已发表论文

长非编码 RNA C1QTNF1 反义 RNA 1 通过海绵化 microRNA-484 上调己糖激酶 2,以促进结直肠癌的恶性进展

 

Authors Jin S, Liu Y, Wang W, Li Z

Received 29 July 2020

Accepted for publication 3 November 2020

Published 24 November 2020 Volume 2020:12 Pages 12053—12066

DOI https://doi.org/10.2147/CMAR.S262096

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Editor who approved publication: Dr Seema Singh

Purpose: The long noncoding RNA C1QTNF1  antisense RNA  1 (C1QTNF1-AS1 ) contributes to hepatocellular carcinoma development. However, its expression and roles in colorectal cancer (CRC) have not been fully explored. Therefore, this study determined the expression and roles of C1QTNF1-AS1  in CRC and elucidated its detailed mechanism of action.
Methods: C1QTNF1-AS1  expression in CRC tissues and cell lines was assessed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). We used Cell Counting Kit-8, flow cytometry, cell migration and invasion assays, and a xenograft tumor model to test the effects of C1QTNF1-AS1  on CRC malignancy. The associations among C1QTNF1-AS1 , microRNA-484 (miR-484), and hexokinase 2  (HK2 ) were explored using luciferase reporter assay, RNA immunoprecipitation, RT–qPCR, and Western blotting.
Results: C1QTNF1-AS1  was overexpressed in CRC and related to poor prognosis. C1QTNF1-AS1  interference inhibited CRC cell proliferation, migration, and invasion but induced apoptosis. Furthermore, C1QTNF1-AS1  deficiency impaired tumor growth in vivo. Mechanistically, C1QTNF1-AS1  adsorbed miR-484, thereby increasing the expression of its target HK2 . Rescue experiments revealed that the effects of C1QTNF1-AS1  deficiency in CRC cells were reversed by inhibiting miR-484 or upregulating HK2 .
Conclusion: C1QTNF1-AS1  drives CRC progression by sponging miR-484 and consequently upregulating HK2 . The C1QTNF1-AS1 /miR-484/HK2  pathway may serve as a diagnostic and therapeutic target for CRC.
Keywords: competitive endogenous RNA, therapeutic target, hexokinase 2