers the depolarization of ΔΨm in 4T1 cells
ROS↑, API induces ROS generation
p‑PI3K↓, The results revealed a significant downregulation of p-PI3K/PI3K, p-AKT/AKT, and Nrf2 in 4T1 cells following API treatment
PI3K↓,
Akt↓,
NRF2↓,
AntiTum↑, API exhibits anti-tumor activity in mice
OS↑, results of animal survival experiments show that API can appropriately prolong the survival of mice with mammary gland tumors

5133-

ART/DHA,

Dihydroartemisinin Exerts Anti-Tumor Activity by Inducing Mitochondrion and Endoplasmic Reticulum Apoptosis and Autophagic Cell Death in Human Glioblastoma Cells

in-vitro,

GBM,

U87MG

in-vitro,

GBM,

U251

AntiTum↑, (DHA) has been shown to exhibit anti-tumor activity in various cancer cells.
tumCV↓, Our results proved that DHA treatment significantly reduced cell viability in a dose- and time-dependent manner by CCK-8 assay.
Apoptosis↓, DHA induced apoptosis of GBM cells through mitochondrial membrane depolarization, release of cytochrome c and activation of caspases-9.
MMP↓,
Cyt‑c↑,
Casp9↑,
CHOP↑, Enhanced expression of GRP78, CHOP and eIF2α and activation of caspase 12 were additionally confirmed that endoplasmic reticulum (ER) stress pathway of apoptosis
GRP78/BiP↑,
eIF2α↑,
Casp12↑,
ER Stress↑, DHA Induced Apoptosis through Mitochondria and Endoplasmic Reticulum (ER) Stress Pathways of Apoptosis in Human GBM Cells
TumAuto↑, ER stress and mitochondrial dysfunction were involved in the DHA-induced autophagy.
ROS↑, Further study revealed that accumulation of reactive oxygen species (ROS) was attributed to the DHA induction of apoptosis and autophagy.

2571-

ART/DHA,

Cancer combination therapies with artemisinin-type drugs

Review,

Var,

AntiTum↑, We and others found that artemisinin and its derivatives also exert profound activity against tumor cells in vitro and in vivo.
ChemoSen↑, Indeed, additive to synergistic interactions of ARS, DHA, or ART have been observed in combination with standard anticancer drugs towards tumor cell lines of diverse origin
hepatoP↝, In a large meta-analysis with 8000 patients, hepatotoxicity occurred in 0.9% of the patients

5169-

Ash,

The Tumor Inhibitor and Antiangiogenic Agent Withaferin A Targets the Intermediate Filament Protein Vimentin

in-vitro,

BC,

MCF-7

AntiTum↑, The natural product withaferin A (WFA) exhibits antitumor and antiangiogenesis activity in vivo, which results from this drug’s potent growth inhibitory activities.
angioG↓,
Vim↓, Here, we show that WFA binds to the intermediate filament (IF) protein, vimentin,

5175-

Ash,

Withaferin A Induces Proteasome Inhibition, Endoplasmic Reticulum Stress, the Heat Shock Response and Acquisition of Thermotolerance

in-vitro,

Cerv,

CCL-102

Inflam↓, In the present study, withaferin A (WA), a steroidal lactone with anti-inflammatory and anti-tumor properties, inhibited proteasome activity
AntiTum↑,
Proteasome↓,
ER Stress↑, and induced endoplasmic reticulum (ER) and cytoplasmic HSP accumulation in Xenopus laevis A6 kidney epithelial cells.
HSPs↑,
GRP94↑, WA induced the accumulation of HSPs including ER chaperones, BiP and GRP94, as well as cytoplasmic/nuclear HSPs, HSP70 and HSP30.
Akt↑, WA-induced an increase in the relative levels of the protein kinase, Akt,
eff↑, WA acted synergistically with mild heat shock to enhance HSP70 and HSP30 accumulation to a greater extent than the sum of both stressors individually
HSP70/HSPA5↑, WA Induced Accumulation of BiP, GRP94, HSP70 and HSP30

4678-

Ash,

Identification of Withaferin A as a Potential Candidate for Anti-Cancer Therapy in Non-Small Cell Lung Cancer

vitro+vivo,

NSCLC,

H1975

ROS↑, WA concurrently induced autophagy and apoptosis and the activation of reactive oxygen species (ROS), which plays an upstream role in mediating WA-elicited effects.
AntiTum↑, In vivo research also demonstrated the anti-tumor effect of WA treatment
CSCs↓, We subsequently demonstrated that WA could inhibit the growth of lung CSCs, decrease side population cells, and inhibit lung cancer spheroid-forming capacity
mTOR↓, at least through downregulation of mTOR/STAT3 signaling
STAT3↓,
ChemoSen↑, combination of WA and chemotherapeutic drugs, including cisplatin and pemetrexed, exerted synergistic effects on the inhibition of epidermal growth factor receptor (EGFR) wild-type lung cancer cell viability.
Keap1↑, Interestingly, we found WA treatment gradually increased KEAP1, while it decreased NRF2 in H1975 cells
NRF2↓,

4819-

ASTX,

Astaxanthin Induces Apoptosis in MCF-7 Cells through a p53-Dependent Pathway

in-vitro,

BC,

MCF-7

5, 10, 25, 50, 75, 100, 125, and 150 μg/mL)

IC50 = 89.742 μg/mL

antiOx↑, It is well known that AXT plays a role as a drug with antioxidant and antitumor properties
AntiTum↑,
TumCD↑, The treatment induced the decrease in cell number in a dose-dependent manner
P53↑, it was observed that the expression of p53 and p21 increased proportionally to the concentration of the AXT treatment.
P21↑,
Apoptosis↑, These findings suggest that the apoptosis of MCF-7 cells induced by AXT operates through a p53-dependent pathway, implying that AXT could potentially have a beneficial role in future breast cancer treatments.
Dose↝, Treatment with 50 μg/mL of AXT led to a viability of the tumor cell of approximately 30% after 48 h.
Casp3↑, The results indicated that caspase-3 activity increased following AXT treatment, reaching a maximum at 48 h post treatment

