中國科學(xué)院神經(jīng)科學(xué)研究所王以政研究組研究發(fā)現(xiàn)TRPC3通道促進卵巢癌的發(fā)生,，這對于進一步了解TRPC3通道以及卵巢癌的發(fā)生具有重要的意義,。這一研究成果公布在Oncogene雜志上。
卵巢癌是發(fā)生于卵巢組織的惡性腫瘤,。卵巢癌有起病隱匿,，早期不易發(fā)現(xiàn)，易轉(zhuǎn)移,，預(yù)后差等特點,。占所有婦科惡性腫瘤的15%左右。卵巢惡性腫瘤的發(fā)病率在女性常見惡性腫瘤中所占的百分率為2.4－5.6%,。在女性生殖道惡性腫瘤中占第三位,，次于宮頸癌和宮體癌。之前香港知名的女企業(yè)家龔如心就是由于卵巢癌去世的
目前卵巢癌的發(fā)病機制仍不清楚,，在這項研究中,，研究人員將TRPC通道與之聯(lián)系了起來。胞質(zhì)自由鈣離子的增加會引起包括細胞生長,、分化與凋亡等的生理改變,。TRPC通道是鈣離子滲透的非選擇性正離子通道。研究人員發(fā)現(xiàn),，TRPC3通道促進卵巢癌的發(fā)生,。人卵巢癌樣品的TRPC3蛋白水平明顯高于正常人的卵巢樣品。下調(diào)人卵巢癌細胞系SKOV3細胞的TRPC3的表達,，可導(dǎo)致增殖的延緩,，抑制介導(dǎo)鈣離子注入的表皮生長因子的作用，Cdc2和CaMKⅡβ的去磷酸化，延長細胞進入M期的過程,。在減少TRPC3的表達可以抑制注射了SKOV3細胞的裸鼠的腫瘤形成,。研究人員認為，卵巢癌的發(fā)生需要TRPC3活性的增加,。（生物谷Bioon.com）
生物谷推薦原始出處：
Oncogene (2009) 28, 1320–1328; doi:10.1038/onc.2008.475
Transient receptor potential channel C3 contributes to the progression of human ovarian cancer
S L Yang1,2, Q Cao3, K C Zhou1,2, Y J Feng3 and Y Z Wang1,2
1Laboratory of Neural Signal Transduction, Institute of Neuroscience, Shanghai Institutes of Biological Sciences, State Key Laboratory of Neuroscience, Shanghai, China
2The Graduate School, Chinese Academy of Science, Shanghai, China
3The Obstetrics and Gynecology Hospital of Medical Center, Fudan University, Shanghai, China
Ovarian cancer (OC) is the leading cause of death from gynecological malignancy. However, the mechanism by which OC develops remains largely unknown. Increases in cytosolic free Ca2+ ([Ca2+]i) can result in different physiological changes including cell growth, differentiation and death. The transient receptor potential (TRP) C channels are nonselective cation channels with permeability to Ca2+. Here we report that TRPC3 channels promote human OC growth. The TRPC3 protein levels in human OC specimens were greatly increased than those in normal ovarian specimens. Downregulating TRPC3 expression in SKOV3 cells, a human OC cell line, led to reduction of proliferation, suppression in epidermal growth factor-induced Ca2+ influx, dephosphorylation of Cdc2 and CaMKIIα and prolonged progression through M phase of these cells. Further, decreased the expression of TRPC3 suppressed the tumor formation generated by injecting SKOV3 cells in nude mice. Together, our results suggest that increased activity of TRPC3 channels is necessary for the development of OCs.
