Research Papers:

Silencing RIF1 decreases cell growth, migration and increases cisplatin sensitivity of human cervical cancer cells

Ying Mei, Chen Peng, Yong-Bin Liu, Jing Wang and Hong-Hao Zhou _

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Oncotarget. 2017; 8:107044-107051. https://doi.org/10.18632/oncotarget.22315

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Ying Mei1,2,3, Chen Peng4, Yong-Bin Liu1,2,3, Jing Wang5 and Hong-Hao Zhou1,2,3

1Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, P. R. China

2Institute of Clinical Pharmacology, Central South University, Hunan Key Laboratory of Pharmacogenetics, Changsha 410078, P. R. China

3Hunan Province Cooperation Innovation Center for Molecular Target New Drug Study, Hengyang 421001, P. R. China

4Department of music therapy, Sam Houston State University, Huntsville TX 77340, USA

5Xiangya school of medicine, Central South University, Changsha 410008, P. R. China

Correspondence to:

Hong-Hao Zhou, email: [email protected]

Keywords: cervical cancer, RIF1, cisplatin, cell cycle, drug resistance

Received: June 12, 2017     Accepted: July 26, 2017     Published: November 06, 2017


Replication timing regulatory factor 1 (RIF1) plays an important role in DNA replication regulation, stem cell pluripotency and DNA repair pathway. However, little is known about the molecular mechanisms and physiological significance of RIF1 in cancer and chemotherapy efficacy. In this study, we found that RIF1 is upregulated in cervical cancer tissues compared with normal tissues both at mRNA and protein levels through online databases. RIF1 knockdown reduced cervical cancer cell growth, colony formation, migration and epithelial–mesenchymal transition (EMT) markers. Flow cytometry analysis indicated that RIF1 knockdown induced apoptosis and G2 cell cycle arrest. Furthermore, RIF1 knockdown increased cisplatin sensitivity, cisplatin-induced G2/M phase arrest, apoptosis and led to defects in DNA repair in a concentration-dependent manner. In terms of mechanism research, increased CDKN1A expression and Bax/Bcl-2/caspase-3 signaling pathway might be involved in the G2/M phase arrest and increased apoptosis in RIF1-silenced cervical cancer cells. Thus, these findings indicate that RIF1 knockdown prior to chemotherapy may be a potential effective therapeutic strategy for cervical cancer.

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