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TRPC1 regulates hypoxia associated events in PTEN-deficient breast cancer cells


Azimi, I and Thompson, EW and Roberts-Thomson, SJ and Monteith, GR, TRPC1 regulates hypoxia associated events in PTEN-deficient breast cancer cells, Calcium Signalling Gordon Research Conference: Intracellular calcium signals: Generation, Function and Therapeutic Intervention, 17-18 June 2017, Lucca, Italy (2017) [Conference Extract]

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TRPC1 was the first member of the non-selective cation transient receptor potential (TRP) ion channel family identified in mammals; however the exact physiological function of TRPC1 as a channel is still not fully understood. TRPC1 knockout mice have been previously described as not having "dramatic" phenotypes. Our unpublished studies identified the TRPC1 ion channel as an integral player of responses to hypoxia, a hallmark of the tumour microenvironment in breast cancer cells, that promotes invasiveness and resistance to chemotherapeutics. TRPC1 was involved in the regulation of specific markers of hypoxia-induced epithelial to mesenchymal transition (EMT), as well as activation of EGFR and STAT3 signalling. TRPC1 also played a role in the regulation of constitutive levels of HIF1α in an Akt-dependent manner in PTEN-deficient MDA-MB-468 and HCC1569 breast cancer cell lines. Furthermore, we identified a close association between the expression of TRPC1 with EMT and metastasis-related genes in breast tumours, as well as survival in basal breast cancer patients. This study presents TRPC1 as a potential therapeutic target for the control of breast cancer metastasis.

Item Details

Item Type:Conference Extract
Keywords:TRPC1, hypoxia, PTEN-deficient, breast cancer
Research Division:Biomedical and Clinical Sciences
Research Group:Pharmacology and pharmaceutical sciences
Research Field:Basic pharmacology
Objective Division:Expanding Knowledge
Objective Group:Expanding knowledge
Objective Field:Expanding knowledge in the health sciences
UTAS Author:Azimi, I (Dr Iman Azimi)
ID Code:151232
Year Published:2017
Deposited By:Pharmacy
Deposited On:2022-07-25
Last Modified:2022-07-28

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