Expression of TRPC6 channels in human epithelial breast cancer cells

Guilbert, Arnaud; Dhennin‐Duthille, Isabelle; Hiani, Yassine El; Haren, Nathalie; Khorsi, Hafida; Sevestre, Henri; Ahidouch, Ahmed; Ouadid-Ahidouch, Halima

doi:10.1186/1471-2407-8-125

Cited by 86 publications

(59 citation statements)

References 39 publications

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“…However, our data showed that only TRPC6 was selectively increased in response to nicotine, while the other subtypes TRPC1/3/4 did not change in HBSMCs. Interestingly this finding differs from a previous study reporting that TRPC6 alone induced OAG-activated calcium influx in human epithelial breast cancer cells [49]. It also differs from our previous study reporting that the enhanced ROCE due to upregulated TRPC6 is a novel pathogenic mechanism contributing to the increased basal [Ca 2+ ] i in pulmonary venous smooth muscle cells (PVSMC) and excessive PVSMC proliferation during the development of hypoxic pulmonary hypertension [50].…”

Section: Discussioncontrasting

confidence: 55%

Nicotine-Induced Airway Smooth Muscle Cell Proliferation Involves TRPC6-Dependent Calcium Influx Via α7 nAChR

Wang

Peng

Hao

et al. 2017

Cell Physiol Biochem

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Background/Aims: The proliferation of human bronchial smooth muscle cells (HBSMCs) is a key pathophysiological component of airway remodeling in chronic obstructive pulmonary disease (COPD) for which pharmacotherapy is limited, and only slight improvements in survival have been achieved in recent decades. Cigarette smoke is a well-recognized risk factor for COPD; however, the pathogenesis of cigarette smoke-induced COPD remains incompletely understood. This study aimed to investigate the mechanisms by which nicotine affects HBSMC proliferation. Methods: Cell viability was assessed with a CCK-8 assay. Proliferation was measured by cell counting and EdU immunostaining. Fluorescence calcium imaging was performed to measure intracellular Ca²⁺ concentration ([Ca²⁺]_i). Results: The results showed that nicotine promotes HBSMC proliferation, which is accompanied by elevated store-operated calcium entry (SOCE), receptor-operated calcium entry (ROCE) and basal [Ca²⁺]_i in HBSMCs. Moreover, we also confirmed that canonical transient receptor potential protein 6 (TRPC6) and α7 nicotinic acetylcholine receptor (α7 nAChR) are involved in nicotine-induced upregulation of cell proliferation. Furthermore, we verified that activation of the PI3K/Akt signaling pathway plays a pivotal role in nicotine-enhanced proliferation and calcium influx in HBSMCs. Inhibition of α7 nAChR significantly decreased Akt phosphorylation levels, and LY294002 inhibited the protein expression levels of TRPC6. Conclusion: Herein, these data provide compelling evidence that calcium entry via the α7 nAChR-PI3K/Akt-TRPC6 signaling pathway plays an important role in the physiological regulation of airway smooth muscle cell proliferation, representing an important target for augmenting airway remodeling.

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Section: Discussioncontrasting

confidence: 55%

Nicotine-Induced Airway Smooth Muscle Cell Proliferation Involves TRPC6-Dependent Calcium Influx Via α7 nAChR

Wang

Peng

Hao

et al. 2017

Cell Physiol Biochem

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“…We have previously demonstrated that TRPC6 and TRPM7 are overexpressed in hBDA at both protein and mRNA levels, and their functional expression was recorded in the MCF-7 cancer cell line and human breast cancer epithelial (hBCE) cells isolated from surgical resection [29,30]. We also reported that TRPM8 expression is regulated by estrogens in breast cancer cells and tissues [31].…”

Section: Introductionmentioning

confidence: 97%

High Expression of Transient Receptor Potential Channels in Human Breast Cancer Epithelial Cells and Tissues: Correlation with Pathological Parameters

