LDH Cancer Research Results

LDH, Lactate Dehydrogenase: Click to Expand ⟱

Source:

Type:

LDH is a general term that refers to the enzyme that catalyzes the interconversion of lactate and pyruvate. LDH is a tetrameric enzyme, meaning it is composed of four subunits.
LDH refers to the enzyme as a whole, while LDHA specifically refers to the M subunit. Elevated LDHA levels are often associated with poor prognosis and aggressive tumor behavior, similar to elevated LDH levels.
leakage of LDH is a well-known indicator of cell membrane integrity and cell viability [35]. LDH leakage results from the breakdown of the plasma membrane and alterations in membrane permeability, and is widely used as a cytotoxicity endpoint.

However, it's worth noting that some studies have shown that LDHA is a more specific and sensitive biomarker for cancer than total LDH, as it is more closely associated with the Warburg effect and cancer metabolism.

Dysregulated LDH activity contributes significantly to cancer development, promoting the Warburg effect (Chen et al., 2007), which involves increased glucose uptake and lactate production, even in the presence of oxygen, to meet the energy demands of rapidly proliferating cancer cells (Warburg and Minami, 1923; Dai et al., 2016b). LDHA overexpression favors pyruvate to lactate conversion, leading to tumor microenvironment acidification and aiding cancer progression and metastasis.

Inhibitors:
Flavonoids, a group of polyphenols abundant in fruit, vegetables, and medicinal plants, function as LDH inhibitors.

LDH is used as a clinical biomarker for Synthetic liver function, nutrition

Tier A — Direct LDH Enzyme Inhibitors (Validated Catalytic Inhibition)

Rank	Compound	Type	LDH Target	Potency Level	Primary Effect	Notes
1	NCI-006	Research drug	LDHA / LDHB	High (in vivo active)	Potent glycolysis suppression	Modern benchmark LDH inhibitor used in metabolic oncology models.
2	(R)-GNE-140	Research drug	LDHA (±LDHB)	High (nM range reported)	Lactate production ↓	Widely used experimental LDH inhibitor.
3	FX11	Research drug	LDHA	High (μM range)	Metabolic crisis in LDHA-dependent tumors	Classic LDHA inhibitor; often increases ROS secondary to metabolic stress.
4	Oxamate	Tool compound	LDH (pyruvate-competitive)	Moderate (mM cellular use)	Reduces lactate flux	Classical LDH inhibitor; requires high concentrations in cells.
5	Gossypol	Natural product derivative	LDHA	Moderate–High	Glycolysis inhibition	Also has other targets; safety considerations apply.
6	Galloflavin	Natural compound	LDH isoforms	Moderate	Lactate production ↓	One of the better-supported “natural-like” LDH inhibitors.

Tier B — Indirect LDH-Axis Modulators (Glycolysis / Lactate Reduction Without Confirmed Direct Catalytic Inhibition)

Rank	Compound	Mechanism Type	LDH Claim Type	Primary Axis	Notes / Caution
1	Lonidamine	MCT/MPC modulation	Lactate axis inhibition	Metabolic transport blockade	Better classified as lactate/pyruvate transport modulator.
2	Stiripentol	Repurposed drug	LDH pathway modulation	Metabolic axis modulation	Emerging oncology interest; primarily neurological drug.
3	Quercetin	Flavonoid	Reported LDH inhibition (mixed evidence)	NF-κB / PI3K modulation	Often LDH-release confusion; direct enzymatic proof limited.
4	Ursolic acid	Triterpenoid	Reported LDH interaction	Warburg modulation	More credible as metabolic signaling modulator.
5	Fisetin	Flavonoid	Docking / indirect reports	Apoptosis / survival signaling	Enzyme inhibition not well validated.
6	Resveratrol	Polyphenol	Indirect glycolysis suppression	AMPK / HIF-1α modulation	Reduces lactate via upstream signaling.
7	Curcumin	Polyphenol	Indirect LDH expression modulation	Inflammation + metabolic signaling	Bioavailability limits translational strength.
8	Berberine	Alkaloid	Indirect metabolic modulation	AMPK activation	Closer to metformin-like metabolic pressure.
9	Honokiol	Lignan	Indirect glycolysis effects	Survival pathway suppression	Not validated as catalytic LDH inhibitor.
10	Silibinin	Flavonolignan	Mixed / indirect reports	Inflammation + metabolic axis	Often misclassified as LDH inhibitor.
11	Kaempferol	Flavonoid	Often LDH-release marker confusion	Glucose transport / signaling	Do not list as direct LDH inhibitor without enzyme data.
12	Oleanolic acid / Limonin / Allicin / Taurine	Natural compounds	Weak / indirect evidence	General metabolic modulation	Should not be categorized as true LDH inhibitors.

