中国科学院神经科学研究所王以政研究组研究发现TRPC3通道促进卵巢癌的发生，这对于进一步了解TRPC3通道以及卵巢癌的发生具有重要的意义。这一研究成果公布在Oncogene杂志上。
卵巢癌是发生于卵巢组织的恶性肿瘤。卵巢癌有起病隐匿，早期不易发现，易转移，预后差等特点。占所有妇科恶性肿瘤的15%左右。卵巢恶性肿瘤的发病率在女性常见恶性肿瘤中所占的百分率为2.4－5.6%。在女性生殖道恶性肿瘤中占第三位，次于宫颈癌和宫体癌。之前香港知名的女企业家龚如心就是由于卵巢癌去世的
目前卵巢癌的发病机制仍不清楚，在这项研究中，研究人员将TRPC通道与之联系了起来。胞质自由钙离子的增加会引起包括细胞生长、分化与凋亡等的生理改变。TRPC通道是钙离子渗透的非选择性正离子通道。研究人员发现，TRPC3通道促进卵巢癌的发生。人卵巢癌样品的TRPC3蛋白水平明显高于正常人的卵巢样品。下调人卵巢癌细胞系SKOV3细胞的TRPC3的表达，可导致增殖的延缓，抑制介导钙离子注入的表皮生长因子的作用，Cdc2和CaMKⅡβ的去磷酸化，延长细胞进入M期的过程。在减少TRPC3的表达可以抑制注射了SKOV3细胞的裸鼠的肿瘤形成。研究人员认为，卵巢癌的发生需要TRPC3活性的增加。（生物谷Bioon.com）
生物谷推荐原始出处：
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.
