Abstract
OCT4 is a transcription factor involved in maintaining stem cell phenotype and pluripotential. However, it remains unclear the expression pattern and biological function of OCT4 isoforms in cervical cancer. Here, we reported that both nuclear OCT4A and cytoplasmic OCT4B were overexpressed in CC. OCT4A was responsible for self-renewal of cervical cancer stem–like cells (CCSCs). Furthermore, OCT4B overexpression in SiHa cervical cancer cell line significantly increased cell proliferation and tumorigenesis by inhibiting apoptosis. Moreover, OCT4B enhanced angiogenesis by the upregulation of CD34, VEGF, HIF-1α and IL-6, and promoted tumor cell mobility to the surrounding tissue by the upregulation of MMP2 and MMP9, and the induction of epithelial-mesenchymal transition (EMT). In conclusion, nuclear OCT4A may serve as a marker of CCSCs and the driving force for cervical cancer metastasis and recurrence, while cytoplasmic OCT4B may cooperate with OCT4A to regulate the progression of cervical cancer through inducing angiogenesis and EMT.
Highlights
Cervical cancer (CC) is the third most common cancer among women worldwide [1]
Similar to the results of IHC, OCT4B transcription was slightly higher than that of OCT4A, but the difference was not significant (Fig. 1E). These results showed that both OCT4A and OCT4B were highly expressed with different subcellular localization in CC at similar levels
IHC analysis of 50 CC tissues showed that positive OCT4 staining was localized in the nucleus, and in the cytoplasm, which is different from the previous description about OCT4 as a nuclear protein
Summary
Cervical cancer (CC) is the third most common cancer among women worldwide [1]. Epidemiological studies have suggested that multiple risk factors are involved in cervical carcinogenesis, including human papillomavirus (HPV) infection, smoking, and sexual behavior[2]. Genetic and molecular events contributing to the initiation and progression of CC have not yet been fully understood. Cancer stem cells (CSCs) including cervical cancer stem cells have become a topic of intensive investigations[4,5]. Aberrant expression of certain stem cell-related nuclear transcription factors, such as OCT4 [6,7], SOX2 [8] and NANOG [9], could contribute to cervical carcinogenesis. The molecular mechanisms by which these factors promote cervical carcinogenesis have not been fully explored
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