MALAT1 promotes the colorectal cancer malignancy by increasing DCP1A expression and miR203 downregulation. Issue 10 (12th July 2018)

• Record Type: Journal Article
• Authors: Wu, Chuanqing; Zhu, Xiaojie; Tao, Kaixiong; Liu, Weizhen; Ruan, Tuo; Wan, Wenze; Zhang, Chun; Zhang, Weikang
• Is Part Of: Molecular carcinogenesis. Volume 57:Issue 10(2018)
• Page Start: 1421
• Page End: 1431
• Publication Date: 2018-07-12
• Subjects: colorectal cancer -- DCP1A -- long non‐coding RNA -- MALAT‐1 -- miR203; Carcinogenesis -- Molecular aspects -- Periodicals; 616.994071
• DOI: 10.1002/mc.22868
• Languages: English
• ISSNs: 0899-1987

Abstract

Abstract : The long non‐coding RNA MALAT1 has been proved to promote the cell proliferation, drug resistance, invasion, and metastasis of colorectal cancer (CRC) in vitro and in vivo by regulating the expression of various oncogenes and their protein products. Our previous work discovered that the expression of the mRNA‐decapping enzymes 1a (DCP1A) is upregulated in CRCs. However, the relationships between MALAT1 and DCP1A in the development of CRC and the underlying mechanisms are still unclear. In this study, we investigated the molecular mechanisms by which MALAT1 and DCP1A may be linked to contribute to the malignancies of CRCs. We found that DCP1A is a direct target molecule of MALAT1. Moreover, by screening the downstream genes of MALAT1, we noticed that microRNA 203(miR203), an oncogene suppressor in numerous cancers, is inversely correlated to both MALAT1 and DCP1A expressions. Following MALAT1 knockdown, we observed overexpression of miR203 accompanied with DCP1A downregulation to a level that reversed the promoted cell proliferation, invasion, and migration in vitro and in vivo, which could be restored by miR203 knockdown or DCP1A overexpression. These results proposed a new molecular mechanism of MALAT‐miR203‐DCP1A axis which is involved with the development and contributes to the malignancy of colorectal cancers.