miR-34a Cancer Research Results

miR-34a, mir-34 precursor family: Click to Expand ⟱

Source:

Type:

MiR-34a expression levels were correlated with tumor differentiation, lymphatic metastasis, clinical stages, and survival rates.

miR-34a is a well-known molecule transcriptionally induced by p53.

-Low miR-34a expression is common in cancers and is often associated with poor prognosis in various cancers, including breast, lung, colorectal, prostate, pancreatic, ovarian, and glioblastoma.
-High miR-34a expression is often associated with better prognosis and improved overall survival in various cancers.

Scientific Papers found: Click to Expand⟱

7907-

Api,

IVT,

Anticancer Potential of Apigenin and Isovitexin with Focus on Oncogenic Metabolism in Cancer Stem Cells

Review,

Var,

ChemoSen↑, Two natural flavonoids, apigenin and isovitexin, have been shown to act synergistically with conventional chemotherapeutic drugs by sensitizing CSCs, ultimately leading to improved therapeutic efficacy.
CSCs↓,
Wnt↓, suppression of the Wnt/β-catenin signaling pathway, the inhibition of nuclear factor-κB protein expression, and the downregulation of the cell cycle via upregulation of p21 and cyclin-dependent kinases
β-catenin/ZEB1↓,
PI3K↓, Figure 3
MMP↓,
TumMeta↓,
MAPK↓,
VEGF↓,
MMP9↓,
TGF-β↓,
Inflam↓,
COX2/PTGS2↓,
IL6↓,
NF-kB↓,
TumCCA↑,
P53↑,
cycD1/CCND1↓,
BAX↑,
Casp↓,
Bcl-2↓,
CD133↓, Brain U87MG and U373MG Apigenin 25–50 μM for 2–21 days ↓Self-renewal capacity, ↓cell growth, ↓clonogenicity, ↓invasiveness ↓CD133, ↓NANOG, ↓SOX2, ↓c-Met, ↓Akt
Nanog↓,
SOX2↓,
Akt↓,
TumCP↓, Breast MDA-MB-231 and MDA-MB-436 Apigenin 2–64 μM for 48 h ↓Proliferation, ↓migration, ↓stemness features, ↓mammospheres, ↓self-renewal capability ↓YAP/TAZ activity, ↓CTGF, ↓CYR61, ↓YAP/TAZ-TEADs
TumCMig↓,
YAP/TEAD↓,
CCN2/CTGF↓,
CCN1/CYR61↓,
SIRT3↓, Breast TNBCs Apigenin 12.5–200 µg/µL for 24 h ↓Stemness properties, ↓mammosphere formation, ↓clonogenic potential ↓SIRT3, ↓SIRT6
SIRT6↓,
PCNA↓, Osteosarcoma U2OS-SC tumors in nude mice Isovitexin 10–40 mg/kg for 2 weeks ↓Tumor growth, ↓tumor size ↓CD133, ↓PCNA, ↓Bcl-2, ↓ DNMT1, ↑apoptotic index, ↑miR-34a
DNMT1↓,
miR-34a↑,

1426-

Bos,

CUR,

Chemo,

Novel evidence for curcumin and boswellic acid induced chemoprevention through regulation of miR-34a and miR-27a in colorectal cancer

in-vivo,

CRC,

10um(cur), 30uM(AKBA)

mouse

in-vitro,

CRC,

HCT116

in-vitro,

CRC,

RKO

in-vitro,

CRC,

SW480

in-vitro,

RCC,

SW-620

in-vitro,

RCC,

HT-29

in-vitro,

CRC,

Caco-2

miR-34a↑, curcumin and AKBA induced upregulation of tumor-suppressive miR-34a and downregulation of miR-27a in CRC cells
miR-27a-3p↓,
TumCG↓,
BAX↑,
Bcl-2↓,
PARP1↓,
TumCCA↑,
Apoptosis↑,
cMyc↓,
CDK4↓,
CDK6↓,
cycD1/CCND1↓,
ChemoSen↑, combined treatment further increased the inhibitory effects
miR-34a↑, miR-34a expression was upregulated by curcumin and further elevated by concurrent treatment with curcumin and AKBA in HCT116 cell
miR-27a-3p↓,