Tier A = Direct catalytic LDH inhibition (enzyme-level validation).
Tier B = Indirect lactate reduction or glycolytic modulation without strong catalytic inhibition evidence.
Important: LDH release assays (cell damage marker) are not proof of LDH enzymatic inhibition.

Scientific Papers found: Click to Expand⟱

4427-

AgNPs,

Silver nanoparticles induce apoptosis and G2/M arrest via PKCζ-dependent signaling in A549 lung cells

in-vitro,

Lung,

A549

tumCV↓, Ag NPs reduced cell viability, increased LDH release, and modulated cell cycle distribution through the accumulation of cells at G2/M and sub-G1 phases (cell death)
LDH↑,
TumCCA↑, G2/M and sub-G1 phases (
BAX↑, Ag NP treatment increased Bax and Bid mRNA levels and downregulated Bcl-2 and Bcl-w mRNAs in a dose-dependent manner.
BID↑,
Bcl-2↓,
PKCδ↓, Ag NPs induce strong toxicity and G2/M cell cycle arrest by a mechanism involving PKCζ downregulation in A549 cells.

2836-

AgNPs,

Gluc,

Glucose capped silver nanoparticles induce cell cycle arrest in HeLa cells

in-vitro,

Cerv,

HeLa

eff↝, AgNPs synthesized are stable up to 10 days without silver and glucose dissolution.
TumCCA↑, AgNPs block the cells in S and G2/M phases, and increase the subG1 cell population.
eff↑, HeLa cells take up abundantly and rapidly AgNPs-G resulting toxic to cells in amount and incubation time dependent manner.
eff↑, The dissolution experiments demonstrated that the observed effects were due only to AgNPs-G since glucose capping prevents Ag+ release.
ROS↑, AgNPs cause toxic responses via induction of oxidative stress as consequence of the generation of intracellular (ROS), depletion of glutathione (GSH), reduction of the superoxide dismutase (SOD) enzyme activity, and increased lipid peroxidation
GSH↓,
SOD↓,
lipid-P↑,
LDH↑, significant LDH levels increase with the highest amount of AgNPs-G and maximum of toxicity was seen at 12 h.

