MCT1 Cancer Research Results

MCT1, Multiple Copies in T-cell malignancy 1: Click to Expand ⟱
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MCT-1 is a transcriptional regulator that plays a crucial role in cell cycle regulation, apoptosis, and cell proliferation. Overexpression of MCT-1 has been observed in: Leukemia, Lymphoma, Breast, Lung, CRC.
Scientific Papers found: Click to Expand⟱
6023- CGA,    Pharmacological advances of the chlorogenic acids family: current insights and future research directions
- Review, AD, NA - Review, Park, NA - Review, IBD, NA
*Aβ↓, chlorogenic acid can reduce Aβ plaques in Alzheimer’s disease model mice by 37%, indicating its neuroprotective potential.
*neuroP↑,
*cardioP↑, Similarly, CGAs offer protection to the cardiovascular system, gastrointestinal tract, kidneys, and liver, while additionally preventing metabolic syndrome and displaying anticancer and antimicrobial capabilities.
*GastroP↑,
*RenoP↑,
*hepatoP↑,
*Obesity↓,
*Bacteria↓,
*BioAv↑, hydroxycinnamoyl-CoA quinate hydroxycinnamoyl transferase, HQT in tomatoes significantly enhances CGA accumulation without significantly altering the levels of other soluble phenolic botanical drugs.
*BioAv↑, Mechanistic studies have shown that dietary fats (such as soybean oil and coconut oil) can significantly enhance the permeability of CGA in the Caco-2 monolayer by increasing cell membrane fluidity
*BioAv↑, Following oral administration of CGA, the acidic environment in the stomach helps maintain the structural stability of CGA, with approximately one-third of the dose entering the blood system through passive diffusion in the small intestine, while the
*ROS↓, CGA pretreatment markedly diminished ROS caused by PD toxins
*GutMicro↑, CGA works with the gut microbiota and its metabolites to alleviate post-infectious irritable bowel syndrome (PI-IBS)
*IBI↑, CGA increases intestinal damage repair, decreases MCT-1 and TFF-3 expression, and suppresses NF-κB expression
*MCT1↓,
*NF-kB↓,
*DNMT1↓, Liver Cancer, DNMT1 protein expression↓