4707-

CUR,

The Potential Role of Curcumin as a Regulator of microRNA in Colorectal Cancer: A Systematic Review

Review,

Var,

miR-497↑, Curcumin was found to cause the upregulation of miR-497, miR-200c, miR-200b, miR-409-3p, miR‐34, miR‐126, miR-145, miR-206, miR-491, miR-141, miR-429, miR-101, and miR-15a
miR-200c↑,
miR-409-3p↑,
miR-34a↑,
miR-126↑,
miR-145↑,
miR-206↑,
miR-491↑,
miR-141↑,
miR-429↑,
miR-101↑,
miR-15↑,
miR-21↓, and the downregulation of miR-21, miR-155, miR‐221, miR‐222, miR-17-5p, miR-130a, miR-27, and miR-20a.
miR-155↓,
miR-221↓,
miR-222↓,
miR-17↓,
miR-130a↓,
miR-27a-3p↓,
miR-20↓,

4708-

CUR,

Molecular mechanisms underlying curcumin-mediated microRNA regulation in carcinogenesis; Focused on gastrointestinal cancers

Review,

GC,

chemoPv↑, Curcumin is well known for its chemopreventive and anti-cancer properties.
AntiCan↑,
*antiOx↑, Mechanistically, curcumin exerts its biological impacts via antioxidant and anti-inflammatory effects through the interaction with various transcription factors and signaling molecules.
*Inflam↓,
miR-21↓, Table 1
miR-34a↑,
miR-200b↑,
miR-27a-3p↓,

405-

CUR,

5-FU,

Curcumin activates a ROS/KEAP1/NRF2/miR-34a/b/c cascade to suppress colorectal cancer metastasis

vitro+vivo,

CRC,

HCT116

15uM

Apoptosis↑, more pronounced increase in apoptosis in p53-deficient when compared to p53-proficient cells
TumCMig↓,
NRF2↑,
ROS↑, antioxidant N-acetylcysteine suppressed the induction of apoptosis by curcumin
MET↑, Curcumin induces MET and inhibits lung-metastases formation via inducing miR-34a
miR-34a↑, Notably, curcumin induced miR-34a and miR-34b/c expression in a ROS/NRF2-dependent and p53-independent manner.

456-

CUR,

Curcumin Promoted miR-34a Expression and Suppressed Proliferation of Gastric Cancer Cells

vitro+vivo,

GC,

SGC-7901

50 μM, 24, 48 and 96 h

miR-34a↑,
TumCP↓,
TumCMig↓,
TumCI↓,
TumCCA↑, inhibited cell cycle progression in G0/G1-S phase
Bcl-2↓,
CDK4/6↓, CDK4
cycD1/CCND1↓,

126-

CUR,

Modulation of miR-34a in curcumin-induced antiproliferation of prostate cancer cells

in-vitro,

Pca,

22Rv1

 1, 5, 10 and 20 μM, 4 days

in-vitro,

Pca,

PC3

in-vitro,

Pca,

DU145

miR-34a↑, curcumin significantly upregulated the expression of miR‐34a, along with the downregulated expression of β‐catenin and c‐myc in three prostate cancer cell lines.
β-catenin/ZEB1↓, curcumin‐induced miR‐34a suppressed the activation of β‐catenin/c‐myc axis and inhibited cell proliferation of prostate cancer cells.
cMyc↓,
P21↑,
cycD1/CCND1↓,
PCNA↓,
TumCG↓, Curcumin inhibited cell growth of prostate cancer cells