2775-

Bos,

The journey of boswellic acids from synthesis to pharmacological activities

Review,

Var,

Review,

AD,

Review,

PSA,

ROS↑, modulation of reactive oxygen species (ROS) formation and the resulting endoplasmic reticulum stress is central to BA’s molecular and cellular anticancer activities
ER Stress↑,
TumCG↓, Cell cycle arrest, growth inhibition, apoptosis induction, and control of inflammation are all the effects of BA’s altered gene expression
Apoptosis↑,
Inflam↓,
ChemoSen↑, BA has additional synergistic effects, increasing both the sensitivity and cytotoxicity of doxorubicin and cisplatin
Casp↑, BA decreases viability and induces apoptosis by activat- ing the caspase-dependent pathway in human pancreatic cancer (PC) cell lines
ERK↓, BA might inhibit the activation of Ak strain transforming (Akt) and extracellular signal–regulated kinase (ERK)1/2,
cl‑PARP↑, initiation of cleavage of PARP were prompted by the treatment with AKBA
AR↓, AKBA affects the androgen receptor by reducing its expression,
cycD1/CCND1↓, decrease in cyclin D1, which inhibits cellular proliferation
VEGFR2↓, In prostate cancer, the downregulation of vascular endothelial growth factor receptor 2–mediated angiogenesis caused by BA
CXCR4↓, Figure 6
radioP↑,
NF-kB↓,
VEGF↓,
P21↑,
Wnt↓,
β-catenin/ZEB1↓,
Cyt‑c↑,
MMP2↓,
MMP1↓,
MMP9↓,
PI3K↓,
MAPK↓,
JNK↑,
*5LO↓, Table 1 (non cancer)
*NRF2↑,
*HO-1↑,
*MDA↓,
*SOD↑,
*hepatoP↑, Preclinical studies demonstrated hepatoprotective impact for BA against different models of hepatotoxicity via tackling oxidative stress, and inflammatory and apoptotic indices
*ALAT↓,
*AST↓,
*LDH↑,
*CRP↓,
*COX2↓,
*GSH↑,
*ROS↓,
*Imm↑, oral administration of biopolymeric fraction (BOS 200) from B. serrata in mice led to immunostimulatory effects
*Dose↝, BA at low concentration tend to stimulate an immune response, as those utilized in the study of Beghelli et al. (2017) however, utilizing higher concentration suppressed the immune response
*eff↑, Useful actions on skin and psoriasis
*neuroP↑, AKBA has substantially diminished the levels of inflammatory markers such as 5-LOX, TNF-, IL-6, and meliorated cognition in lipopolysaccharide-induced neuroinflammation rodent models
*cognitive↑,
*IL6↓,
*TNF-α↓,

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

5880-

CAR,

In vitro and in vivo antitumor potential of carvacrol nanoemulsion against human lung adenocarcinoma A549 cells via mitochondrial mediated apoptosis

vitro+vivo,

Lung,

A549

nude mice, present study commenced to formulate CANE by an energy intensive ultrasonication method.

in-vitro,

Nor,

BEAS-2B

in-vitro,

Lung,

PC9

Dose↝, prepare a carvacrol nanoemulsion (CANE) using an ultrasonication technique and further evaluation of its anticancer potential against human lung adenocarcinoma A549 cells. (160nm)
mt-ROS↑, The CANE induced reactive oxygen species (ROS) production in A549 cells,
p‑JNK↑, leading to activation of key regulators of apoptosis such as p-JNK, Bax and Bcl2 as well as release of cytochrome C, and activation of the caspase cascade.
BAX↑,
Cyt‑c↑,
Casp↑,
AntiTum↑, CANE displayed a strong antitumor potential in vivo using an athymic nude mice model.
ER Stress↑, Abnormally high ROS levels create ER stress with the involvement of three major signaling proteins IRE1-α, PERK and ATF-6
LDH↑, higher LDH activity, which is a well-established biomarker released by damaged cells, was observed in CANE-treated cells
selectivity↑, CANE displayed no cytotoxicity up to 100 µg/ml against normal bronchial epithelium cells (BEAS-2B)
Apoptosis↑, Induction of apoptosis and ROS production in the presence of CANE
DNAdam↑, potential role on DNA damage and chromatin condensation
IRE1↑, We observed a higher expression of IRE1-α in CANE treated cells
XBP-1↑, similar expression pattern for XBP-1
CHOP↓, down-regulation of CHOP, p-eIF2α, and GRP78 was observed in CANE-treated cells
p‑eIF2α↓,
GRP78/BiP↓,
Ca+2↑, increase of Ca+2 levels in CANE-treated cells. A 2.5 fold higher Ca+2 was observed at 100 μg/ml CANE treated cells
MMP↓, CANE severely altered mitochondrial membrane potential (Δψm) in a dose-dependent manner.
Bcl-2↓, up- and down-regulation of pro-apoptotic (Bax) and anti-apoptotic (Bcl2) proteins
Casp3↑, higher levels of cleaved caspase-9 and caspase-3 in cells treated with CANE in a dose-dependent manner
Casp9↑,
eff↓, To confirm this, A549 cells were first treated with N-acetyl-L-cysteine NAC (5 mM), a strong scavenger of ROS, prior to CANE (100 µg/ml) treatment and observed a marked reduction in ROS generation
TumW↓, A significant (p < 0.05) 34.2 and 62.1% reduction in tumor weight was observed in the mice treated with 50 and 100 mg/Kg CANE, orally three times in a week
Weight↑, body weights of 100 mg/kg CANE treated mice remained static up to the second week and increased further up to 4 weeks
eff↑, ultrasonication consider as simple, cost-effective, clean and prompt aseptic technique16, wherein large droplets ruptured into small droplets by ultrasound leading to the formation of nano-scale droplets
eff↑, We selected polysorbate 80 as a surfactant (HLB, 15), which is regarded as safe for using in pharmaceutical and food industries1