4818-

ASTX,

MEL,

Effect of astaxanthin and melatonin on cell viability and DNA damage in human breast cancer cell lines

in-vitro,

BC,

MDA-MB-231

in-vitro,

BC,

T47D

in-vitro,

Nor,

MCF10

TumCD↑, Astaxanthin increases the melatonin-induced cell death in breast cancer cells
DNAdam↑, Astaxanthin-melatonin combination and DNA damages in breast cancer cells
*antiOx↑, strong anti-oxidative, anti-tumoral, and anti-inflammatory effects.
*AntiTum↑,
Inflam↓,
tumCV↓, Astaxanthin at lower doses than melatonin reduced cell viability and Bcl2 expression, induced apoptosis and DNA damage in MDA-MB-231 and T47D.
Bcl-2↓,
Apoptosis↓,
selectivity↑, Meanwhile, the effects of astaxanthin on cell cytotoxicity, apoptosis, and DNA damage in MCF10A cells are insignificant compared to MDA-MB-231 and T47D.
eff↑, Furthermore, the presence of astaxanthin increased the function of melatonin-induced cell death in breast cancer cells.
Dose↓, The results showed that very low doses of astaxanthin reduced survival rate, induced apoptosis, reduced the expression of Bcl2 proteins, and destroyed the DNA in cancerous cells

4804-

ASTX,

Astaxanthin in cancer therapy and prevention (Review)

Review,

Var,

Review,

AD,

*antiOx↑, gained significant attention for its potent antioxidant, anti-inflammatory and anti-proliferative properties.
*Inflam↓,
ChemoSen⇅, In some instances, it reduces the cytotoxicity of cisplatin, particularly with cisplatin on the SKBR3 breast cancer cell line, indicating a potential protective effect. In certain cases, AXT enhances the cytotoxic effect of the chemotherapy drugs
chemoP↑, The present review detailed both in vitro and in vivo studies highlighting the effectiveness of AXT in sensitizing cancer cells to chemotherapy, thereby enhancing therapeutic outcomes and potentially reducing treatment-related side effects.
BioAv↑, incorporation of AXT in nanoparticle-based delivery systems has further improved its bioavailability
TumCP↑, AXT exhibits hormetic effects on U251-MG, T98G and CRT-MG cell lines, where low doses stimulate cell proliferation
ROS⇅, while higher doses induce apoptosis by triggering a dose-dependent oxidative stress response, significantly increasing reactive oxygen species (ROS) levels and promoting apoptosis
Apoptosis↑,
PI3K↑, AXT activates the PI3K/Akt/GSK3β pathway, leading to the upregulation of nuclear factor erythroid 2-related factor 2 (Nrf2), a transcription factor, in SH-SY5Y cells under oxygen and glucose deprivation conditions
Akt↑,
GSK‐3β↑,
NRF2↑,
AntiCan↑, antioxidant, AXT has the potential to act as both an anticancer drug and a neuroprotectant.
*neuroP↑, AXT protects against oxidative stress, which causes mitochondrial dysfunction and apoptosis, thereby reducing the detrimental effects associated with neurodegenerative diseases such as Alzheimer's, Parkinson's
eff↑, The synergistic cytotoxic effect of AXT with melatonin showed enhanced efficacy in the T47D cell line compared with the MDA-MB-231 line
AntiTum↑, AXT effectively reduced tumor size and the number of cancer cells in mice, supporting its potential anti-tumor activity.

4813-

ASTX,

Astaxanthin Prevents Oxidative Damage and Cell Apoptosis Under Oxidative Stress Involving the Restoration of Mitochondrial Function

in-vitro,

AD,

*antiOx↑, Astaxanthin (ASTA), a natural compound known for its potent antioxidant properties, shows the biological activities in anti-apoptosis and antitumor.
*Apoptosis↓,
*AntiTum↑,
*ROS↓, ASTA significantly reduced H2O2-induced mitochondrial dysfunctions and restored the intracellular reactive oxygen species (ROS), mitochondrial membrane potential, and respiratory capacity.
*MMP↑, Astaxanthin depresses oxidative stress-induced depolarization of mitochondrial membrane potential and restores the mitochondrial respiratory capacity.
*neuroP↑, Oxidative stress (OS) is one of the factors that result in cell damage and the development of neurological diseases such as Alzheimer's disease (AD).

5424-

ASTX,

Astaxanthin exerts an adjunctive anti-cancer effect through the modulation of gut microbiota and mucosal immunity

in-vivo,

Nor,

mice

*GutMicro↑, Astaxanthin synergistically enhances the anticancer effects of sorafenib by modulating intestinal flora.
AntiCan↑,
eff↑, Astaxanthin significantly promotes the proliferation of Akkermansia, a microorganism with enhanced anti-tumor immune effects.
AntiTum↑, Therefore, it strengthens the body's anti-tumor immune response and synergistically boosts the therapeutic efficacy of drugs.
ChemoSen↑,

5448-

ATV,

Beyond cardiovascular health: The pharmacotherapeutic potential of statins in oncology

Review,

Var,

Apoptosis↑, Despite statins’ ability to induce apoptosis or autophagy, arrest cell cycle, or modulate favorable epigenetic reprogramming, their efficacy is highly context-dependent
TumAuto↑,
TumCCA↑,
BioAv↓, Challenges such as statin resistance, low bioavailability and pharmacokinetic variability further complicate their application in oncology.
eff↑, including nanoparticle-based drug delivery systems and combination therapies with chemotherapy, radiotherapy or immunotherapy, appear to help overcome these limitations.
HMGCR↓, statins reduce cholesterol levels by targeting HMGCR
LDL↓,
cardioP↑, statins have become a cornerstone in the management of hypercholesterolemia and the prevention of cardiovascular diseases [23], [24], [25], [26].
AntiTum↑, Notably, while research suggests that statins possess anti-tumor effects, evidence remains conflicting and highly context-dependent
ChemoSen↑, suggest that statins can sensitize cancer cells to chemotherapy and radiotherapy, potentially improving treatment outcomes,
RadioS↑,
toxicity↓, Statins are widely regarded as safe and well-tolerated. However, like any medication, they are not without potential side effects, though these are generally mild [232].

