Abstract
Ovarian cancer is a highly deadly disease, which is often diagnosed at a late stage with metastases. However, most ovarian cancers relapse after surgery combined with platinum-based chemotherapy. Cancer stem cells (CSCs) are stem-like cells that possess high tumorigenic capability and display higher resistant capability against current therapies. However, our knowledge of ovarian CSCs and their molecular mechanism remains sparse. In the current study, we found that KDM4C, a histone demethylase, was required for ovarian cancer stem cell (CSC) maintenance. Depletion of KDM4C significantly reduced the CSC population and sphere formation in vitro. Moreover, we found that KDM4C can regulate the expression of stem cell factor OCT-4 via binding to its promoter. These data indicate that KDM4C is relevant for ovarian CSC maintenance and underscore its importance as a potential therapeutic target.
Highlights
Ovarian cancer has the highest mortality rate of any gynecological malignancies around the world [1]
KDM4C Is Upregulated in the cancer stem cells (CSCs) Population in Ovarian Cancer Cell Lines
Our results demonstrated that KDM4C and KDM5C were significantly increased in SKOV-3 spheres, while the rest of the histone demethylases showed comparable mRNA expression levels (Figure 1(b))
Summary
Ovarian cancer has the highest mortality rate of any gynecological malignancies around the world [1]. Surgery and chemotherapy are the main treatments for ovarian cancer, whereas a large majority of patients with advanced ovarian cancer relapse due to therapy resistance [2]. To overcome this dilemma in ovarian cancer, it is important to understand the molecular mechanism underlying therapy resistance of ovarian cancer [3]. The recently proposed hypothesis of cancer stem cells (CSCs), known as tumor-initiating cells, may provide a more effective approach for the treatment of ovarian cancer. CSCs display higher resistant capability against current therapies and are believed to be responsible for tumor metastasis [5, 6]. Understanding of the molecular regulation mechanism of CSCs might provide new targets for treatment of ovarian cancer
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