6223- CUR,    Curcumin Rewires the Tumor Metabolic Landscape: Mechanisms and Clinical Prospects
- Review, Var, NA
Ferroptosis↑, including the induction of ferroptosis by regulating the SLC7A11/GPX4 axis
GutMicro↑, and modulating gut microbiota metabolism. I
Akt↓, it inhibits pro-tumorigenic signals such as Akt/mTOR, NF-κB, Wnt/β-catenin, and STAT3, thereby blocking tumor proliferation, invasion, and metastasis
mTOR↓,
NF-kB↓,
Wnt↓,
β-catenin/ZEB1↓,
STAT3↓,
TumCP↓,
TumCI↓,
TumMeta↓,
AMPK↑, activates tumor-suppressive and cytoprotective pathways, including AMPK, p53, and nuclear factor erythroid 2-related factor 2 (Nrf2), which induce cell cycle arrest and apoptosis
P53↑,
NRF2↑,
TumCCA↑,
Apoptosis↑,
Casp↑, activation of the Caspase cascade
GPx4↓, as well as ferroptosis by inhibiting the solute carrier family 7 member 11 (SLC7A11)/glutathione peroxidase 4 (GPX4) axis [5]
DNMTs↓, inhibiting epigenetic regulatory mechanisms such as DNMTs and HDACs.
HDAC↓,
VEGF↓, inhibiting VEGF signaling and enhances the immune microenvironment by improving T cell and NK cell function
Imm↑,
NK cell↑,
Warburg↓, Curcumin effectively reverses the Warburg effect and interferes with glucose metabolism by targeting HIF-1α and inhibiting key enzymes, including hexokinase 2 (HK2), pyruvate kinase M2 (PKM2), and lactate dehydrogenase A (LDHA)
Hif1a↓,
HK2↓,
PKM2↓,
LDHA↓,
GLUT1↓, as well as the functions of glucose transporter 1 (GLUT1) and monocarboxylate transporters (MCTs) [12].
MCT1↓,
AMPK↑, curcumin activates signaling pathways such as AMPK, downregulates fatty acid synthase (FASN) and stearoyl-CoA desaturase (SCD1),
FASN↓,
SCD1↓,
GLS↓, Curcumin extensively intervenes in amino acid metabolism by inhibiting the activity of glutaminase (GLS), ornithine decarboxylase (ODC), and other enzymes,
Apoptosis↑, inducing apoptosis through mechanisms such as disrupting the electron transport chain, reducing membrane potential, and promoting the generation of reactive oxygen species (ROS)
ETC↓,
MMP↓,
ROS↑,
lipid-P↑, curcumin induces lipid peroxidation and collapses redox homeostasis, thereby activating the ferroptosis program [
ChemoSen↑, blocking invasion and metastasis, and enhancing chemosensitivity.
PDK1↓, In hypoxic pancreatic cancer cells, curcumin downregulates the expression of GLUT1, HK2, LDHA, and PDK1 by inhibiting the Beclin1/HIF-1α axis, which results in reduced ATP production and inhibited cell proliferation [
Beclin-1↓,
ATP↓,
Glycolysis↓, inhibiting glycolysis
GlucoseCon↓, decreased glucose uptake and increased lactate production
lactateProd↑,
MMPs↓, reduces MMP, GSH, and G6PD activities
GSH↓, inhibition of SLC7A11 to limit GSH synthesis, thereby triggering the collapse of the antioxidant defense system
G6PD↓,
OXPHOS↓, downregulate OXPHOS and glycolysis activities
SREBP2↓, curcumin treatment leads to a marked downregulation of the mRNA expression of SREBP and its target genes. inhibiting the expression of NPC1L1, SREBP-2, and HNF1α
COX2↓, curcumin exerts anti-tumor effects by downregulating the expression of NF-κB, COX-2, and AP-1
AP-1↓,
NADH↓, decreased GPx4 and FSP1 expression, induced ferroptosis by inhibiting GSH-GPx4 and FSP1-CoQ 10-NADH pathways
NRF2↑, it inhibits GPX4 and activates Nrf2 and heme oxygenase-1 (HO-1). This results in an abnormal accumulation of intracellular Fe2+, ROS, lipid peroxides, and malondialdehyde (MDA), along with a depletion of GSH
HO-1↑,
Iron↑,
MDA↑,
*ROS↓, studies have demonstrated that the topical application of curcumin on the skin exerts antitumor effects by synergistically downregulating COX-2 and ODC activities, alleviating oxidative damage, and concurrently inhibiting inflammatory proliferation i
*Inflam↓,

2308- CUR,    Counteracting Action of Curcumin on High Glucose-Induced Chemoresistance in Hepatic Carcinoma Cells
- in-vitro, Liver, HepG2
GlucoseCon↓, Curcumin obviated the hyperglycemia-induced modulations like elevated glucose consumption, lactate production, and extracellular acidification, and diminished nitric oxide and reactive oxygen species (ROS) production
lactateProd↓,
ECAR↓,
NO↓,
ROS↑, Curcumin favors the ROS production in HepG2 cells in normal as well as hyperglycemic conditions. ROS production was detected in cancer cells treated with curcumin, or doxorubicin, or their combinations in NG or HG medium for 24 h
HK2↓, HKII, PFK1, GAPDH, PKM2, LDH-A, IDH3A, and FASN. Metabolite transporters and receptors (GLUT-1, MCT-1, MCT-4, and HCAR-1) were also found upregulated in high glucose exposed HepG2 cells. Curcumin inhibited the elevated expression of these enzymes, tr
PFK1↓,
GAPDH↓,
PKM2↓,
LDHA↓,
FASN↓,
GLUT1↓, Curcumin treatment was able to significantly decrease the expression of GLUT1, HKII, and HIF-1α in HepG2 cells either incubated in NG or HG medium.
MCT1↓,
MCT4↓,
HCAR1↓,
SDH↑, Curcumin also uplifted the SDH expression, which was inhibited in high glucose condition
ChemoSen↑, Curcumin Prevents High Glucose-Induced Chemoresistance
ROS↑, Treatment of cells with doxorubicin in presence of curcumin was found to cooperatively augment the ROS level in cells of both NG and HG groups.
BioAv↑, Curcumin Favors Drug Accumulation in Cancer Cells
P53↑, An increased expression of p53 in curcumin-treated cells can be suggestive of susceptibility towards cytotoxic action of anticancer drugs
NF-kB↓, curcumin has therapeutic benefits in hyperglycemia-associated pathological manifestations and through NF-κB inhibition
pH↑, Curcumin treatment was found to resist the lowering of pH of culture supernatant both in NG as well in HG medium.

