NDLI: SOX4 contributes to the progression of cervical cancer and the resistance to the chemotherapeutic drug through ABCG2.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Sun, R. Jiang, B. Qi, H. Zhang, X. Yang, J. Duan, J. Li, Y. Li, G.
Description	Country affiliation: China Author Affiliation: Sun R ( Cancer Research Institute, Central South University, Changsha, China.); Jiang B ( Key Laboratory of Carcinogenesis, National Health and Family Planning Commission, Changsha, China.); Qi H ( Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha, China.); Zhang X ( Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine in Henan Province, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, China.); Yang J ( Cancer Research Institute, Central South University, Changsha, China.); Duan J ( Key Laboratory of Carcinogenesis, National Health and Family Planning Commission, Changsha, China.); Li Y ( Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha, China.); Li G ( The Third Affiliated Hospital, Xinxiang Medical University, Xinxiang, China.)
Abstract	SOX4, a member of the SOX (sex-determining region Y-related HMG box) transcription factor family, has been reported to be abnormally expressed in a wide variety of cancers, and to exert a pleiotropic function. However, its function in progression of cervical cancer (CC) remains unknown. In this study, we found that SOX4 was highly expressed in CC cells and tissues, and overexpression of SOX4 in CC CaSki cells enhanced tumor clone formation and cell proliferation, and accelerated cell cycle progress. Meanwhile, downregulation of SOX4 by shRNA in CaSki cells inhibited cell proliferation, and slowed cell cycle progress, indicating that SOX4 contributes to the development of CC. In addition, SOX4 overexpression by gene transfer reduced the sensitivity of CaSki cells in response to the chemotherapeutic drug cisplatin, and SOX4 downregulation by RNA interference increased the sensitivity of CaSki cells in response to cisplatin. Moreover, SOX4 overexpression upregulated multiple drug resistant gene ABCG2, and SOX4 downregulation inhibited ABCG2 expression. Taken together, these results suggested that SOX4 functions to modulate cancer proliferation by regulation of cell cycle, and inhibit cancer cell sensitivity to therapeutic drug via upregulation of ABCG2. Thus, SOX4 may be a target for CC chemotherapy.
File Format	HTM / HTML
e-ISSN	20414889
DOI	10.1038/cddis.2015.290
Journal	Cell Death and Disease
Volume Number	6
Language	English
Publisher	Nature Publishing Group
Publisher Date	2015-11-19
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Research Support, Non-u.s. Gov't Uterine Cervical Neoplasms Cell Proliferation Mice, Inbred Balb C Drug Resistance, Neoplasm Heterografts Neoplasm Proteins Genetics Physiology Enoyl-coa Hydratase Drug Therapy Antineoplastic Agents Soxc Transcription Factors Pharmacology Metabolism Cisplatin Disease Progression Atp-binding Cassette Transporters Discipline Cell Biology Pathology Animals Cell Cycle Mice, Nude Mice Hela Cells
Content Type	Text
Resource Type	Article

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