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circ_0136666 Facilitates the Progression of Colorectal Cancer via miR-383/CREB1 Axis

Authors Li Y, Zang H, Zhang X, Huang G

Received 29 February 2020

Accepted for publication 9 July 2020

Published 4 August 2020 Volume 2020:12 Pages 6795—6806


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 4

Editor who approved publication: Dr Ahmet Emre Eskazan

Yuhui Li, Hongliang Zang, Xue Zhang, Guomin Huang

Department of General Surgery, China-Japan Union Hospital of Jilin University, Changchun, Jilin, People’s Republic of China

Correspondence: Guomin Huang
Department of General Surgery, China-Japan Union Hospital of Jilin University, No. 829 Xinmin Avenue, Changchun, Jilin 130012, People’s Republic of China
Tel +86-13504426968

Background: The changes in dietary patterns cause an increased incidence of colorectal cancer (CRC) globally. We aimed to explore the mechanism behind circular RNA circ_0136666 in the progression of CRC.
Materials and Methods: The expression of circ_0136666, miR-383 and cAMP response element binding protein 1 (CREB1) was detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell proliferation, apoptosis and glycolysis were measured by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), flow cytometry and glucose or lactate detection kit, respectively. The combination between miR-383 and circ_0136666 or CREB1 in 293T cells was predicted by Circular RNA Interactome or Starbase software and confirmed by dual-luciferase reporter assay. Western blot assay was performed to detect the abundance of CREB1, hexokinase 2 (HK2) and lactate dehydrogenase A (LDHA) in CRC cells. Murine xenograft model was established to verify the function of circ_0136666 in vivo.
Results: circ_0136666 was aberrantly up-regulated in CRC tissues and cells, and it promoted the proliferation and glycolysis and inhibited the apoptosis of CRC cells. circ_0136666 accelerated the progression of CRC through directly targeting and down-regulating miR-383. CREB1 could bind to miR-383 in 293T cells. The overexpression of CREB1 reversed the inhibitory effects of miR-383 accumulation on the proliferation and glycolysis and the promoting impact on the apoptosis of CRC cells. The enrichment of CREB1 was modulated by circ_0136666/miR-383 signaling in CRC cells. The glycolysis-related proteins (HK2 and LDHA) were modulated by circ_0136666/miR-383/CREB1 axis in CRC cells. circ_0136666 accelerated the growth of CRC tumors via circ_0136666/miR-383/CREB1 axis in vivo.
Conclusion: circ_0136666 deteriorated CRC through miR-383/CREB1 axis. circ_0136666/miR-383/CREB1 axis might be an underlying therapeutic target for CRC therapy.

Keywords: colorectal cancer, circ_0136666, miR-383, CREB1, proliferation, apoptosis, glycolysis

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