1579-

Citrate,

Effect of Food Additive Citric Acid on The Growth of Human Esophageal Carcinoma Cell Line EC109

in-vitro,

ESCC,

Eca109

TumCP↓, higher citric acid concentrations (800, 1600 μg/ml)
e-LDH↑, incubation with either 400, 800 or 1600 µg/ml CA for 48 hours caused a significant increase (P<0.01) in LDH release by 1.67-fold, 2.79fold and 3.16-fold, respectively
MMP↓,
Ca+2?, CA level can directly regulate several metabolic pathways and increase calcium uptake from foods
PFK↓, potential inhibitor of PFK
Glycolysis↓, increasingly evidences have indicated that a high level of citrate could inhibit the glycolytic pathway

1869-

DCA,

Dichloroacetate induces autophagy in colorectal cancer cells and tumours

in-vitro,

CRC,

HT-29

in-vitro,

CRC,

HCT116

in-vitro,

Pca,

PC3

in-vitro,

CRC,

HT-29

LC3II↑, Increased expression of the autophagy markers LC3B II was observed following DCA treatment both in vitro and in vivo
ROS↑, increased production of reactive oxygen species (ROS)
mTOR↓, mTOR inhibition
MCT1↓, DCA is a possible competitive MCT-1 inhibitor
NADH:NAD↓, increased NAD+/NADH ratios
NAD↑,
TumAuto↑, DCA induces autophagy in cancer cells accompanied by ROS production and mTOR inhibition, reduced lactate excretion, reduced kPL and increased NAD+/NADH ratio.
lactateProd↓, DCA treatment reduces lactate excretion with no change in glucose uptake
LDH↑, Increased LDH activity

2841-

FIS,

Fisetin, an Anti-Inflammatory Agent, Overcomes Radioresistance by Activating the PERK-ATF4-CHOP Axis in Liver Cancer

in-vitro,

Nor,

RAW264.7

LPS-induced Raw264.7 cells

in-vitro,

Liver,

HepG2

10, 25, 100, and 200 μM, 24 h

in-vitro,

Liver,

Hep3B

in-vitro,

Liver,

HUH7

*Inflam↓, fisetin reduced the LPS-induced production of pro-inflammation markers, such as TNF-α, IL-1β, and IL-6, demonstrating the anti-inflammatory effects of fisetin
*TNF-α↓,
*IL1β↓,
*IL6↓,
Apoptosis↓, fisetin induced apoptotic cell death and ER stress through intracellular calcium (Ca2+) release, the PERK-ATF4-CHOP signaling pathway, and induction of GRP78 exosomes.
ER Stress↑,
Ca+2↑,
PERK↑, inducing the GRP78-PERK-ATF4-CHOP pathway in fisetin-treated radioresistant liver cancer cells.
ATF4↑, fisetin treatment of HepG2 and Hep3B cells resulted in the upregulation of ATF4 and CHOP in a time-dependent manner
CHOP↑,
GRP78/BiP↑,
tumCV↓, fisetin decreased the cell viability and increased LDH activity in HepG2, Hep3B, and Huh7 cells in a concentration-dependent manner
LDH↑,
Casp3↑, caspase-3 activity was significantly enhanced
cl‑Casp3↑, fisetin treatment significantly increased the pro-apoptotic markers, including cleaved caspase-3, caspase-8, and caspase-9
cl‑Casp8↑,
cl‑Casp9↑,
p‑eIF2α↑, fisetin treatment increased CHOP, p-eIF2α, ATF4, p-PERK, and GRP78 levels
RadioS↑, Radiation Combined with Fisetin Overcomes Radioresistance