5364-

AV,

A New Biomaterial Derived from Aloe vera—Acemannan from Basic Studies to Clinical Application

Review,

Var,

BioAv↑, Acemannan (AC) is considered to be a natural polysaccharide with good biodegradability and biocompatibility extracted from Aloe vera
AntiTum↑, AC has the potential to treat various diseases, such as oral diseases, systemic metabolic diseases, cardiovascular system diseases, and benign and malignant tumors [12].
cardioP↑,

5365-

AV,

Aloe Vera Polysaccharides as Therapeutic Agents: Benefits Versus Side Effects in Biomedical Applications

Review,

Nor,

Review,

IBD,

Review,

Diabetic,

*Wound Healing↑, Traditionally recognized for its anti-inflammatory and antimicrobial effects, which are very important in wound healing, the Aloe Vera relies on its polysaccharides
*Imm↑, which confer immunomodulatory, antioxidant, and tissue-regenerative properties.
*antiOx↑,
*AntiDiabetic↑, graphical abstract
*AntiCan↑,
*Inflam↓, The anti-inflammatory properties of Aloe Vera polysaccharides are primarily mediated through the inhibition of key inflammatory pathways.
*NF-kB↓, Acemannan and other polysaccharides suppress the activation of nuclear factor-kappa B (NF-κB), a transcription factor that regulates the expression of pro-inflammatory genes.
*COX2↓, By inhibiting NF-κB [48,49], Aloe Vera polysaccharides reduce the production of cyclooxygenase-2 (COX-2) and lipoxygenase (LOX),
*5LO↓,
*IL1β↓, Aloe Vera polysaccharides downregulate the expression of pro-inflammatory cytokines like IL-1β, IL-6, and TNF-α, while upregulating anti-inflammatory cytokines such as IL-10
*IL6↓,
*TNF-α↓,
*IL10↑,
*other↓, This dual action helps to mitigate inflammation in conditions such as arthritis, dermatitis, and inflammatory bowel disease (IBD)
*ROS↓, Aloe Vera polysaccharides exhibit potent antioxidant activity by scavenging reactive oxygen species (ROS) and free radicals,
*SOD↑, The polysaccharides enhance the activity of endogenous antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), which neutralize oxidative stress and protect cells from damage [17,63].
*Catalase↑,
*GPx↑,
*lipid-P↓, This property is particularly beneficial in preventing lipid peroxidation, DNA damage, and protein oxidation, processes associated with chronic diseases and aging
*DNAdam↓,
*GutMicro↑, Aloe Vera polysaccharides support gastrointestinal health, acting as prebiotics and promoting the growth of beneficial gut microbiota such as Lactobacillus and Bifidobacterium species [64].
*ZO-1↑, enhance the integrity of the intestinal epithelial barrier by upregulating the expression of tight junction proteins such as occludin and zonula occludens-1 (ZO-1) [51,54].
AntiTum↑, Certain polysaccharides in Aloe Vera, including acemannan, have demonstrated antitumoral effects by inducing apoptosis (programmed cell death) in cancer cells.
Casp3↑, This is achieved through the activation of caspase-3 and caspase-9, key enzymes in the apoptotic pathway [45,48].
Casp9↑,
angioG↓, Aloe Vera polysaccharides also inhibit angiogenesis and metastasis by downregulating matrix metalloproteinases (MMPs) and VEGF [75].
MMPs↓,
VEGF↓,
NK cell↑, Moreover, these polysaccharides enhance the immune system’s ability to recognize and destroy cancer cells through stimulating natural killer (NK) cells and cytotoxic T lymphocytes (CTLs) [43,55].

5577-

B-Gluc,

Lentinan progress in inflammatory diseases and tumor diseases

Review,

Var,

Review,

IBD,

AntiTum↑, LNT are macromolecules with a β-1,3-D-glucan and its unique molecular structure is closely related to its pharmacological activity, and the glucan of the β-glycosidic bond is the key structure for its antitumor function [6, 7].
GutMicro↑, LNT could also improve the imbalance of gut microbial colonies [25].
*Inflam↓, LNT exerts its anti-inflammatory effect by downregulating cell surface TNFR1 to inhibit TNF-α-induced NF-κB activation
*TNF-α↓,
*NF-kB↓,
ChemoSen↑, LNT combined with cisplatin can not only reduce the dose of cisplatin, but also promote the activation of the intrinsic apoptosis pathway through the regulation of signals, leading to apoptosis of liver cancer cells
OS↑, LNT combined with pentafluorouracil improved survival time for advanced gastric cancer, which is consistent with the results of a meta-study of five randomized controlled trials [78, 79].
Imm↑, Although LNT has been approved in Japan as an immune agent for chemotherapy in gastric cancer
IL6↓, significantly enhance the immune function of CD4 cells, increase NK cells and reduce IL-6 levels
ERK↓, Studies have shown that LNT can inhibit the ERK/MAPK signaling pathway by regulating miR-340, thereby promoting apoptosis in osteosarcoma cells
MAPK↓,
*antiOx↑, LNT is an shiitake extract with anti-inflammatory, antioxidant, anti-tumor and other biological activities and functions.
eff↑, Furthermore,studies also found that LNT selenium nanoparticles can promote apoptosis by acting on specific signaling pathways [96, 97].

5580-

B-Gluc,

Lentinan, a Shiitake Mushroom β-Glucan, Downregulates the Enhanced PD-L1 Expression Induced by Platinum Compounds in Gastric Cancer Cells

in-vitro,

GC,

MKN45

PD-L1↓, lentinan treatment inhibited the platinum drug-stimulated expression of PD-L1 in gastric cancer cells mainly by suppressing MAPK signaling
MAPK↓,
OS↑, Lentinan has been reported to improve the overall survival of cancer patients receiving chemotherapy [23, 24] through its antitumor and immunomodulatory activitie
AntiTum↑,
Imm↑,

876-

B-Gluc,

Clinical and Physiological Perspectives of β-Glucans: The Past, Present, and Future

Review,

NA,

AntiTum↑,

5501-

Ba,

Therapeutic effects and mechanisms of action of Baicalein on stomach cancer: a comprehensive systematic literature review

Review,

GC,

AntiCan↑, The review demonstrated that BC exerts therapeutic effects on GC through multiple biochemical mechanisms.
Apoptosis↑, BC plays an important role in inducing apoptosis, inhibiting cell proliferation, and suppressing metastasis in GC cells.
TumCP↓,
TumMeta↓,
BAX↑, graphical abstract
TumAuto↑,
ROS↑,
NRF2↝, BC induced apoptosis and autophagy in MGC-803, SGC-7901, and HGC-27 cells, enhancing cisplatin sensitivity via suppression of the AKT/mTOR pathway and modulation of the Nrf2/Keap1 axis.
PI3K↓,
Akt↓,
NF-kB↓,
TGF-β↓,
SMAD4↓,
GPx4↓, It induces autophagy and ferroptosis, partly through p53 activation and suppression of SLC7A11/GPX4, and disrupts mitochondrial membrane potential via reactive oxygen species (ROS) generation [31, 37]
MMP↓,
*HO-1↑, BC stabilizes Nrf2, leading to the induction of antioxidant enzymes such as HO-1, GST, and NQO1, which mitigate oxidative stress and contribute to its antitumor effects [38].
*GSTs↑,
*antiOx↑,
*AntiTum↑,
*NRF2↑,
ChemoSen↑, BC induced apoptosis and autophagy in MGC-803, SGC-7901, and HGC-27 cells, enhancing cisplatin sensitivity via suppression of the AKT/mTOR pathway and modulation of the Nrf2/Keap1 axis.
Akt↓,
mTOR↓,
FAK↓, reducing FAK expression
Ki-67↓, Immunohistochemical analysis also revealed lower Ki-67 levels, indicating reduced cellular proliferation.