679-

EGCG,

5-FU,

Epigallocatechin-3-gallate targets cancer stem-like cells and enhances 5-fluorouracil chemosensitivity in colorectal cancer

in-vitro,

CRC,

NOTCH1↓, Furthermore, EGCG suppressed Notch1
BMI1↓,
SUZ12↓,
EZH2↓,
miR-34a↑,
miR-200c↑,
miR-145↑,
CSCs↓, (EGCG), an active catechin present in green tea, has been shown to suppress CSC growth in various cancers

1654-

FA,

Molecular mechanism of ferulic acid and its derivatives in tumor progression

Review,

Var,

AntiCan↑, FA has anti-inflammatory, analgesic, anti-radiation, and immune-enhancing effects and also shows anticancer activity,
Inflam↓,
RadioS↑,
ROS↑, FA can cause mitochondrial apoptosis by inducing the generation of intracellular reactive oxygen species (ROS)
Apoptosis↑,
TumCCA↑, G0/G1 phase
TumCMig↑, inducing autophagy; inhibiting cell migration, invasion, and angiogenesis
TumCI↓,
angioG↓,
ChemoSen↑, synergistically improving the efficacy of chemotherapy drugs and reducing adverse reactions.
ChemoSideEff↓,
P53↑, FA could increase the expression level of p53 in MIA PaCa-2 pancreatic cancer cells
cycD1/CCND1↓, while reducing the expression levels of cyclin D1 and cyclin-dependent kinase (CDK) 4/6.
CDK4↓,
CDK6↓,
TumW↓, FA treatment was found to reduce tumor weight in a dose-dependent manner, increase miR-34a expression, downregulate Bcl-2 protein expression, and upregulate caspase-3 protein expression
miR-34a↑,
Bcl-2↓,
Casp3↑,
BAX↑,
β-catenin/ZEB1↓, isoferulic acid dose-dependently downregulated the expression of β-catenin and MYC proto-oncogene (c-Myc), inducing apoptosis
cMyc↓,
Bax:Bcl2↑, FXS-3 can inhibit the activity of A549 cells by upregulating the Bax/Bcl-2 ratio
SOD↓, After treatment with FA, Cao et al. [40] observed an increase in ROS production and a decrease in superoxide dismutase activity and glutathione content in EC-1 and TE-4 oesophageal cancer cells
GSH↓,
LDH↓, FA could promote the release of lactate dehydrogenase (LDH)
ERK↑, A can activate the ERK1/2 pathway
eff↑, conjugated zinc oxide nanoparticles with FA (ZnONPs-FA) to act on hepatoma Huh-7 and HepG2 cells. The results showed that ZnONPs-FA could induce oxidative DNA damage and apoptosis by inducing ROS production.
JAK2↓, by inhibiting the JAK2/STAT6 immune signaling pathway
STAT6↓,
NF-kB↓, thus inhibiting the activation of NF-κB
PYCR1↓, FA can target PYCR1 and inhibit its enzyme activity in a concentration-dependent manner.
PI3K↓, FA inhibits the activation of the PI3K/AKT pathway
Akt↓,
mTOR↓, FA could significantly reduce the expression level of mTOR mRNA and Ki-67 protein in A549 lung cancer graft tissue
Ki-67↓,
VEGF↓,
FGFR1↓, FA is a novel FGFR1 inhibitor
EMT↓, FA can inhibit EMT
CAIX↓, selectively inhibit CAIX
LC3II↑, Autophagy vacuoles and increased LC3-II and p62 autophagy proteins were observed after treatment with this compound
p62↑,
PKM2↓, FA could inhibit the expression of PKM2 and block aerobic glycolysis
Glycolysis↓,
*BioAv↓, FA has poor solubility in water and a poor ability to pass through biological barriers [118]; therefore, the extent to which it is metabolized in vivo after oral administration is largely unknown

997-

GA,

The Inhibitory Mechanisms of Tumor PD-L1 Expression by Natural Bioactive Gallic Acid in Non-Small-Cell Lung Cancer (NSCLC) Cells

in-vitro,

Lung,

A549

400 μM @48hrs

in-vitro,

Lung,

H292

100 μM@48hrs

in-vitro,

Nor,

HUVECs

400 μM GA inducing around 8% cell death which indicated that this concentration does not make much toxicity in normal cells  ****

