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tid		Target	TRPC1	Cancers General Effect on Target

Name	Transient Receptor Potential Canonical 1
Source
Type

<b>TRPC1</b> is a calcium-permeable ion channel protein that regulates key signaling pathways in many cell types, with roles in physiology and disease (including cancer).
<pre>
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.
</pre>

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.

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