2534-

M-Blu,

doxoR,

PDT,

Methylene Blue-Mediated Photodynamic Therapy in Combination With Doxorubicin: A Novel Approach in the Treatment of HT-29 Colon Cancer Cells

in-vitro,

CRC,

HT-29

LDH↑, present study, the results strongly suggest that the groups treated with DOX + MB + L 610/830 nm had the highest rates of LDH release
ROS↑, Several studies have shown that PDT via different mechanisms, including ROS generation, damage to cellular components (for example lipids, proteins, and nucleic acids) and, as a result, disrupting the integrity of the cell membrane

2430-

PBG,

The cytotoxic effects of propolis on breast cancer cells involve PI3K/Akt and ERK1/2 pathways, mitochondrial membrane potential, and reactive oxygen species generation

in-vitro,

BC,

MDA-MB-231

TumCP↓, CP extract exhibited antiproliferative and cytotoxic effects on MDA MB-231 cells, what may be probably related to PI3K/Akt and ERK1/2 pathways.
TP53↓, decreased expression of apoptosis-related genes (TP53, CASP3, BAX and P21)
Casp3↓,
BAX↓,
P21↓,
ROS↑, These results suggested that CP cytotoxic effects on MDA MB-231 cells might be associated with the intracellular ROS production
eff↓, CP-induced ROS generation was reduced after cotreatment with the antioxidant NAC, which increased the percentage of viable cells, suggesting that CP-induced necrotic-related cell death could be associated with ROS production
MMP↓, Necrosis death is associated with mitochondrial dysfunction and our propolis sample reduced the MMP and increased LDH levels.
LDH↑,
ATP↓, rupture of mitochondrial membrane, loss of adenosine triphosphate (ATP),
Ca+2↑, excessive ROS production, intracellular [Ca+2] elevation, osmotic shock,

3374-

QC,

Therapeutic effects of quercetin in oral cancer therapy: a systematic review of preclinical evidence focused on oxidative damage, apoptosis and anti-metastasis

Review,

Oral,

Review,

AD,

α-SMA↓, In oral cancer cells, quercetin could inhibit EMT via up-regulation of claudin-1 and E-cadherin and down-regulation of α-SMA, vimentin, fibronectin, and Slug [29]
α-SMA↑, OSC20 Invasion: ↓Migration, ↑Expression of epithelial markers (E-cadherin & claudin-1), ↑Expression of mesenchymal markers (fibronectin, vimentin, & α-SMA),
TumCP↓, quercetin significantly reduced cancer cell proliferation, cell viability, tumor volume, invasion, metastasis and migration
tumCV↓,
TumVol↓,
TumCI↓,
TumMeta↓,
TumCMig↓,
ROS↑, This anti-cancer agent induced oxidative stress and apoptosis in the cancer cells.
Apoptosis↑,
BioAv↓, The efficacy of quercetin (as lipophilic) is much impacted by its poor absorption rates, which define its bioavailability. The research on quercetin's bioavailability in animal models shows it may be as low as 10%
*neuroP↑, quercetin has been observed to exhibit neuroprotective effects in Alzheimer's disease through its anti-oxidants, and anti-inflammatory properties and inhibition of amyloid-β (Aβ) fibril formation
*antiOx↑,
*Inflam↓,
*Aβ↓,
*cardioP↑, Additionally, quercetin protects the heart by stopping oxidative stress, inflammation, apoptosis, and protein kinases
MMP↓, ↓MMP, ↑Cytosolic Cyt. C,
Cyt‑c↑,
MMP2↓, ↓Activation MMP-2 & MMP-9, ↓Expression levels of EMT inducers & MMPs, Downregulated Twist & Slug
MMP9↓,
EMT↓,
MMPs↓,
Twist↓,
Slug↓,
Ca+2↑, ↑Apoptosis, ↑ROS, ↑Ca2+ production, ↑Activities of caspase‑3, caspase‑8 & caspase‑9
AIF↑, ↑Mitochondrial release of Cyt. C, AIF, & Endo G
Endon↑,
P-gp↓, ↓ Protein levels of P-gp, & P-gp Expression
LDH↑, ↑LDH release
HK2↓, CAL27 cells) 80µM/24h Molecular markers: ↓Activities of HK, PK, & LDH, ↓Glycolysis, ↓Glucose uptake, ↓Lactate production, ↓Viability, ↓G3BP1, & YWHA2 protein levels
PKA↓,
Glycolysis↓,
GlucoseCon↓,
lactateProd↓,
GRP78/BiP↑, Quercetin controls the activation of intracellular Ca2+ and calpain-1, which then activates GRP78, caspase-12, and C/EBP homologous protein (CHOP) in oral cancer cells
Casp12↑,
CHOP↑,