5251-

Ba,

The Fascinating Effects of Baicalein on Cancer: A Review

Review,

Var,

AntiTum↑, The anti-tumor functions of baicalein are mainly due to its capacities to inhibit complexes of cyclins to regulate the cell cycle, to scavenge oxidative radicals, to attenuate mitogen activated protein kinase (MAPK), protein kinase B (Akt) or mammali
TumCCA↓,
ROS↓,
MAPK↓,
Akt↓,
mTOR↓,
Casp3↑, , to induce apoptosis by activating caspase-9/-3 and to inhibit tumorinvasion and metastasis by reducing the expression of matrix metalloproteinase-2/-9 (MMP-2/-9).
Casp9↑,
TumCI↓,
TumMeta↓,
MMP2↓,
MMP9↓,
Securin↓, Baicalein also induced cell death by reducing the expression of securin, while also inhibiting cancer cell death by affecting the expression of p-AKT and γ-H2AX [26].
γH2AX↝,
N-cadherin↓, Baicalein also decreased the expression of metastasis-associated molecules, including N-cadherin, vimentin, ZEB1, and ZEB2.
Vim↓,
Zeb1↓,
ZEB2↓,
TumCMig↓, researchers demonstrated that baiclalein inhibited cellular adhesion, migration, invasion, and growth of HCC cells both in vitro and in vivo.
TumCG↑,
12LOX↓, Baicalein is an inhibitor of 12-LOX and induced apoptosis, morphological changes, and carbonic anhydrase expression in PaCa cells.
DR5↑, Baicalein lessened this resistance to TRAIL by upregulating DR5 expression and promoting the expression of ROS, thus causing TRAIL sensitization in PC3 cells [85]
ROS↑,
RadioS↑, baicalein increased the sensitivity of prostate cancer cells to radiation without affecting this sensitivity in normal cells
ChemoSen↑, Combination therapy of baicalein with paclitaxel, which were assembled by nanoparticles, was demonstrated to have synergistic anticancer effects in A549 lung cancer cells and in mice bearing A549/PTX drug-resistant lung cancer xenografts [97].
BioAv↓, It is worth noting that the bioavailability of baicalein in vivo remains low.

2022-

BBR,

GoldNP,

Rad,

Berberine-loaded Janus gold mesoporous silica nanocarriers for chemo/radio/photothermal therapy of liver cancer and radiation-induced injury inhibition

in-vitro,

Liver,

SMMC-7721 cell

in-vitro,

Nor,

HL7702

*toxicity↓, Berberine (Ber), an isoquinolin alkaloid with low toxicity and protective effects against radiotherapy
radioP↑,
BioAv↑, We preloaded Ber into folic acid targeting Janus gold mesoporous silica nanocarriers (FA-JGMSNs) for overcoming the poor bioavailability of Ber.
AntiTum↑, highly efficient anti-tumor effect, good biosafety
selectivity↑, as well as the effective protection of normal tissue of this nanoplatform.
eff↑, These selective distributions of Ber in cancer cells and normal cells originated from selective endocytosis as well as pH-responsive drug release, which were conducive to achieving an improved therapeutic effect of Ber.
chemoP↑, Notably, chemo/radio/photothermal therapeutics didn’t cause the amounts of deaths of HL-7702 cells, indicating an excellent biosafety of the triple-model therapy.

