Long noncoding RNA SFTA1P promoted apoptosis and increased cisplatin chemosensitivity via regulating the hnRNP-U-GADD45A axis in lung squamous cell carcinoma
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Ling Li1,2, Ji-Ye Yin1,2, Fa-Zhong He1,2, Ma-Sha Huang1,2, Tao Zhu1,2, Yuan-Feng Gao1,2, Yi-Xin Chen1,2, Dong-Bo Zhou3, Xiang Chen4, Lun-Quan Sun5, Wei Zhang1,2, Hong-Hao Zhou1,2 and Zhao-Qian Liu1,2
1Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, P. R. China
2Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University, Changsha 410078, P. R. China
3Department of Gerontology, Xiangya Hospital, Central South University, Changsha 410008, P. R. China
4Department of Dermatology, Xiangya Hospital, Central South University, Changsha 410008, P. R. China
5Center for Molecular Medicine, Xiangya Hospital, Key Laboratory of Molecular Radiation Oncology of Hunan Province, Central South University, Changsha 410008, P. R. China
Zhao-Qian Liu, email: firstname.lastname@example.org
Keywords: lung squamous cell carcinoma; long noncoding RNA SFTA1P; hnRNP-U- GADD45A; apoptosis; cisplatin chemosensitivity
Received: July 28, 2017 Accepted: August 24, 2017 Published: October 27, 2017
Chemotherapeutic insensitivity remains one of the major obstacles in clinical treatment of lung squamous cell carcinoma (LSCC). Recently, increasing evidence has suggested that long non-coding RNAs (lncRNAs) promote tumorigenesis in many cancer types. However, the potential biological roles and regulatory mechanisms of lncRNAs in response to cisplatin treatment are poorly understood. Here, we found that lncRNA SFTA1P (surfactant associated 1, pseudogene), highly expressed in lung, was down-regulated in LSCC tissues and could be induced upon cisplatin treatment in LSCC cells. Elevated SFTA1P induced apoptosis and enhanced the sensitivity to cisplatin of LSCC cells. We further identified that hnRNP-U (heterogeneous nuclear ribonucleoprotein U) was down-regulated in LSCCs and positively correlated with patients’ poor prognosis as well as SFTA1P. Mechanistic studies revealed that SFTA1P could up-regulate hnRNP-U expression. In addition, we identified that hnRNP-U enhanced cisplatin-induced apoptosis through up-regulation of GADD45A, high expression of which was correlated with good prognosis in LSCC patients. Our findings demonstrated that SFTA1P might serve as a useful biomarker for LSCC diagnosis and a predictor for cisplatin chemotherapy response in patients with LSCC.
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