3369-

QC,

Pharmacological basis and new insights of quercetin action in respect to its anti-cancer effects

Review,

Pca,

FAK↓, Quercetin can inhibit HGF-induced melanoma cell migration by inhibiting the activation of c-Met and its downstream Gabl, FAK and PAK [84]
TumCCA↑, stimulation of cell cycle arrest at the G1 stage
p‑pRB↓, mediated through regulation of p21 CDK inhibitor and suppression of pRb phosphorylation resulting in E2F1 sequestering.
CDK2↑, low dose of quercetin has brought minor DNA injury and Chk2 induction
CycB/CCNB1↓, quercetin has a role in the reduction of cyclin B1 and CDK1 levels,
CDK1↓,
EMT↓, quercetin suppresses epithelial to mesenchymal transition (EMT) and cell proliferation through modulation of Sonic Hedgehog signaling pathway
PI3K↓, quercetin on other pathways such as PI3K, MAPK and WNT pathways have also been validated in cervical cancer
MAPK↓,
Wnt↓,
ROS↑, colorectal cancer, quercetin has been shown to suppress carcinogenesis through various mechanisms including affecting cell proliferation, production of reactive oxygen species and expression of miR-21
miR-21↑,
Akt↓, Figure 1 anti-cancer mechanisms
NF-kB↓,
FasL↑,
Bak↑,
BAX↑,
Bcl-2↓,
Casp3↓,
Casp9↑,
P53↑,
p38↑,
MAPK↑,
Cyt‑c↑,
PARP↓,
CHOP↑,
ROS↓,
LDH↑,
GRP78/BiP↑,
ERK↑,
MDA↓,
SOD↑,
GSH↑,
NRF2↑,
VEGF↓,
PDGF↓,
EGF↓,
FGF↓,
TNF-α↓,
TGF-β↓,
VEGFR2↓,
EGFR↓,
FGFR1↓,
mTOR↓,
cMyc↓,
MMPs↓,
LC3B-II↑,
Beclin-1↑,
IL1β↓,
CRP↓,
IL10↓,
COX2↓,
IL6↓,
TLR4↓,
Shh↓,
HER2/EBBR2↓,
NOTCH↓,
DR5↑, quercetin has enhanced DR5 expression in prostate cancer cells
HSP70/HSPA5↓, Quercetin has also suppressed the upsurge of hsp70 expression in prostate cancer cells following heat treatment and enhanced the quantity of subG1 cells
CSCs↓, Quercetin could also suppress cancer stem cell attributes and metastatic aptitude of isolated prostate cancer cells through modulating JNK signaling pathway
angioG↓, Quercetin inhibits angiogenesis-mediated of human prostate cancer cells through negatively modulating angiogenic factors (TGF-β, VEGF, PDGF, EGF, bFGF, Ang-1, Ang-2, MMP-2, and MMP-9)
MMP2↓,
MMP9↓,
IGFBP3↑, Quercetin via increasing the level of IGFBP-3 could induce apoptosis in PC-3 cells
uPA↓, Quercetin through decreasing uPA and uPAR expression and suppressing cell survival protein and Ras/Raf signaling molecules could decrease prostate cancer progression
uPAR↓,
RAS↓,
Raf↓,
TSP-1↑, Quercetin through TSP-1 enhancement could effectively inhibit angiogenesis