2674-

BBR,

Berberine: A novel therapeutic strategy for cancer

Review,

Var,

Review,

IBD,

Inflam↓, anti-inflammatory, antidiabetic, antibacterial, antiparasitic, antidiarrheal, antihypertensive, hypolipidemic, and fungicide.
AntiCan↑, elaborated on the anticancer effects of BBR through the regulation of different molecular pathways such as: inducing apoptosis, autophagy, arresting cell cycle, and inhibiting metastasis and invasion.
Apoptosis↑,
TumAuto↑,
TumCCA↑,
TumMeta↓,
TumCI↓,
eff↑, BBR is shown to have beneficial effects on cancer immunotherapy.
eff↑, BBR inhibited the release of Interleukin 1 beta (IL-1β), Interferon gamma (IFN-γ), Interleukin 6 (IL-6), and Tumor Necrosis Factor-alpha (TNF-α) from LPS stimulated lymphocytes by acting as a dopamine receptor antagonist
CD4+↓, BBR inhibited the proliferation of CD4+ T cells and down-regulated TNF-α and IL-1 and thus, improved autoimmune neuropathy.
TNF-α↓,
IL1↓,
BioAv↓, On the other hand, P-Glycoprotein (P-gp), a secretive pump located in the epithelial cell membrane, restricts the oral bioavailability of a variety of medications, such as BBR. The use of P-gp inhibitors is a common and effective way to prevent this
BioAv↓, Regardless of its low bioavailability, BBR has shown great therapeutic efficacy in the treatment of a number of diseases.
other↓, BBR has been also used as an effective therapeutic agent for Inflammatory Bowel Disease (IBD) for several years
AMPK↑, inhibitory effects on inflammation by regulating different mechanisms such as 5′ Adenosine Monophosphate-Activated Protein Kinase (AMPK. Increase of AMPK
MAPK↓, Mitogen-Activated Protein Kinase (MAPK), and NF-κB signaling pathways
NF-kB↓,
IL6↓, inhibiting the expression of proinflammatory genes such as IL-1, IL-6, Monocyte Chemoattractant Protein 1 (MCP1), TNF-α, Prostaglandin E2 (PGE2), and Cyclooxygenase-2 (COX-2)
MCP1↓,
PGE2↓,
COX2↓,
*ROS↓, BBR protected PC-12 cells (normal) from oxidative damage by suppressing ROS through PI3K/AKT/mTOR signaling pathways
*antiOx↑, BBR therapy improved the antioxidant function of mice intestinal tissue by enhancing the levels of glutathione peroxidase and catalase enzymes.
*GPx↑,
*Catalase↑,
AntiTum↑, Besides, BBR leaves great antitumor effects on multiple types of cancer such as breast cancer,69 bladder cancer,70 hepatocarcinoma,71 and colon cancer.72
TumCP↓, BBR exerts its antitumor activity by inhibiting proliferation, inducing apoptosis and autophagy, and suppressing angiogenesis and metastasis
angioG↓,
Fas↑, by increasing the amounts of Fas receptor (death receptor)/FasL (Fas ligand), ROS, ATM, p53, Retinoblastoma protein (Rb), caspase-9,8,3, TNF-α, Bcl2-associated X protein (Bax), BID
FasL↑,
ROS↑,
ATM↑,
P53↑,
RB1↑,
Casp9↑,
Casp8↑,
Casp3↓,
BAX↑,
Bcl-2↓, and declining Bcl2, Bcl-X, c-IAP1 (inhibitor of apoptosis protein), X-linked inhibitor of apoptosis protein (XIAP), and Survivin levels
Bcl-xL↓,
IAP1↓,
XIAP↓,
survivin↓,
MMP2↓, Furthermore, BBR suppressed Matrix Metalloproteinase-2 (MMP-2), and MMP-9 expression.
MMP9↓,
CycB/CCNB1↓, Inhibition of cyclin B1, cdc2, cdc25c
CDC25↓,
CDC25↓,
Cyt‑c↑, BBR inhibited tumor cell proliferation and migration and induced mitochondria-mediated apoptosis pathway in Triple Negative Breast Cancer (TNBC) by: stimulating cytochrome c release from mitochondria to cytosol
MMP↓, decreased the mitochondrial membrane potential, and enabled cytochrome c release from mitochondria to cytosol
RenoP↑, BBR significantly reduced the destructive effects of cisplatin on the kidney by inhibiting autophagy, and exerted nephroprotective effects.
mTOR↓, U87 cell, Inhibition of m-TOR signaling
MDM2↓, Downregulation of MDM2
LC3II↑, Increase of LC3-II and beclin-1
ERK↓, BBR stimulated AMPK signaling, resulting in reduced extracellular signal–regulated kinase (ERK) activity and COX-2 expression in B16F-10 lung melanoma cells
COX2↓,
MMP3↓, reducing MMP-3 in SGC7901 GC and AGS cells
TGF-β↓, BBR suppressed the invasion and migration of prostate cancer PC-3 cells by inhibiting TGF-β-related signaling molecules which induced Epithelial-Mesenchymal Transition (EMT) such as Bone morphogenetic protein 7 (BMP7),
EMT↑,
ROCK1↓, inhibiting metastasis-associated proteins such as ROCK1, FAK, Ras Homolog Family Member A (RhoA), NF-κB and u-PA, leading to in vitro inhibition of MMP-1 and MMP-13.
FAK↓,
RAS↓,
Rho↓,
NF-kB↓,
uPA↓,
MMP1↓,
MMP13↓,
ChemoSen↑, recent studies have indicated that it can be used in combination with chemotherapy agents

5584-

BetA,

Betulinic acid induces apoptosis through a direct effect on mitochondria in neuroectodermal tumors

in-vitro,

GBM,

A172

in-vitro,

GBM,

U118MG

in-vitro,

GBM,

U251

Apoptosis↑, BetA induced apoptosis by a direct effect on mitochondria independent of accumulation of wild-type p53 protein and independent of death-inducing ligand/receptor systems such as CD95.
P53↑,
Cyt‑c↑, release of soluble apoptogenic factors such as cytochrome c or AIF from mitochondria into the cytosol, where they induced activation of caspases.
AIF↑,
Casp↑,
AntiTum↑, BetA exhibited potent antitumor activity on neuroblastoma cells resistant to CD95- or doxorubicin-triggered apoptosis and on primary tumor cells from patients with neuroectodermal tumors.
MMP↓, BetA resulted in loss of the mitochondrial membrane potential

2724-

BetA,

Down-regulation of NOX4 by betulinic acid protects against cerebral ischemia-reperfusion in mice

in-vivo,

Nor,

mice

in-vivo,

Stroke,

AntiTum↑, Betulinic acid is mainly known for its anti-tumor and anti-inflammatory activities.
*Inflam↓,
*ROS↓, Our previous study showed that betulinic acid could decrease the reactive oxygen species (ROS) production by regulating the expression of NADPH oxidase.
*NOX4↓, Pre-treatment with betulinic acid (50 mg/kg/day for 7 days via gavage) prior to MCA occlusion prevented the ischemia/reperfusion-induced up-regulation of NOX4 and ROS production.
*Apoptosis↓, treatment with betulinic acid could markedly blunt the ischemia/reperfusion-induced neuronal apoptosis
neuroP↑, betulinic acid protects against cerebral ischemia/reperfusion injury in mice

2760-

BetA,

A Review on Preparation of Betulinic Acid and Its Biological Activities

Review,

Var,

Review,

Stroke,

AntiTum↑, BA is considered a future promising antitumor compound
Cyt‑c↑, BA stimulated mitochondria to release cytochrome c and Smac and cause further apoptosis reactions
Smad1↑,
Sepsis↓, Administration of 10 and 30 mg/kg of BA significantly improved survival against sepsis and attenuated lung injury.
NF-kB↓, BA inhibited nuclear factor-kappa B (NF-κB) expression in the lung and decreased levels of cytokine, intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1 (MCP-1) and matrix metalloproteinase-9 (MMP-9)
ICAM-1↓,
MCP1↓,
MMP9↓,
COX2↓, In hPBMCs, BA suppressed cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PEG2) production by inhibiting extracellular regulated kinase (ERK) and Akt phosphorylation and thereby modulated the NF-κB signaling pathway
PGE2↓,
ERK↓,
p‑Akt↓,
*ROS↓, BA significantly decreased the mortality of mice against endotoxin shock and inhibited the production of PEG2 in two of the most susceptible organs, lungs and livers [80]. Moreover, BA reduced reactive oxygen species (ROS) formation
*LDH↓, and the release of lactate dehydrogenase
*hepatoP↑, hepatoprotective effect of BA from Tecomella undulata.
*SOD↑, Pretreatment of BA prevented the depletion of hepatic antioxidants superoxide dismutase (SOD) and catalase (CAT), reduced glutathione (GSH) and ascorbic acid (AA) and decreased the CCl4-induced LPO level
*Catalase↑,
*GSH↑,
*AST↓, A also attenuated the elevation of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) plasma level,
*ALAT↓,
*RenoP↑, BA also exhibits renal-protective effects. Renal fibrosis is an end-stage renal disease symptom that develops from chronic kidney disease (CKD).
*ROS↓, BA protected against this ischemia-reperfusion injury in a mice model by enhancing blood flow and reducing oxidative stress and nitrosative stress
*α-SMA↓, Moreover, BA reduced the expression of α-smooth muscle actin (α-SMA) and collagen-I