PD-L1↓, GA strongly decreases the expression levels of PD-L1 protein in A549 and H292 NSCLC cells
p‑EGFR↓,
p‑PI3K↓,
p‑Akt↓,
P53↑, GA upregulates the expression levels of p53 protein in a concentration-dependent manner
miR-34a↑, p53 indirectly regulates the expression levels of PD-L1 through inducing miR-34a in cancer cells
*toxicity↓, 400 μM GA inducing around 8% cell death which indicated that this concentration does not make much toxicity in normal cells

7468-

HNK,

Honokiol and Its Emerging Role in Breast Cancer Therapy

Review,

BC,

*ROS↓, HNK inhibits essential oncogenic pathways and reduces oxidative stress, inflammation, metabolic reprogramming, and cancer stemness.
*Inflam↓,
CSCs↓,
ChemoSen↑, HNK demonstrates synergistic activity with chemotherapy, endocrine therapy, targeted therapy, and immune checkpoint inhibitors, increasing sensitivity to treatment across models of ER+, PR+, and HER2+ BrCas, as well as triple-negative breast cancers
BioAv↑, Nanotechnological delivery systems enhance the solubility, bioavailability, and intratumoral accumulation of HNK, increasing its translational capacity.
ROS↑, HNK increases intracellular reactive oxygen species (ROS) levels in cancer cells, coinciding with a time-dependent loss of mitochondrial membrane potential (ΔΨm), indicating that ROS production is closely linked to mitochondrial damage
MMP↓,
mtDam↑,
TumCCA↑, HNK causes G0/G1 cell cycle arrest by downregulating cyclin D1 and CDK4, as well as promoting intrinsic apoptosis-like pathways marked by increases in caspase-3 and caspase-9 activities
cycD1/CCND1↓,
CDK4↓,
Casp3↑,
Casp9↑,
Bcl-2↓, reducing the anti-apoptotic Bcl-2 and Bcl-xL, and increasing the pro-apoptotic Bax
Bcl-xL↓,
BAX↑,
p‑STAT3↓, HNK suppresses the phosphorylation of STAT3 in MDA-MB-231
AMPK↑, HNK was found to activate the LKB1–AMPK axis and induce miR-34a expression in MCF7, SKBR3, and SUM149 cells, thereby inhibiting EMT, stemness, and oncogenic leptin signaling in an LKB1-dependent manner
miR-34a↑,
EMT↓,
HH↓, HNK can induce apoptosis by suppressing essential components of the Hh pathway, including SHH [28], Gli1, and Ptch1 [26], as well as downregulating NF-κB
Shh↓,
Gli1↓,
PTCH1↓,
NF-kB↓,
TNF-α↓, reduces the production of inflammatory cytokines, including TNF-α and IL-6
IL6↓,
Glycolysis↓, HNK suppresses HIF-1α-controlled glycolysis by downregulating glycolytic metabolic enzymes, disrupting glucose uptake, and inhibiting tumor growth.
GlucoseCon↓,
BioAv↓, This limitation is primarily attributed to pharmacokinetic challenges, including poor aqueous solubility, low oral bioavailability, rapid metabolism, and the lack of standardized dosing regimens,
BioAv↓, Preclinical studies demonstrate that following oral administration at 40 mg/kg, HNK is rapidly absorbed (Tmax ≈ 20 min) but exhibits low systemic exposure [75], due to extensive first-pass metabolism and high hepatic extraction
Half-Life↝, While the plasma elimination half-life is moderately prolonged (t½ ≈ 290 min),

7894-

IVT,

Isovitexin Inhibits Stemness and Induces Apoptosis in Hepatocellular Carcinoma SK-Hep-1 Spheroids by Upregulating miR-34a Expression

in-vitro,

HCC,

SK-HEP-1

CD44↓, ISOV suppressed sphere and colony formation, and decreased CD44+ cell populations
CSCs↓,
ABCG2↓, ABCG2, ALDH1, and NANOG mRNA levels were decreased, while there was a concomitant increase in miR-34a levels
ALDH1A1↓,
Nanog↓,
miR-34a↑,
BAX↑, ISOV increased Bax protein levels, and reduced Bcl-2 and Mcl-1 protein levels in SK-SC
Bcl-2↓,
Mcl-1↓,
Apoptosis↑, We suggest that ISOV-mediated miR-34a upregulation induces apoptosis and suppresses the stemness of SK-SC.