4480-

SeNPs,

Chit,

Biogenic synthesized selenium nanoparticles combined chitosan nanoparticles controlled lung cancer growth via ROS generation and mitochondrial damage pathway

in-vitro,

Lung,

A549

 55.285 and 30.9 nm, for SeNPs and Se-chitosan NPs, respectively.

Chito-NPs of 24.09 µg/mL, whereas for SeNPs it was 18.56 µg/mL

in-vitro,

Nor,

HK-2

selectivity↑, (MCF-10) were not significantly cytotoxically affected by SeNPs and Se-chitosan NPs.
*toxicity↓,
ROS↑, SeNP and Se-chitosan NP treatment resulted in increased ROS generation and caused mitochondrial dysfunction
mtDam↑,
Apoptosis↑, Chito-NPs, SeNPs, and Se-chitosan NPs cause apoptosis and death in A549 cells.
LDH↑, Chito-NPs, SeNPs, and Se-chitosan NPs increase the LDH release

2093-

TQ,

Regulation of NF-κB Expression by Thymoquinone; A Role in Regulating Pro-Inflammatory Cytokines and Programmed Cell Death in Hepatic Cancer Cells

in-vitro,

Liver,

HepG2

TQ (125–1000 ug/mL).

in-vitro,

Nor,

TumCD↑, evidence of the cytotoxic effects of TQ on HepG2 cells
selectivity↑, These findings indicate the selective regulation of HepG2 cell proliferation by TQ treatment without the detectable toxic effect of the normal hepatocytes
Casp3↑, TQ mediates the activation of Casp3, DLC1, and NF-κB, providing a new function of TQ in treating hepatocellular carcinoma (HCC).
DLC1↑,
NF-kB↑,
LDH↑, relative LDH production increased significantly in HepG2 cells treated with 500 ug/m
*toxicity↓, normal hepatocyte cells showed negligible differentiation in cell viability rate

Showing Research Papers: 1 to 14 of 14

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 14

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 1, GSH↑, 1, HO-1↑, 1, MDA↓, 1, NRF2↑, 1, ROS↓, 1, SOD↑, 1,

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1, LDH↑, 1,

Migration ⓘ

5LO↓, 1,

Immune & Inflammatory Signaling ⓘ

COX2↓, 1, CRP↓, 1, IL1β↓, 1, IL6↓, 2, Imm↑, 1, Inflam↓, 2, TNF-α↓, 2,

Protein Aggregation ⓘ

Aβ↓, 1,

Drug Metabolism & Resistance ⓘ

Dose↝, 1, eff↑, 1,

Clinical Biomarkers ⓘ

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

Functional Outcomes ⓘ

cardioP↑, 1, cognitive↑, 1, hepatoP↑, 1, neuroP↑, 2, toxicity↓, 2,
Total Targets: 30

Scientific Paper Hit Count for: LDH, Lactate Dehydrogenase

2 Silver-NanoParticles
2 Quercetin
1 Glucose
1 Boswellia (frankincense)
1 brusatol
1 Brucea javanica
1 Carvacrol
1 Citric Acid
1 Dichloroacetate
1 Fisetin
1 Methylene blue
1 doxorubicin
1 Photodynamic Therapy
1 Propolis -bee glue
1 Selenium NanoParticles
1 chitosan
1 Thymoquinone

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

LDH Cancer Research Results

Tier A — Direct LDH Enzyme Inhibitors (Validated Catalytic Inhibition)

Tier B — Indirect LDH-Axis Modulators (Glycolysis / Lactate Reduction Without Confirmed Direct Catalytic Inhibition)

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

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 ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Core Metabolism/Glycolysis ⓘ

Migration ⓘ

Immune & Inflammatory Signaling ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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