5718-

BF,

Bufalin inhibits CYP3A4 activity in vitro and in vivo

in-vivo,

Nor,

Wistar rats

CYP3A4↓, Bufalin showed a modest but significant inhibition of CYP3A4 both in vitro and in vivo.
Apoptosis↑, Bufalin has been shown to induce apoptosis in human leukemia HL-60 cells and human tumor cells12, 13, 14, 15, 16, 17, 18.
AntiTum↑, In conclusion, the present study demonstrates that bufalin, which has been reported to exhibit significant anti-tumor activity12, 13, 14, 15, 16, 17, 18,

5628-

Bif,

immuno,

Bifidobacterium modulation of tumor immunotherapy and its mechanism

Review,

Var,

Imm↑, his review will focus on the immunomodulatory effects of Bifidobacteria in malignancies and the possible mechanisms of action of Bifidobacteria on immunotherapy
Risk↓, Bifidobacteria have a role in the prevention of intestinal cancer in healthy intestinal microbiota by influencing intestinal probiotics metabolism and enhancing the host immune response;
GutMicro↑,
AntiTum↑, Bifidobacteria has been shown to positively induce an anti-tumor immune response [32].
OS↑, Bifidobacterium longum 420 significantly increased the survival of mice carrying renal cell carcinoma tumors treated with anti-PD-1 and anti-CTLA-4 antibodies
selectivity↑, Bifidobacteria have been shown to selectively accumulate in tumors upon entry into the blood stream, possibly due to the hypoxic microenvironment’s
eff↑, (e.g., probiotic strains such as Bifidobacterium bifidum) to enhance the efficacy of cancer immunotherapy is still in its infancy,

5629-

Bif,

ProBio,

Gut microbiota shapes cancer immunotherapy responses

Review,

Var,

eff↑, oral administration of Bifidobacterium enhanced the anti-tumor efficacy of PD-L1 inhibitors by promoting dendritic cell (DC) maturation and increasing tumor-specific CD8 + T cell activity.
DCells↑,
CD8+↑,
eff↑, One study analyzing plasma samples from colorectal cancer (CRC) patients treated with ACT and chemotherapy found that responders had significantly higher blood levels of Bifidobacterium, Lactobacillus, and Enterococcus, indicating that the blood micr
AntiTum↑, Inosine, a purine metabolite produced by Akkermansia muciniphila and Bifidobacterium longum, enhances antitumor immunity by inhibiting UBA6 expression in tumor cells,
other↑, Likewise, vitamin B6, synthesized by Lactobacillus acidophilus and Bifidobacterium bifidum, boosts T lymphocyte proliferation and promotes antitumor immunity by stimulating T cell activity
selectivity↑, Additionally, Bifidobacterium preferentially accumulates in tumors . Bifidobacterium, for example, migrates to colonize and enrich CRC tumors198
GutMicro↑, Microbiome analysis revealed enrichment of beneficial bacteria (Bifidobacterium longum, Lachnospiraceae, Ruminococcaceae) and a decline in potentially detrimental species such as Bacteroides.

5686-

BJ,

BRU,

A review of Brucea javanica: metabolites, pharmacology and clinical application

Review,

Var,

AntiTum↑, Notably, multiple metabolites in BJ demonstrate anti-tumor effects through various signaling pathways
other↝, well-known metabolites such as Brusatol and Bruceine D.
ChemoSen↑, Multiple clinical studies have demonstrated that the co-administration of BJ with other pharmacological agents in individuals with cancer can enhance therapeutic efficacy, improve patients’ quality of life, and mitigate adverse reactions
QoL↑,
chemoP↑,
*Inflam↓, Brusatol (Zhou et al., 2018) has been shown to reduce inflammation in RAW264.7 cells
NF-kB↓, nhibition of NF-ΚB and ras homolog gene families, member A/rho-associated kinase (RhoA/ROCK) signaling pathways.
TumCP↓, Brusatol has exhibited notable effects in inhibiting proliferation, invasion, and metastasis in a murine model of liver transplantation tumor in humans.
TumCI↓,
TumMeta↓,
Hif1a↓, In colorectal cancer, Brusatol functions by facilitating the degradation process of hypoxia-inducible factor-1 (HIF-1α) (Oh et al., 2017), mediated by prolyl hydroxylase (PHD), while concurrently suppressing NRF2
NRF2↓,
STAT3↓, impede the proliferation and migration of osteosarcoma cells through the inhibition of the STAT3 signaling pathway.
COX2↓, BJO (Lou et al., 2010) induced apoptosis of T24 bladder cancer cells, possibly by upregulating caspase-3 and caspase-9 expression by activating the caspase pathway and inhibiting the NF-ΚB and Cyclooxygenase-2 (COX-2).
Casp3↑,
Casp9↑,
ROS↑, Figure 10
EGFR↓,
NRF2↑, brusatol and dehydrobruceine B (DHB) effectively increased the concentration of reactive oxygen species (ROS) by activating the NRF2 pathway

5690-

BJ,

BRU,

Brusatol: A potential sensitizing agent for cancer therapy from Brucea javanica

Review,

Var,

NRF2↓, Brusatol is a potent Nrf2 inhibitor for future cancer treatment.
TumCG↓, Brusatol exhibits significant tumor inhibition in multiple cancers.
ChemoSen↑, also exhibits significant synergistic antitumor effects in combination with chemotherapeutic agents
ROS↑, Graphical Abstract
NF-kB↓,
Akt↓,
mTOR↓,
TumCCA↑,
Apoptosis↑,
PARP↑,
Casp↑,
P53↓,
Bcl-2↓,
PI3K↓,
JAK2↓,
EMT↓,
p27↑,
ROCK1↓,
MMP2↓,
MMP9↓,
NRF2↓, which is the reason why brusatol is called an Nrf2 inhibitor [15]. Brusatol is a potent Nrf2 inhibitor
AntiTum↑, Brusatol shows significant antitumor effects in vitro and in vivo
HO-1↓, Moreover, brusatol inhibited the expression of Nrf2 downstream genes, such as HO-1 [19], [31], [32], NQO1 [43], [44], VEGF [45], and AKR1C1 [46].
NQO1↓,
VEGF↓,
MRP1↓, brusatol reduced both the mRNA and protein levels of NQO1, HO-1, MDR1, and MRP5
RadioS↑, Improvement of sensitivity to radiotherapy and phototherapy
PhotoS↑,
toxicity↝, the toxicity of brusatol is a problem that can not be ignored.

