Abstract
Epithelial ovarian carcinomas account for more than 90% of human ovarian cancers and have become the primary cause of death for gynecological malignancies. Unlimited cell proliferation and resistance to cell apoptosis contribute to the development of ovarian cancers. However, the underlying mechanisms involved in these processes in epithelial ovarian carcinomas are yet poorly understood. In the present study, we examined the Hippo signaling gene expression and investigated the effects of Sphingosine 1-phosphate (S1P) on cell proliferation and the underlying mechanisms in human ovarian cancer cell lines, OVCAR3 and SKOV3. Our results demonstrate that S1P disrupts Hippo signaling by reducing YAP phosphorylation and increasing the expression of CCN1 and CCN2 in both ovarian cancer cells. Furthermore, the increase in CCN1/CCN2 expression contributes to the S1P-induced increase in cancer cell proliferation.
Highlights
IntroductionEpithelial ovarian carcinomas (EOC) account for more than 90% of human ovarian cancers, which have become the primary cause of death for gynecological malignancies in the western countries [1]
Sphingosine 1-phosphate (S1P) induces a decrease in phosphorylated Yes-associated protein (YAP) and a nucleus translocation of YAP in OVCAR3 and SKOV3 cells
We examined the Hippo signaling gene expression levels and found that all of the genes examined are expressed in two Epithelial ovarian carcinomas (EOC) cell lines, even though two cell lines have the different genetic background
Summary
Epithelial ovarian carcinomas (EOC) account for more than 90% of human ovarian cancers, which have become the primary cause of death for gynecological malignancies in the western countries [1]. Lacking highly sensitive and specific methods for early detection, a majority of patients with the initial diagnosis of EOC are at advanced stages (FIGO classification stage III and stage IV) [1]. The clinical outcomes in advanced EOC remain comparatively poor [1]. Finding a reliable method for early diagnosis of this malignant disease is urgently required. Two major processes, unlimited cell proliferation and resistance to cell apoptosis, contribute to the development of ovarian cancers. The underlying mechanisms involved in these processes in EOC are yet poorly understood
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