6538-

MeSal,

ASA,

Salicylate induces AMPK and inhibits c-MYC to activate a NRF2/ARE/miR-34a/b/c cascade resulting in suppression of colorectal cancer metastasis

in-vitro,

CRC,

chemoPv↑, Aspirin and its active metabolite salicylate have emerged as promising agents for the chemoprevention of colorectal cancer (CRC).
AMPK↑, Salicylate activated AMPK, thereby activating NRF2, which directly induced miR-34a/b/c expression via ARE motifs.
NRF2↑, Salicylate activates NRF2 via AMPK in CRC cells
miR-34a↑,
cMyc↓, Consistently, it has been shown that aspirin down-regulates c-MYC levels in numerous cancer entities
tumCV↓, Salicylate inhibits cell viability and induces apoptosis in CRC cells
Apoptosis↑,
TumCI↓, Salicylate inhibits migration, invasion and induces MET in CRC cells
TumCMig↓,
MET↑,

222-

MFrot,

MF,

LF-MF inhibits iron metabolism and suppresses lung cancer through activation of P53-miR-34a-E2F1/E2F3 pathway

in-vitro,

Lung,

A549

 0.4T, 7.5 Hz

 inhibits iron metabolism

TumCG↓,
OS↑,
miR-34a↑, enhanced miR-34a transcription
E2Fs↓, E2F1/E2F3
P53↑,
TfR1/CD71↓, TfR1 protein levels
Ferritin↓, inhibits iron metabolism

2084-

TQ,

Thymoquinone, as an anticancer molecule: from basic research to clinical investigation