2024-

Bos,

Antiproliferative and cell cycle arrest potentials of 3-O-acetyl-11-keto-β-boswellic acid against MCF-7 cells in vitro

in-vitro,

BC,

MCF-7

 101.1

in-vitro,

Nor,

MCF10

275.2

MMP↓, mitochondrial membrane potential (ΔΨm) was reduced by increasing AKBA concentration with a significant release of cytochrome c.
Cyt‑c↑,
ROS↑, A significant increase in reactive oxygen species formation was observed. Compared with the untreated control, 1.32-, 1.61- and 2.44-fold ROS generation increases were achieved following 50, 100 and 200 µg mL−1 AKBA
Casp8↑, activated the production of caspase 8 and caspase 9 in a dose-dependent pattern
Casp9↑,
AntiTum↑, antitumoral activity against MCF-7 cells in a dose-dependent pattern with a reduction rate of 21.65 ± 6.63, 32.37 ± 6.97, 54.29 ± 5.35 and 61.42 ± 4.14% for the concentrations 50, 100, 200 and 400 µg mL−1, respectively
selectivity↑, cell inhibition rate with calculated IC50 of 101.1 and 275.2 for MCF-7 and MCF-10A, respectively
TumCCA↑, finally arrested the MCF-7 cell cycle at the G1 phase.

5702-

BRU,

BJ,

Brusatol inhibits metastasis of triple-negative breast cancer through metabolic reprogramming

in-vitro,

BC,

AntiTum↑, Brusatol (BRU), a natural compound with reported anti-tumor activity and low toxicity, has not been explored in the context of cancer metastasis or metabolic reprogramming.
PPP↓, BRU inhibited metabolic pathways, including the pentose phosphate pathway (PPP), glycolysis, and the tricarboxylic acid (TCA) cycle, while significantly reducing NADPH levels and exacerbating redox stress.
Glycolysis↓,
TCA↓,
NADPH↓,
ROS↑, levated levels of reactive oxygen species (ROS)
chemoP↑, enhance anti-tumor efficacy while reducing chemotherapy-associated toxicity.
e-LDH↑, BRU treatment further enhanced extracellular LDH activity in matrix-detached cells in a concentration-dependent manner
TumMeta↓, Brusatol inhibits TNBC metastasis
Glycolysis↓, BRU extensively inhibits glycolytic capacity in ECM-detached cells under metabolic stress

2047-

Buty,

Sodium butyrate inhibits migration and induces AMPK-mTOR pathway-dependent autophagy and ROS-mediated apoptosis via the miR-139-5p/Bmi-1 axis in human bladder cancer cells

in-vitro,

CRC,

T24/HTB-9

0-10mM

in-vitro,

Nor,

SV-HUC-1

in-vitro,

Bladder,

5637

in-vivo,

NA,

200 mg/kg/day, i.g., n = 5

mice

HDAC↓, Sodium butyrate (NaB) is a histone deacetylase inhibitor and exerts remarkable antitumor effects in various cancer cells
AntiTum↑,
TumCMig↓, NaB inhibited migration
AMPK↑, induced AMPK/mTOR pathway-activated autophagy and reactive oxygen species (ROS) overproduction via the miR-139-5p/Bmi-1 axis
mTOR↑,
TumAuto↑,
ROS↑, NaB initiates ROS overproduction
miR-139-5p↑, NaB upregulates miR-139-5p and depletes Bmi-1 in bladder cancer cells
BMI1↓,
TumCI?, NaB significantly inhibited cell migration dose-dependently
E-cadherin↑, E-cadherin was markedly increased, while the expression of N-cadherin, Vimentin, and Snail was decreased
N-cadherin↓,
Vim↓,
Snail↓,
cl‑PARP↑, increased expression levels of cleaved PARP, cleaved caspase-3, and Bax and the concurrent decrease in Bcl-2 and Bcl-xl
cl‑Casp3↑,
BAX↑,
Bcl-2↓,
Bcl-xL↓,
MMP↓, impairs mitochondrial membrane potential
PINK1↑, activates the PINK1/ PARKIN pathway
PARK2↑,
TumMeta↓, NaB inhibits tumor metastasis and growth in vivo
TumCG↓,
LC3II↑, a significant increase in the levels of cleaved caspase3, p-AMPK, and LC3B-II along with decreased Bmi-1 and Vimentin
p62↓, elevated LC3B-II levels and degradation of p62
eff↓, NAC abolished the impairment of MMP and ROS overproduction. Interestingly, NAC also significantly inhibited apoptosis induced by NaB

1205-

Caff,

immuno,

Caffeine-enhanced anti-tumor activity of anti-PD1 monoclonal antibody

in-vivo,

Melanoma,

B16-F10

OS↑,
CD4+↑, increase in infiltration of CD4+ and CD8+ T lymphocytes into the B16F10 melanoma tumors.
CD8+↑,
AntiTum↑,
TNF-α↑, increased intra-tumoral TNF-α and IFN-γ levels
IFN-γ↑, increased intra-tumoral TNF-α and IFN-γ levels

2012-

CAP,

Capsaicin induces cytotoxicity in human osteosarcoma MG63 cells through TRPV1-dependent and -independent pathways

NA,

OS,

MG63

0-40 μM

20 μM

AntiTum↑, capsaicin induces apoptosis in various tumor cells as a mechanism of its anti-tumor activity
Apoptosis↑, capsaicin-induced apoptosis and the activation of transient receptor potential receptor vanilloid 1 (TRPV1) in a dose- and time-dependent manner in human osteosarcoma MG63 cells in vitro
TRPV1↑, TRPV1 activation is required for the capsaicin-induced overproduction of ROS and decrease in SOD activity
ROS↑, overproduction of reactive oxygen species (ROS)
SOD↓, decrease in superoxide dismutase (SOD) activity
AMPK↑, capsaicin induced the activation of adenosine 5ʹ-monophosphate-activated protein kinase (AMPK), p53 and C-jun N-terminal kinase (JNK)
P53↑,
JNK↑,
Bcl-2↓, decrease in the level of B-cell lymphoma 2 (Bcl-2)
Cyt‑c↑, increase in the levels of Cytochrome C
cl‑Casp3↑, cleaved-caspase-3
cl‑PARP↑, cleaved polyadenosine diphosphate-ribose polymerase (PARP) in a time-dependent manner following capsaicin treatment in MG63 cells
Ca+2↑, Once the channel is activated, it can enable the rapid increase of intracellular calcium (Ca2+) levels and initiate cell death
MMP↓, several independent studies have demonstrated that capsaicin disrupted MMP (Δψm)

