Title: Long non-coding RNA SPRY4-IT1 promotes gallbladder carcinoma progression
Abstract: // Liang Yang 1, * , Xi Cheng 1, * , Naijian Ge 2 , Weixing Guo 3 , Feiling Feng 4 , Fuying Wan 1 1 Radiation Center, East Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai, 201805, China 2 Mini-Invasive Intervention Center, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai, 200438, China 3 Hepatic Surgical Department VI, Eastern Hepatobiliary Surgery Hospital, The Second Military Medical University, Shanghai, 200438, China 4 Department of Biliary Tract, Eastern Hepatobiliary Surgery Hospital, The Second Military Medical University, Shanghai 200438, China * Liang Yang, Xi Cheng and Naikian Ge contributed equally to this work Correspondence to: Weixing Guo, email: [email protected] Feiling Feng, email: [email protected] Keywords: SPRY4-IT1, lncRNA, GBC, metastasis, EMT Received: September 20, 2016 Accepted: October 24, 2016 Published: November 25, 2016 ABSTRACT Gallbladder carcinoma (GBC) is the most common malignancy of the bile duct and patients with GBC have extremely poor prognoses. Long non-coding RNAs (lncRNAs) are found to be dysregulated in a variety of cancers, including GBC. SPRY4-IT1 has been recently revealed as oncogenic regulator in many cancers. However, whether SPRY4-IT1 is involved in GBC progression remains largely unknown. To investigate the role of SPRY4-IT1 in GBC, we evaluated the expression SPRY4-IT1 in GBC tissues and cell lines, and investigated the effect of SPRY4-IT1 knockdown on cell proliferation, migration and invasion of GBC in vitro . Our result showed that SPRY4-IT1 was upregulated in GBC tissues. Further experiments revealed that SPRY4-IT1 knockdown significantly inhibited GBC cell proliferation. Furthermore, inhibitory effects of SPRY4-IT1 on cell migration and invasion were partly associated with EMT process. In conclusion, these data suggest that SPRY4-IT1 could be an oncogene for GBC, and may be served as a candidate target for new therapies in human GBC.