466- CUR,    Curcumin circumvent lactate-induced chemoresistance in hepatic cancer cells through modulation of hydroxycarboxylic acid receptor-1
- in-vitro, Liver, HepG2 - in-vitro, Liver, HuT78
GlucoseCon↓,
lactateProd↓,
pH↑,
NO↑,
LAR↓,
Hif1a↓, gene and protein
LDHA↓,
MCT1↓,
MDR1↓,
STAT3↓,
HCAR1↓,

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

946- Nimb,    Nimbolide retards T cell lymphoma progression by altering apoptosis, glucose metabolism, pH regulation, and ROS homeostasis
- in-vivo, NA, NA
Apoptosis↑,
Bcl-2↓,
P53↑, up-regulated expression of p53,
cl‑Casp3↑,
Cyt‑c↑,
ROS↑, induced ROS production by suppressing the expression of antioxidant regulatory enzymes, namely superoxide dismutase and catalase
SOD↓,
Catalase↓,
Glycolysis↓,
GLUT3↓,
LDHA↓, LDHA inhibitor
MCT1↓,
NHE1↓,
ATPase↓,
CAIX↓,


Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↓, 1,   Ferroptosis↑, 1,   GPx4↓, 1,   GSH↓, 1,   HO-1↑, 1,   Iron↑, 1,   lipid-P↑, 1,   MDA↑, 1,   NADH↓, 1,   NRF2↑, 2,   OXPHOS↓, 1,   ROS↑, 5,   SOD↓, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   ETC↓, 1,   MMP↓, 1,   SDH↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 2,   CAIX↓, 1,   ECAR↓, 1,   FASN↓, 2,   G6PD↓, 1,   GAPDH↓, 1,   GLS↓, 1,   GlucoseCon↓, 3,   Glycolysis↓, 2,   HK2↓, 2,   lactateProd↓, 3,   lactateProd↑, 1,   LAR↓, 1,   LDH↑, 1,   LDHA↓, 4,   MCT4↓, 1,   NAD↑, 1,   NADH:NAD↓, 1,   PDK1↓, 1,   PFK1↓, 1,   PKM2↓, 2,   SCD1↓, 1,   SREBP2↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 3,   Bcl-2↓, 1,   Casp↑, 1,   cl‑Casp3↑, 1,   Cyt‑c↑, 1,   Ferroptosis↑, 1,   MCT1↓, 5,  

Autophagy & Lysosomes ⓘ

Beclin-1↓, 1,   LC3II↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNMTs↓, 1,   P53↑, 3,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

HDAC↓, 1,   mTOR↓, 2,   STAT3↓, 2,   Wnt↓, 1,  

Migration ⓘ

AP-1↓, 1,   ATPase↓, 1,   MMPs↓, 1,   TumCI↓, 1,   TumCP↓, 1,   TumMeta↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 2,   NO↓, 1,   NO↑, 1,   VEGF↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 2,   GLUT3↓, 1,   NHE1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   HCAR1↓, 2,   Imm↑, 1,   NF-kB↓, 2,   NK cell↑, 1,  

Cellular Microenvironment ⓘ

pH↑, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   ChemoSen↑, 2,   MDR1↓, 1,  

Clinical Biomarkers ⓘ

GutMicro↑, 1,   LDH↑, 1,  
Total Targets: 84

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

ROS↓, 2,  

Cell Death ⓘ

MCT1↓, 1,  

DNA Damage & Repair ⓘ

DNMT1↓, 1,  

Barriers & Transport ⓘ

GastroP↑, 1,   IBI↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   NF-kB↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 3,  

Clinical Biomarkers ⓘ

GutMicro↑, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   hepatoP↑, 1,   neuroP↑, 1,   Obesity↓, 1,   RenoP↑, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 16

Scientific Paper Hit Count for: MCT1, Multiple Copies in T-cell malignancy 1
3 Curcumin
1 Chlorogenic acid
1 Dichloroacetate
1 Nimbolide
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

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