2017-

CAP,

Spice Up Your Kidney: A Review on the Effects of Capsaicin in Renal Physiology and Disease

Review,

Var,

RenoP↑, observed experimental benefits in preventing acute kidney injury
AntiTum↑, anti-tumoral properties of capsaicin on different types of cancer cells are well-acknowledged
AMPK↑, activating the AMPK/mTOR
mTOR↑,
PD-1↓, capsaicin promotes the inhibition of the PD-L1/PD-1 checkpoint
PD-L1↓,

2020-

CAP,

Capsaicinoids and Their Effects on Cancer: The “Double-Edged Sword” Postulate from the Molecular Scale

Review,

Var,

AntiTum↑, highlighting its antitumor properties mediated by cytotoxicity and immunological adjuvancy against at least 74 varieties of cancer,
selectivity↑, while non-cancer cells tend to have greater tolerance
TRPV1↑, activation or phosphorylation of TRPV1
MMP↓, leads to cell membrane depolarization through the influx of Na2+ and Ca2+,
Ca+2↑,
ER Stress↑, endoplasmic reticulum stress [73], and the inhibition of angiogenesis
angioG↓,
Casp3?, increase in caspase-3 activation, PARP-1 cleavage
cl‑PARP↑,
selectivity↑, oxidative stress threshold reached by these could be potentially higher than that caused in normal cells (tNOX−) when exposed to CAP, possibly also contributing to the selectivity of its effects
ROS↑, increase in the production of reactive oxygen species (ROS),
*ROS∅, Remarkably, in this same work, cells derived from the normal epithelium of human pancreatic ducts (HPDE6-E6E7) showed high tolerance to the same treatment by keeping their ROS levels stable
selectivity↑, In this sense, non-transformed human astrocytes from a primary culture showed greater tolerance to CAP, as they did not experience any of the mentioned effects when exposed to the same treatment

Showing Research Papers: 1 to 50 of 126
Page 1 of 3 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 126

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

Bacteria↓, 1, CD8+↑, 2, Sepsis↓, 1,
Total Targets: 215

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 10, Catalase↑, 3, GPx↑, 2, GSH↑, 2, GSTs↑, 1, HO-1↑, 2, lipid-P↓, 1, MPO↓, 1, NOX4↓, 1, NRF2↑, 3, ROS↓, 7, ROS∅, 1, SOD↑, 4, TBARS↓, 1,

Mitochondria & Bioenergetics ⓘ

MMP↑, 1, mtDam↑, 1,

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1, LDH↓, 1,

Cell Death ⓘ

Apoptosis↓, 2, iNOS↓, 1,

Transcription & Epigenetics ⓘ

other↓, 1,

Protein Folding & ER Stress ⓘ

ER Stress↓, 1, HSP70/HSPA5↑, 1,

DNA Damage & Repair ⓘ

DNAdam↓, 2,

Migration ⓘ

5LO↓, 1, ZO-1↑, 1, α-SMA↓, 1,

Angiogenesis & Vasculature ⓘ

p‑eNOS↑, 1,

Immune & Inflammatory Signaling ⓘ

COX2↓, 1, IL10↑, 1, IL1β↓, 1, IL6↓, 1, Imm↑, 2, Inflam↓, 9, NF-kB↓, 2, TNF-α↓, 2,

Hormonal & Nuclear Receptors ⓘ

RAAS↓, 1,

Clinical Biomarkers ⓘ

ALAT↓, 1, AST↓, 1, GutMicro↑, 2, IL6↓, 1, LDH↓, 1,

Functional Outcomes ⓘ

AntiCan↑, 1, AntiDiabetic↑, 1, AntiTum↑, 4, cardioP↑, 2, cognitive↑, 1, hepatoP↑, 1, memory↑, 1, neuroP↑, 4, RenoP↑, 1, toxicity↓, 1, Wound Healing↑, 1,

Infection & Microbiome ⓘ

Bacteria↓, 1,
Total Targets: 54

Scientific Paper Hit Count for: AntiTum, AntiTumor

6 chitosan
6 Selenite (Sodium)
5 Silver-NanoParticles
5 Astaxanthin
5 immunotherapy
4 Chlorogenic acid
4 Quercetin
4 Selenium NanoParticles
3 Astragalus
3 Ashwagandha(Withaferin A)
3 beta-glucans
3 Betulinic acid
3 Brucea javanica
3 brusatol
3 Capsaicin
3 Copper and Cu NanoParticles
3 Disulfiram
3 Hydrogen Gas
3 Resveratrol
3 Spermidine
2 Auranofin
2 Cisplatin
2 Allicin (mainly Garlic)
2 Artemisinin
2 Melatonin
2 Aloe anthraquinones
2 Baicalein
2 Berberine
2 Radiotherapy/Radiation
2 Bifidobacterium
2 Carvacrol
2 Chlorophyllin
2 Gemcitabine (Gemzar)
2 Gambogic Acid
2 Vitamin C (Ascorbic Acid)
2 Magnolol
2 Naringin
2 Psoralidin
2 Shikonin
2 Thymol-Thymus vulgaris
1 3-bromopyruvate
1 acetazolamide
1 Apigenin (mainly Parsley)
1 Atorvastatin
1 Gold NanoParticles
1 Bufalin/Huachansu
1 probiotics
1 Boswellia (frankincense)
1 Butyrate
1 Caffeine
1 Carnosine
1 Celastrol
1 Prebiotic
1 Choline
1 Camptothecin
1 Ellagic acid
1 EGCG (Epigallocatechin Gallate)
1 Ferulic acid
1 HydroxyTyrosol
1 IP6 (Inosital 1,2,3,4,5,6-hexakisphosphate)
1 Methylene blue
1 Honokiol
1 Magnetic Fields
1 Moringa oleifera
1 Bicarbonate(Sodium)
1 Oleuropein
1 Oxygen, Hyperbaric
1 Phenylbutyrate
1 Piperlongumine
1 Pterostilbene
1 Curcumin
1 Radio Frequency
1 salinomycin
1 Selenium
1 Chemotherapy
1 Sulforaphane (mainly Broccoli)
1 erastin
1 statins
1 Citric Acid
1 Urolithin
1 Zerumbone

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:913  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

AntiTum Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Hormonal & Nuclear Receptors ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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