剪接体相关因子CTNNBL1促进卵巢癌的增殖和侵袭。
Spliceosome-associated factor CTNNBL1 promotes proliferation and invasion in ovarian cancer.
作者信息
Li Yingwei, Guo Haiyang, Jin Chengjuan, Qiu Chunping, Gao Min, Zhang Lei, Liu Zhaojian, Kong Beihua
机构信息
Department of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Jinan 250012, China.
Princess Margaret Cancer Center, University Health Network, Toronto, Ontario, Canada.
出版信息
Exp Cell Res. 2017 Aug 1;357(1):124-134. doi: 10.1016/j.yexcr.2017.05.008. Epub 2017 May 10.
Ovarian cancer is the most lethal gynecologic malignancy and the molecular pathogenesis of high-grade serous ovarian carcinoma has not been completely characterized. Numerous studies have shown that altered splicing patterns and splicing factors were found to contribute to tumor development and progression. In this study, we demonstrated that spliceosome-associated factor CTNNBL1 was significantly upregulated in high-grade serous ovarian carcinoma, the elevated level of CTNNBL1 indicates poor prognosis in patients with high-grade serous ovarian carcinoma. Functional characterization revealed that CTNNBL1 promoted the proliferation and invasion of ovarian cancer cells in vitro. Furthermore, through transcriptome analysis, we found CTNNBL1 regulates multiple splicing events and gene expression in ovarian cancer cells. Importantly, we identified IFI16 and FOXM1 splicing was regulated by CTNNBL1. To our knowledge, this is the first study exploring the expression, functional roles and regulated splicing events of CTNNBL1 in ovarian cancer.
卵巢癌是最致命的妇科恶性肿瘤，高级别浆液性卵巢癌的分子发病机制尚未完全明确。大量研究表明，剪接模式和剪接因子的改变与肿瘤的发生发展有关。在本研究中，我们发现剪接体相关因子CTNNBL1在高级别浆液性卵巢癌中显著上调，CTNNBL1水平升高提示高级别浆液性卵巢癌患者预后不良。功能研究表明，CTNNBL1在体外促进卵巢癌细胞的增殖和侵袭。此外，通过转录组分析，我们发现CTNNBL1调节卵巢癌细胞中的多个剪接事件和基因表达。重要的是，我们确定IFI16和FOXM1的剪接受CTNNBL1调控。据我们所知，这是第一项探索CTNNBL1在卵巢癌中的表达、功能作用及调控剪接事件的研究。
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