TRPC1 Cancer Research Results

TRPC1, Transient Receptor Potential Canonical 1: Click to Expand ⟱
Source:
Type:
TRPC1 is a calcium-permeable ion channel protein that regulates key signaling pathways in many cell types, with roles in physiology and disease (including cancer). 
TRPC1 is upregulated in several cancer types, including breast cancer.
Since it contributes to Ca²⁺ influx, its overexpression can enhance signaling pathways that drive:
 -Proliferation
 -Migration & invasion
 -Epithelial–mesenchymal transition (EMT)
 -Chemoresistance

Breast cancer cell lines
MCF-7 (ER⁺, luminal type)
-TRPC1 is expressed and contributes to store-operated calcium entry (SOCE).
-Silencing or inhibiting TRPC1 tends to reduce proliferation and increase sensitivity to apoptosis.
MDA-MB-231 (triple-negative, invasive type)
-TRPC1 is generally upregulated compared to non-tumorigenic breast epithelial cells (like MCF10A or HBL-100).
-Promotes migration and invasion through calcium-dependent activation of signaling pathways (e.g., NFAT, ERK, AKT).
-Knockdown reduces motility and metastatic potential in vitro.
HBL-100 (SV40-transformed, non-malignant reference)
-TRPC1 expression is lower than in true malignant lines like MDA-MB-231.
-Often used as a “control” to highlight that TRPC1 is upregulated during malignant transformation.


Scientific Papers found: Click to Expand⟱
4425- MF,  doxoR,    Brief Magnetic Field Exposure Stimulates Doxorubicin Uptake into Breast Cancer Cells in Association with TRPC1 Expression: A Precision Oncology Methodology to Enhance Chemotherapeutic Outcome
- in-vitro, BC, 4T1 - in-vitro, BC, MCF-7
ChemoSen↑, PEMF therapy may enhance DOX cytotoxicity in breast cancer cells,
TRPC1↑, increased by TRPC1 overexpression,
Dose↓, PEMF exposure enhances DOX-mediated killing of breast cancer cells, reducing the IC50 value of DOX by half, whereas muscle cells, representative of collateral tissues, were less sensitive to PEMF-enhanced DOX-mediated cytotoxicity
selectivity↑, whereas muscle cells, representative of collateral tissues, were less sensitive to PEMF-enhanced DOX-mediated cytotoxicity.

4356- MF,    Pulsed electromagnetic fields synergize with graphene to enhance dental pulp stem cell-derived neurogenesis by selectively targeting TRPC1 channels
- in-vitro, Nor, NA
*Diff↑, brief PEMF exposure promotes in vitro differentiation by activating a TRPC1-mitochondrial axis
*TRPC1↑,
*ROS↑, PEMF-stimulated neurogenic induction of hDPSCs through their mutual capacity to activate TRPC1with subsequent ROS production.


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:


Migration ⓘ

TRPC1↑, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   Dose↓, 1,   selectivity↑, 1,  
Total Targets: 4

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

Diff↑, 1,  

Migration ⓘ

TRPC1↑, 1,  
Total Targets: 3

Scientific Paper Hit Count for: TRPC1, Transient Receptor Potential Canonical 1
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#:1376  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

Home Page