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Effect and mechanism of long non-coding RNA ZEB2-AS1 in the occurrence and development of colon cancer

1 Department of Anorectal Surgery, Dalian Municipal Central Hospital, Dalian, Liaoning 116033, China
2 Department of General Surgery, Shaoxing People's Hospital (Shaoxing Hospital, Zhejiang University School of Medicine)
3 Department of Medical Oncology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou 310000, China
4 Department of Orthopedics, The Sixth People's Hospital of Cixi, Ningbo 315300, China

Special Issues: Advanced Big Data Analysis for Precision Medicine

Objective: Clarify the expression changes, biological functions and related mechanisms of long non-coding RNA (lncRNA) ZEB2-AS1 in colon cancer tissues. Methods: The expression levels of ZEB2-AS1 in colon cancer tissues and adjacent tissues were detected by qRT-PCR and in situ hybridization methods. Cell biology experiments were performed to detect the proliferation, migration and apoptosis of colon cancer cells when the level of ZEB2-AS1 was overexpression or silencing. Then, Western blot was performed to analyze the effect of ZEB2-AS1 on the expression levels of β-catenin protein and related genes in the signal pathway. Results: We found that the expression level of ZEB2-AS1 in colon cancer tissues was significantly up-regulated compared with that in adjacent normal tissues. In colon cancer cell line of HCT8, overexpression of ZEB2-AS1 could promote cell proliferation and migration, while silencing ZEB2-AS1 would enhance cell apoptosis and inhibit proliferation. Study on the mechanism of ZEB2-AS1 showed that it could promote the expression of β-catenin, activate downstream genes to be transcribed and promote the occurrence and development of tumors. Conclusion: ZEB2-AS1 could promote colon cancer cell proliferation and inhibit apoptosis to promote the progression of colon cancer by upregulating the expression of β-catenin protein. ZEB2-AS1 may be a useful new target for treating colon cancer patients.
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© 2019 the Author(s), licensee AIMS Press. This is an open access article distributed under the terms of the Creative Commons Attribution Licese (http://creativecommons.org/licenses/by/4.0)

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