Review,

Var,

*ROS↓, An interesting study reported that thymoquinone is actually a potent apoptosis inducer in cancer cells, but it exerts antiapoptotic effect through attenuating oxidative stress in other types of cell injury
*chemoPv↑, antioxidant activity of thymoquinone is responsible for its chemopreventive activities
ROS↑, other studies reported thymoquinone induce apoptosis in cancer cells by exerting oxidative damage
ROS⇅, Another hypothesis states that thymoquinone acts as an antioxidant at lower concentrations and a prooxidant at higher concentrations
MUC4↓, Torres et al. [17] revealed that thymoquinone down-regulates glycoprotein mucin 4 (MUC4)
selectivity↑, thymoquinone was found to inhibit DNA synthesis, proliferation, and viability of cancerous cells, such as LNCaP, C4-B, DU145, and PC-3, but not noncancerous BPH-1 prostate epithelial cells [20].
AR↓, Down-regulation of androgen receptor (AR) and cell proliferation regulator E2F-1 was indicated as the mechanism behind thymoquinone’s action in prostate cancer
cycD1/CCND1↓, expression of STAT3-regulated gene products, such as cyclin D1, Bcl-2, Bcl-xL, survivin, Mcl-1 and vascular endothelial growth factor (VEGF), was inhibited by thymoquinone, which ultimately increased apoptosis and killed cancer cells
Bcl-2↓,
Bcl-xL↓,
survivin↓,
Mcl-1↓,
VEGF↓,
cl‑PARP↑, induction of the cleavage of poly-(ADP-ribose) polymerase (PARP
ROS↑, In ALL cell line CEM-ss, thymoquinone treatment generated reactive oxygen species (ROS) and HSP70
HSP70/HSPA5↑,
P53↑, thymoquinone can induce apoptosis in MCF-7 breast cancer cells via the up-regulation of p53 expression
miR-34a↑, Thymoquinone significantly increased the expression of miR-34a via p53, and down-regulated Rac1 expression
Rac1↓,
TumCCA↑, In hepatic carcinoma, thymoquinone induced cell cycle arrest and apoptosis by repressing the Notch signaling pathway
NOTCH↓,
NF-kB↓, Evidence revealed that thymoquinone suppresses tumor necrosis factor (TNF-α)-induced NF-kappa B (NF-κB) activation
IκB↓, consequently inhibits the activation of I kappa B alpha (I-κBα) kinase, I-κBα phosphorylation, I-κBα degradation, p65 phosphorylation
p‑p65↓,
IAP1↓, down-regulated the expression of NF-κB -regulated antiapoptotic gene products, like IAP1, IAP2, XIAP Bcl-2, Bcl-xL;
IAP2/BIRC3↑,
XIAP↓,
TNF-α↓, It also inhibited monocyte chemo-attractant protein-1 (MCP-1), TNF-α, interleukin (IL)-1β and COX-2, ultimately reducing the NF-κB activation in pancreatic ductal adenocarcinoma cells
COX2/PTGS2↓,
Inflam↓, indicating its role as an inhibitor of proinflammatory pathways
α-tubulin↓, Without affecting the tubulin levels in normal human fibroblast, thymoquinone induces degradation of α and β tubulin proteins in human astrocytoma U87 cells and in T lymphoblastic leukaemia Jurkat cells, and thus exerts anticancer activity
Twist↓, thymoquinone treatment inhibits TWIST1 promoter activity and decreases its expression in breast cancer cell lines; leading to the inhibition of epithelial-mesenchymal transition (EMT)
EMT↓,
mTOR↓, thymoquinone also attenuated mTOR activity, and inhibited PI3K/Akt signaling in bladder cancer
PI3K↓,
Akt↓,
BioAv↓, Thymoquinone is chemically hydrophobic, which causes its poor solubility, and thus bioavailability. bioavailability of thymoquinone was reported ~58% with a lag time of ~23 min
ChemoSen↑, Some studies revealed that thymoquinone in combination with other chemotherapeutic drugs can show better anticancer activities
BioAv↑, Thymoquinone-loaded liposomes (TQ-LP) and thymoquinone loaded in liposomes modified with Triton X-100 (XLP) with diameters of about 100 nm were found to maintain stability, improve bioavailability and maintain thymoquinone’s anticancer activity
PTEN↑, Thymoquinone also induces apoptosis by up-regulating PTEN
chemoPv↑, A recent study showed that thymoquinone can potentiate the chemopreventive effect of vitamin D during the initiation phase of colon cancer in rat model
RadioS↑, thymoquinone also mediates radiosensitization and cancer chemo-radiotherapy
*Half-Life↝, Thymoquinone-loaded nanostructured lipid carrier (TQ-NLC) has been developed to improve its bioavailability (elimination half-life ~5 hours)
*BioAv↝, calculated absolute bioavailability of thymoquinone was reported ~58% with a lag time of ~23 min by Alkharfy et al.

7887-

VT,

IVT,

Dietary Flavonoids Vitexin and Isovitexin: New Insights into Their Functional Roles in Human Health and Disease Prevention

