Long non-coding RNA SPRY4-IT1 promotes cell proliferation and invasion by regulation of Cdc20 in pancreatic cancer cells

• Published in: PloS one 2018-02, Vol.13 (2), p.e0193483
• Main Authors: Guo, Wenhao, Zhong, Kunhong, Wei, Heng, Nie, Chunlai, Yuan, Zhu
• Format: Article
• Language: English
• Subjects: Analysis; Apoptosis; Apoptosis - genetics; Arabidopsis Proteins - genetics; Assaying; Biology and life sciences; Cancer; Cancer cells; Carcinoma; Cdc20 Proteins - genetics; Cell cycle; Cell Cycle Checkpoints - genetics; Cell growth; Cell Line, Tumor; Cell migration; Cell proliferation; Cell Proliferation - genetics; Colorectal cancer; Development and progression; Esophagus; G1 phase; Gene expression; Gene Expression Regulation, Neoplastic - genetics; Gene Knockdown Techniques; Genetic aspects; Humans; Inhibition; Medical prognosis; Medicine and Health Sciences; Metastasis; MicroRNA; Neoplasm Invasiveness; Non-coding RNA; Ovarian cancer; Pancreatic cancer; Pancreatic Neoplasms - pathology; Physiological aspects; Polymerase chain reaction; Research and Analysis Methods; Ribonucleic acid; RNA; RNA, Long Noncoding - genetics; Transcription; Transfection; Western blotting; Wound healing
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0193483

Accumulating evidence has demonstrated that long non-coding RNAs (lncRNAs) play a critical role in the development of human cancers including pancreatic cancer. Long non-coding RNA SPRY4-IT1 (sprouty4-intron transcript 1) has been reported to play an oncogenic role in various types of human carcinomas. However, the role of SPRY4-IT1 in pancreatic cancer is unclear. The objective of this study was to determine the function of SPRY4-IT1 on proliferation and invasion in pancreatic cancer. In the current study, we dissected the function and mechanism of SPRY4-IT1 by multiple approaches including Real-time RT-PCR, Western blotting analysis, MTT assay, Wound healing assay, Transwell assay, and transfection. We found that down-regulation of SPRY4-IT1 inhibited cell growth and induced cell apoptosis in pancreatic cancer cells. Moreover, SPRY4-IT1 knockdown induced cell cycle arrest at G0/G1 phase. Furthermore, inhibition of SPRY4-IT1 retarded cell migration and invasion in pancreatic cancer cells. Overexpression of SPRY4-IT1 enhanced cell growth and invasion, and inhibited cell apoptosis in pancreatic cancer cells. Mechanistically, suppression of SPRY4-IT1 inhibited the expression of Cdc20 in pancreatic cancer cells. Our findings demonstrated that inhibition of SPRY4-IT1 could be a potential therapeutic approach for the treatment of pancreatic cancer.