Differential Role of Transient Receptor Potential Channels in Ca2+ Entry and Proliferation of Prostate Cancer Epithelial Cells

Thebault, Stéphanie; Flourakis, Matthieu; Vanoverberghe, Karine; Vandermoere, Franck; Roudbaraki, Morad; Lehen’kyi, V’yacheslav; Slomianny, Christian; Beck, Benjamin; Mariot, Pascal; Bonnal, J; Mauroy, Brigitte; Shuba, Yaroslav; Capiod, Thierry; Skryma, Roman; Prevarskaya, Natalia

doi:10.1158/0008-5472.can-05-0376

Cited by 179 publications

(153 citation statements)

References 44 publications

Supporting

Mentioning

145

Contrasting

Unclassified

Order By: Relevance

“…Oscillatory [Ca 2+ ] i activity may be especially suited to the specificity of Ca 2+ signalling [26], as the possibility of amplitude and frequency signal encoding permits distinct effectors to be targeted. Recent data suggested that Ca 2+ entry through TRPC6 enhances primary hPCE cell proliferation [12]. In our study, we not only uncover the involvement of TRPC6 in HGFinduced Ca 2+ entry in DU145 and PC3 cells but also show the likely role of this channel in the enhancement of the proliferative effects of HGF, because exposure to HGF causes TRPC6 overexpression.…”

Section: Discussionsupporting

confidence: 66%

“…TRPC6 channels function as store-operated calcium channels that account for the sustained calcium inflow triggered by the IP 3 -evoked depletion of intracellular Ca 2+ stores [9]. Furthermore, TRPC6, as a receptoroperated Ca 2+ channel in primary hPCE cells, is also directly activated by DAG [11,12]. Although it is not clear whether HGF can induce Ca 2+ entry independent of store depletion in DU145 cells, our results suggest that TRPC6 is instrumental to HGF-induced calcium entry in DU145 and PC3 cells.…”

Section: Discussionmentioning

confidence: 99%

“…For PCR, specific sense and antisense primers were selected. The human TRPC6 primers (NM_004621) were as follows: sense 5′-GAACTTAGCAATGAACTGGCAGT-3′ and antisense 5′-CATATCATGCCTATTACCCAGGA-3′, with a product length 625 bp for TRPC6 and 277 bp for TRPC6γ [12]. The human c-MET primers (NM_000245) were as follows: sense 5′-GTTTCCCAATTTCTGACC-3′ and antisense 5′-TATATCAAAGGTGTTTAC-3′, with a product length of 516 bp.…”

Section: Reverse Transcription-polymerase Chain Reaction Analysis (Rtmentioning

confidence: 99%

“…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%

See 3 more Smart Citations

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

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionsupporting

confidence: 66%

Section: Discussionmentioning

confidence: 99%

Section: Reverse Transcription-polymerase Chain Reaction Analysis (Rtmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

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

View full text Add to dashboard Cite

show abstract

“…Under physiologic conditions, many aspects of these processes are mediated by members of the Ca 2 þ -binding protein (Nelson and Chazin, 1998). Since considerable evidence shows that intracellular Ca 2 þ deregulation is crucial for tumour growth and development (Durham and Walton, 1982;Huang et al, 2005;Ding et al, 2006;Thebault et al, 2006), understanding the genetic mechanisms of the Ca 2 þ -binding protein genes involved in carcinogenesis is imperative for the development of new therapeutic strategies.…”

mentioning

confidence: 99%

Network-based analysis of calcium-binding protein genes identifies Grp94 as a target in human oral carcinogenesis

et al. 2007

View full text Add to dashboard Cite

To characterise Ca 2 þ -binding protein gene expression changes in oral squamous cell carcinomas (OSCCs), we compared the gene expression profiles in OSCC-derived cell lines with normal oral tissues. One hundred Ca 2 þ -binding protein genes differentially expressed in OSCCs were identified, and genetic pathways associated with expression changes were generated. Among genes mapped to the network with the highest significance, glucose-regulated protein 94 kDa (Grp94) was evaluated further for mRNA and protein expression in the OSCC cell lines, primary OSCCs, and oral premalignant lesions (OPLs). A significant (Po0.001) overexpression of Grp94 protein was observed in all cell lines compared to normal oral epithelium. Immunohistochemical analysis showed highly expressed Grp94 in primary OSCCs and OPLs, whereas most of the corresponding normal tissues had no protein immunoreaction. Real-time quantitative reverse transcriptase-PCR data agreed with the protein expression status. Moreover, overexpression of Grp94 in primary tumours was significantly (Po0.001) correlated with poor disease-free survival. The results suggested that Grp94 may have potential clinical application as a novel diagnosis and prognostic biomarker for human OSCCs.

show abstract

Roles of Ion Transport in Control of Cell Motility

Stock

Ludwig

Hanley

et al. 2013

Comprehensive Physiology

View full text Add to dashboard Cite

Cell motility is an essential feature of life. It is essential for reproduction, propagation, embryonic development, and healing processes such as wound closure and a successful immune defense. If out of control, cell motility can become life-threatening as, for example, in metastasis or autoimmune diseases. Regardless of whether ciliary/flagellar or amoeboid movement, controlled motility always requires a concerted action of ion channels and transporters, cytoskeletal elements, and signaling cascades. Ion transport across the plasma membrane contributes to cell motility by affecting the membrane potential and voltage-sensitive ion channels, by inducing local volume changes with the help of aquaporins and by modulating cytosolic Ca(2+) and H(+) concentrations. Voltage-sensitive ion channels serve as voltage detectors in electric fields thus enabling galvanotaxis; local swelling facilitates the outgrowth of protrusions at the leading edge while local shrinkage accompanies the retraction of the cell rear; the cytosolic Ca(2+) concentration exerts its main effect on cytoskeletal dynamics via motor proteins such as myosin or dynein; and both, the intracellular and the extracellular H(+) concentration modulate cell migration and adhesion by tuning the activity of enzymes and signaling molecules in the cytosol as well as the activation state of adhesion molecules at the cell surface. In addition to the actual process of ion transport, both, channels and transporters contribute to cell migration by being part of focal adhesion complexes and/or physically interacting with components of the cytoskeleton. The present article provides an overview of how the numerous ion-transport mechanisms contribute to the various modes of cell motility.

show abstract

Differential Role of Transient Receptor Potential Channels in Ca2+ Entry and Proliferation of Prostate Cancer Epithelial Cells

Cited by 179 publications

References 44 publications

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

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

Network-based analysis of calcium-binding protein genes identifies Grp94 as a target in human oral carcinogenesis

Roles of Ion Transport in Control of Cell Motility

Contact Info

Product

Resources

About