DMBX1 knockdown inhibits colorectal cancer cell proliferation and migration via down-regulating c-Myc expression

Author:

Zhang Qian1,Xu Junrong1,Ma Zihan2,Wang Haifeng3,Wei Wei2,Duan Ying2,Wang Yuan1,Hao Jie1,Fang Hangrong,Gou Siqi,Wang Juanhong

Affiliation:

1. Department of Gastroenterology, Xi'an No. 3 Hospital, The Affiliated Hospital of Northwest University

2. Department of Pathology, Xi'an No. 3 Hospital, The Affiliated Hospital of Northwest University

3. Department of Clinical laboratory, Xi'an No. 3 Hospital, The Affiliated Hospital of Northwest University

Abstract

Abstract Background: Diencephalon/mesencephalon homeobox 1(DMBX1) is associated with the progression of some malignant tumors. Nevertheless, it is not known whether DMBX1 regulates the development of colorectal cancer (CRC). Methods:The Cancer Genome Atlas (TCGA) dataset was selected to evaluate DMBX1 expression in CRC and normal tissues. The mRNA levels of DMBX1 were analyzed in the four CRC cell lines by RT-qPCR. The biological roles of DMBX1 knockdown were investigated by a series of functional experiments in CRC. Furthermore, western blotting and rescue experiments were conducted to determine the potential molecular mechanisms of DMBX1. Results:DMBX1 was overexpressed in CRC. Knockdown of DMBX1 suppressed CRC cell proliferation and migration, and increased cell apoptosis. In addition, the expression of c-Myc was distinctly down-regulated after DMBX1 Knockdown. Finally, rescue experiments verified that the upregulation of c-Myc immensely restored the abilities of proliferation and migration in DMBX1-knockdown CRC cells. Conclusions:DMBX1 could exert its oncogenic role through the regulation of c-Myc in CRC. DMBX1 might serve as a possible therapeutic target for CRC patients.

Publisher

Research Square Platform LLC

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