Chl Cancer Research Results

Chl, chloride: Click to Expand ⟱
Source:
Type:
Chloride ion channels and transporters encompass a diverse family of proteins that help regulate membrane potential, cell volume, and intracellular pH.

-Chloride channels facilitate the movement of chloride ions across cell membranes, contributing to processes such as electrical signaling, regulation of cell volume, and maintenance of intracellular pH.
-They include several families and subtypes, such as the CLC family, volume-regulated anion channels (VRACs), and chloride intracellular channel (CLIC) proteins.
-These channels are involved in cell-cycle regulation, apoptosis, and migration—all processes that can influence tumor growth and metastasis.

-Members of the CLC family (e.g., CLC-3) have been reported to be overexpressed in certain cancers like gliomas, breast cancer, and prostate cancer, where they may contribute to enhanced cellular proliferation and invasiveness.
-Chloride intracellular channel proteins (e.g., CLIC1) have been found to have increased expression in cancers including colorectal, lung, and ovarian carcinomas. Elevated levels of CLIC1, for instance, have been linked to increased tumor aggressiveness.
Scientific Papers found: Click to Expand⟱
8021- IVM,    The antiparasitic agent ivermectin induces chloride-dependent membrane hyperpolarization and cell death in leukemia cells
- vitro+vivo, AML, HL-60 - NA, lymphoma, U937 - NA, Pca, DU145
AntiP↑, From these screens, we identified ivermectin, a derivative of avermectin B1 that is licensed for the treatment of the parasitic infections, strongyloidiasis and onchocerciasis, but is also effective against other worm infestations.
TumCD↑, ivermectin induced cell death at low micromolar concentrations in acute myeloid leukemia cell lines and primary patient samples preferentially over normal hematopoietic cells.
selectivity↑,
TumCG↓, Ivermectin also delayed tumor growth in 3 independent mouse models of leukemia at concentrations that appear pharmacologically achievable.
i-Chl↑, Ivermectin increased intracellular chloride ion concentrations and cell size in leukemia cells.
ROS↑, Ivermectin also increased reactive oxygen species generation that was functionally important for ivermectin-induced cell death.
ChemoSen↑, Finally, ivermectin synergized with cytarabine and daunorubicin that also increase reactive oxygen species production.

8040- IVM,    Ivermectin, a potential anticancer drug derived from an antiparasitic drug
- Review, Var, NA
Akt↓, inhibition by IVM of the Akt/mTOR pathway to induce autophagy and p-21-activated kinase 1(PAK1)was the target of IVM for breast cancer
mTOR↓,
TumAuto↑,
TumCP↓, IVM could inhibit the proliferation of the canine breast tumor cell lines CMT7364 and CIPp by blocking the cell cycle without increasing apoptosis, and the mechanism of IVM may be related to the inhibition of the Wnt pathway
TumCCA↑,
Wnt↓,
YAP/TEAD↓,
MMP↓, IVM could significantly reduce the mitochondrial membrane potential and inhibit mitochondrial respiration and ATP production.
mitResp↓,
ATP↓,
eff↓, acetyl-L-cysteine (NAC), could reverse IVM-induced inhibition
eff↑, it was found that IVM could enhance the drug activity of the anti-androgen drug enzalutamide in the prostate cancer cell line LNCaP and reverse the resistance of the prostate cancer cell line PC3 to docetaxel
ROS↑, induction of reactive oxygen species (ROS) production.
ChemoSen↑, IVM can enhance the efficacy of cisplatin to improve the treatment of epithelial ovarian cancer, and the mechanism is related to the inhibition of the Akt/mTOR pathway
PAK1↓, IVM also had a cytotoxic effect on a variety of nasopharyngeal cancer cells in vitro, and the mechanism is related to the reduction of PAK1 kinase activity to inhibit the MAPK pathway.
MAPK↓,
EMT↓, IVM could reduce the metastasis of lung cancer cells by inhibiting EMT.
Beclin-1/ATG6↑, IVM in the breast cancer cell lines MCF-7 and MDA-MB-231 significantly increased intracellular autophagic flux and the expression of key autophagy proteins such as LC3, Bclin1, Atg5
ATG5↑,
CSCs↓, Further studies showed that IVM could inhibit CSCs by regulating the PAK1-STAT3 axis
STAT3↝,
P-gp/ABCB1↓, Several studies have confirmed that IVM could reverse drug resistance by inhibiting P-gp and MDR-associated proteins
MDR1↓,
HSP27↓, Inhibit HSP27 Prostate cancer, Lung cancer Colorectal cancer
Chl↑, Activate chloride channels Leukemia
TFE3↑, Increase TFE3 Activity Melanoma


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

AntiP↑, 1,   TFE3↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 1,   mitResp↓, 1,   MMP↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   MAPK↓, 1,   TumCD↑, 1,   YAP/TEAD↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

HSP27↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG5↑, 1,   Beclin-1/ATG6↑, 1,   TumAuto↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

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

CSCs↓, 1,   EMT↓, 1,   mTOR↓, 1,   STAT3↝, 1,   TumCG↓, 1,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

Chl↑, 1,   i-Chl↑, 1,   PAK1↓, 1,   TumCP↓, 1,  

Barriers & Transport(tgid=15) ⓘ

P-gp/ABCB1↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 2,   eff↓, 1,   eff↑, 1,   MDR1↓, 1,   selectivity↑, 1,  
Total Targets: 31

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: Chl, chloride
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#:1204  State#:%  Dir#:2
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