LncRNA ST8SIA6-AS1 promotes colorectal cancer cell proliferation, migration and invasion by regulating the miR-5195/PCBP2 axis

C.-M. Huang, G.-Y. Cao, C.-X. Yang, Y. Chen, G.-D. Liu, B.-W. Xu, X. Zhang

Department of Gastrointestinal Surgery, Suqian First Hospital, Suqian, P.R. China. xianzhang9988@163.com

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• Oncology

OBJECTIVE: Long non-coding RNAs (lncRNAs) have been reported to play a vital role in the development and progression of various cancers, including colorectal cancer (CRC). Although the dysregulation of lncRNA ST8SIA6-AS1 participates in the development of multiple malignancies, the underlying molecular mechanisms of ST8SIA6-AS1 in regulating CRC progression remain to be fully discovered.
PATIENTS AND METHODS: The expression level of lncRNA ST8SIA6-AS1 was examined in the tumor tissues and paracancerous tissues of CRC patients. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was utilized to examine the expression levels of ST8SIA6-AS1, miR-5195, and Poly-(C) Binding Protein 2 (PCBP2). The protein expression level of PCBP2 was detected by Western blotting. MTT assay was performed to measure the proliferation of HCT-116 and SW480 cells. Cell migration and invasion abilities were measured by transwell assay. Luciferase reporter assay was used to examine the interaction between miR-5195 and ST8SIA6-AS1 or PCBP2.
RESULTS: This study revealed that lncRNA ST8SIA6-AS1 was upregulated in CRC tissues and cells. Knockdown of ST8SIA6-AS1 inhibited proliferation, migration, and invasion of CRC cells. Moreover, ST8SIA6-AS1 was proved to inhibit miR-5195 expression by directly targeting miR-5195. In addition, it was demonstrated that overexpression of miR-5195 inhibited CRC progression. Furthermore, PCBP2 was shown to enhance sh-ST8SIA6-AS1 and miR-5195 mimics-attenuated cell proliferation, migration, and invasion by directly binding to miR-5195.
CONCLUSIONS: Our study revealed that ST8SIA6-AS1 promoted CRC progression via the miR-5195/PCBP2 axis. This study may provide an improved understanding of the pathogenesis of CRC.

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