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Circ_0060927 promotes colorectal cancer development by sponging miR-331-3p and upregulating TBX2
Dian Yin1, XiaoLu Zhai1, Xiu Feng1
1Department of Oncology, Nantong First People's Hospital and Second Affiliated Hospital of Nantong University, 666 Shengli Road, Chongchuan District, Nantong City, Jiangsu, China.
Background:
The dysregulation of circular RNAs (circRNAs) is closely associated with the pathogenesis of colorectal cancer (CRC). The present study aimed to elucidate the biological function and mechanism of circ_0060927 in CRC.
Methods:
5-ethynyl-2'-deoxyuridine, Cell Counting Kit-8 (CCK-8), flow cytometry and transwell assays, as well as Xenograft tumor models were adopted for in vitro and in vivo analyses. The interaction between microRNA-331-3p (miR-331-3p) and circ_0060927 or T-box transcription factor 2 (TBX2) was verified by the dual-luciferase reporter and RNA pull-down assays.
Results:
Circ_0060927 deficiency inhibited cell proliferation, autophagy, migration, and invasion and increased cell apoptosis and necrosis in CRC cells, as well as inhibited tumor growth in vivo. Circ_0060927 could bind to miR-331-3p, and circ_0060927 regulated CRC cell behaviors via sponging miR-331-3p. TBX2 was targeted by miR-331-3p, and miR-331-3p targeted TBX2 to exert the anti-cancer role in CRC cells. Mechanically, circ_0060927 regulated TBX2 expression by sequestering miR-331-3p in CRC cells.
Conclusion:
Circ_0060927 downregulation inhibited CRC progression by regulating the miR-331-3p/TBX2 axis, which might offer a potential treatment target for CRC.
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