Review,

AD,

Review,

Var,

*antiOx↑, antioxidant, anti-inflammatory, anticancer, antibacterial, and neuroprotective mechanisms.
*Inflam↓,
*AntiCan↑,
*Bacteria↓,
*neuroP↑, cardiovascular protection, blood sugar regulation, anti-obesity, anticancer, antioxidant, anti-inflammatory, and neuroprotective properties.
*Obesity↓,
*cardioP↑, Vitexin exerts a cardioprotective effect against DOX-induced cardiac toxicity by reducing oxidative stress, lowering cardiac inflammatory cytokines, increasing FOXO3a, and inhibiting caspase-3 activation.
*ROS↓, Sprague-Dawley rat hearts, H9c2 cells 10 μM Reducing ROS levels; improving mitochondrial activity, mitochondrial membrane potential, and ATP content; markedly increasing MFN2 expression and reducing the recruitment of Drp1 in mitochondria.
*MMP↑,
*ATP↑,
*MFN2↑,
*DRP1/DNM1L↓,
*FOXO3↑, Protect against DOX-induced acute cardiotoxicity Rats 30 mg/kg Vitexin induced elevated FOXO3a protein expression levels, by suppressing oxidative stress
*NRF2↑, vitexin activated nuclear factor-erythroid 2-related factor 2 (Nrf2) in HUVEC under high glucose.
*Ferroptosis↓, Diabetic nephropathy HK-2 cells/DN rat 0–40 μM Vitexin could alleviate diabetic nephropathy by attenuated ferroptosis via activating GPX4
*GPx4↑,
TumCP↓, Gastric cancer Nude mice/GC cells 2 mg/kg 10–160 μM Vitexin inhibited the malignant progression of GC in vitro and in vivo by suppressing HMGB1-mediated activation of PI3K/Akt/HIF-1α signaling pathway.
HMGB1↓,
PI3K↓,
Akt↓,
Hif1a↓,
CDK1↓, Colon cancer HCT-116 cells 1–300 μM Inhibit colon cancer HCT-116 cell proliferation by suppressing CDK1/cyclin B expression, leading to cell cycle arrest in the G2/M phase.
CycB/CCNB1↓,
TumCCA↑,
Apoptosis↑, Isovitexin Colon cancer Promoted apoptosis and suppressed cell proliferation by activating the p53 signaling pathway.
P53↑,
NF-kB↓, Non-small cell lung cancer cells A549/ H1299 cells, nude mice 1–120 μM Suppressed NF-κB, AKT and ERK activation. [24] Vitexin A549 cells, nude mice 0–40 μM Reduced the levels of p-PI3K, p-Akt, and p-mTOR.
ERK↓,
p‑PI3K↓,
miR-34a↑, Isovitexin Hepatocarcinoma SK-Hep-1 cells Mediated miR-34a upregulation induces apoptosis and suppresses the stemness of SK-SC.
Apoptosis↑,
CSCs?,
*MAPK↓, Isovitexin Acute lung injury RAW 264.7 cells 0–50 μM Inhibiting MAPK and NF-κB and activating HO-1/Nrf2 pathways.
*HO-1↑,
*hepatoP↑, EAH mice 5 mg/kg Vitexin ameliorated hepatic injury in EAH mice through activation of the AMPK/AKT/GSK-3β pathway and upregulation of the Nrf2 gene.
*AMPK↑,
*Akt↑,
*GSK‐3β↑,
*chemoP↑, Vitexin exerts a cardioprotective effect against DOX-induced cardiac toxicity by reducing oxidative stress, lowering cardiac inflammatory cytokines, increasing FOXO3a, and inhibiting caspase-3 activation.
*Casp3↓,
*IRes↝, Vitexin and isovitexin flavonoids not only affected the absorption of peripheral glucose in insulin and non-insulin sensitive tissues but also showed the potential to restore insulin resistance in HepG2 cells by enhancing cellular uptake of glucose.
*GlucoseCon↑,
ChemoSen↑, When combined with doxorubicin (Dox), vitexin can reduce tumor growth and show synergistic effects in in vivo tests, increasing antitumor efficacy.
*GSH↑, Vitexin also increased Nrf2 expression and boosted GSH and antioxidant enzymes such as SOD, CAT, GPx, and GST.
*SOD↑,
*ATF2↑,
*GPx↑,
*GSTs↑,
*AntiAge↑, In Caenorhabditis elegans, studies have shown that vitexin and isovitexin, as putative SKN-1/Nrf2 activators, increase lifespan and support a healthy lifespan.
*Stroke↓, It has been demonstrated that vitexin protects against a cerebral ischemia/reperfusion (I/R)-induced increase in the permeability of brain endothelial cells
*AChE↓, vitexin treatment significantly inhibited acetylcholinesterase activity and markedly downregulated the expression of ace-1 and ace-2.
*ACE/ACE1↓,
*ACE2↓,
*GutMicro↑, Vitexin and isovitexin have also shown promising potential in modulating intestinal microbiota and in turn play a significant role in regulating various diseases such as overweight
*MPO↓, Vitexin can also resist Helicobacter pylori infection, which may be related to its anti-myeloperoxidase (MPO) enzyme activity and inhibition of H- and K-ATPase activity
*H+/K+-ATPase↓,
*AntiDiabetic↑, Antidiabetic Vitexin and Isovitexin Inhibits α-glucosidase/α-amylase, promotes GLUT4, modulates gut microbiota
*GLUT4↑,
*Obesity↓, Anti-obesity Vitexin Activates AMPKα, inhibits C/EBPα, FAS, activates Hedgehog signaling
*HH↓,
*RenoP↑, vitexin protects the kidneys and prevents the formation of kidney stones by inhibiting pyroptosis, apoptosis, epithelial–mesenchymal transition (EMT), and macrophage activation.
*BioAv↓, Vitexin and isovitexin have poor absorption in the gastrointestinal tract, with significant first-pass effects in the intestine (approximately 94%), stomach (30%), and liver (50%), resulting in a lower bioavailability (F) (approximately 5%).
*BioAv↝, The absorption and metabolism processes of vitexin and isovitexin in the human body are complex, and their bioavailability is influenced by multiple factors, including the action of the gut microbiota, interactions with dietary components, first-pass
*BioAv↑, The vitexin-loaded bilayer nanoparticles are designed by assembling soybean peptides and coating them with a goblet cell-targeting peptide. They significantly increase the bioaccessibility and bioavailability of vitexin