Dhennin‐Duthille

Gautier²,

Faouzi³

et al. 2011

Cell Physiol Biochem

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223

206

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Background: Transient Receptor Potential (TRP) channels are expressed in many solid tumors. However, their expression in breast cancer remains largely unknown. Here, we investigated the profile expression of 13 TRP channels in human breast ductal adenocarcinoma (hBDA) and performed a correlation between their overexpression and pathological parameters. Methods: The TRP channels expression was determined by RT-PCR in hBDA tissue, in human breast cancer epithelial (hBCE) primary culture and in MCF-7 cell line. The TRP protein level was evaluated by immunohistochemistry in hBDA tissue samples of 59 patients. Results: TRPC1, TRPC6, TRPM7, TRPM8, and TRPV6 channels were overexpressed in hBDA compared to the adjacent non-tumoral tissue. Most interestingly, TRPC1, TRPM7 and TRPM8 expression strongly correlated with proliferative parameters (SBR grade, Ki67 proliferation index, and tumor size), and TRPV6 was mainly overexpressed in the invasive breast cancer cells. Using laser capture microdissection, we found that TRPV6 expression was higher in invasive areas, compared to the corresponding non-invasive ones. Moreover, TRPV6 silencing inhibited MDA-MB-231 migration and invasion, and MCF-7 migration. Conclusion: TRP channels are aberrantly expressed in hBDA, hBCE primary cultures, and cell lines, and associated with pathological parameters. The high expression of TRP channels in tumors suggests the potential of these channels for diagnostic, prognosis and/or therapeutic approaches in human breast ductal adenocarcinoma.

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“…Through a phospholipase C (PLC)-dependent mechanism, they can be activated by G-protein coupled receptors or receptor tyrosine kinases [7]. Recently, it has been shown that TRPC6 contributes to the proliferation of some types of cancer cells [8][9][10]. In addition, in the primary human prostate cancer epithelial (hPCE) cells and LNCaP cells, agonist-mediated stimulation of α 1 -adrenergic receptors requires the coupled activation of TRPC6 channels and nuclear factors of activated T cells to promote cell proliferation [11,12].…”

Section: Introductionmentioning

confidence: 99%

The role of TRPC6 in HGF-induced cell proliferation of human prostate cancer DU145 and PC3 cells

Wang¹,

Yue²,

Li³

et al. 2010

Asian J Androl

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Hepatocyte growth factor (HGF) is a glycoprotein that induces prostate cancer cell proliferation, migration and invasion. The activation of transient receptor potential canonical 6 (TRPC6) channels is considered important in promoting prostate cancer cell proliferation. In this study, we assessed the role of endogenous TRPC6 channels in the HGF-induced cell proliferation of prostate cancer. Reverse transcription-PCR and Western blotting were used to investigate TRPC6 expression. Electrophysiological techniques (whole-cell patch clamp configuration) and Ca 2+ imaging analysis were used to investigate the channel activity in cells. The effects of TRPC6 channels on cell cycle progression, cell apoptosis and cell growth were also examined. TRPC6 and c-MET were expressed in DU145 and PC3 cells. In addition, functional TRPC6 channels were present in DU145 and PC3 cells, and TRPC6 knockdown suppressed TRPC-like currents evoked by oleoyl-2-acetyl-sn-glycerol (OAG). Inhibition of TRPC6 channels in DU145 and PC3 cells abolished OAG-and HGF-induced Ca 2+ entry. Furthermore, inhibition of TRPC6 channels arrested DU145 and PC3 cells at the G2/M phase and suppressed HGF-induced cell proliferation. Collectively, our results indicate that TRPC6 has an important role in HGF-induced DU145 and PC3 cell proliferation.

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Expression of TRPC6 channels in human epithelial breast cancer cells

Cited by 86 publications

References 39 publications

Nicotine-Induced Airway Smooth Muscle Cell Proliferation Involves TRPC6-Dependent Calcium Influx Via α7 nAChR

Nicotine-Induced Airway Smooth Muscle Cell Proliferation Involves TRPC6-Dependent Calcium Influx Via α7 nAChR

High Expression of Transient Receptor Potential Channels in Human Breast Cancer Epithelial Cells and Tissues: Correlation with Pathological Parameters

The role of TRPC6 in HGF-induced cell proliferation of human prostate cancer DU145 and PC3 cells

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