Showing Research Papers: 1 to 16 of 16

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 16

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

ACE/ACE1↓, 1, ACE2↓, 1, H+/K+-ATPase↓, 1, IRes↝, 1, Stroke↓, 1,

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2, Ferroptosis↓, 1, GPx↑, 1, GPx4↑, 1, GSH↑, 1, GSTs↑, 1, HO-1↑, 1, MFN2↑, 1, MPO↓, 1, NRF2↑, 1, ROS↓, 3, SOD↑, 1,

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 1, DRP1/DNM1L↓, 1, MMP↑, 1,

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1, GlucoseCon↑, 1,

Cell Death(tgid=5) ⓘ

Akt↑, 1, ATF2↑, 1, Casp3↓, 1, Ferroptosis↓, 1, MAPK↓, 1,

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

FOXO3↑, 1, GSK‐3β↑, 1, HH↓, 1,

Barriers & Transport(tgid=15) ⓘ

GLUT4↑, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 3,

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 2, BioAv↑, 1, BioAv↝, 2, Half-Life↝, 1,

Clinical Biomarkers(tgid=22) ⓘ

GutMicro↑, 1,

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1, AntiCan↑, 1, AntiDiabetic↑, 1, cardioP↑, 1, chemoP↑, 1, chemoPv↑, 1, hepatoP↑, 1, neuroP↑, 1, Obesity↓, 2, RenoP↑, 1, toxicity↓, 1,

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,
Total Targets: 50

Scientific Paper Hit Count for: miR-34a, mir-34 precursor family

6 Curcumin
3 Isovitexin
2 5-fluorouracil
1 Apigenin (mainly Parsley)
1 Boswellia (frankincense)
1 Chemotherapy
1 EGCG (Epigallocatechin Gallate)
1 Ferulic acid
1 Gallic acid
1 Honokiol
1 Methyl salicylate / Sweet Birch oil
1 Aspirin
1 Magnetic Field Rotating
1 Magnetic Fields
1 Thymoquinone
1 Vitexin

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#:450  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

miR-34a Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Metal & Cofactor Biology(tgid=2) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Hormonal & Nuclear Receptors(tgid=20) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Synaptic & Neurotransmission(tgid=18) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

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