JOURNAL OF BIOLOGICAL REGULATORS & HOMEOSTATIC AGENTS Vol. 33, no. 2, 331-343 (2019)
LncRNA MALAT1 promotes colorectal cancer development by sponging miR-363-3p to regulate EZH2 expression.
- 1 Department of Anorectal Surgery, The First People’s Hospital of Wenling, Zhejiang Province, China.
- 2 Department of General Surgery, The First People’s Hospital of Wenling, Zhejiang Province, China.
- # Contributed equally
LncRNA MALAT1 is reported to play a potential role in human cancers. Hence, we investigated the effects of MALAT1 on colorectal cancer in vitro and in vivo, and further validated whether MALAT1 affected colorectal cancer development and EZH2 expression via regulating miR-363-3p. The fresh colorectal cancer tissues, adjacent non-tumor tissues, FHC, LOVO, SW620, CL40 and HCT116 cells were analyzed in this study. MALAT1, miR-363-3p and EZH2 expression levels were assessed using qRT-PCR and Western blot. Cell proliferation, migration and invasion were also measured. Binding effects between MALAT1 and miR-363-3p, or miR-363-3p and EZH2 3’UTR were detected by dual luciferase assay. We observed that MALAT1 was highly expressed in colorectal cancer tissues and cells, and MALAT1 knockdown inhibited cell proliferation as well as expression levels of EZH2 by upregulated miR-363-3p in cell models and in vivo. Moreover, miR-363-3p functions as a downstream target of MALAT1, meanwhile EZH2 was a target of miR-363-3p, suggesting MALAT1 might regulate miR-363-3p and/or EZH2 expression. Collectively, we concluded that MALAT1 functioned as a ceRNA to promote colorectal cancer development and EZH2 expression through sponging miR-363-3p in vitro and in vivo.
Cancer development, Colorectal cancer, EZH2, MALAT1, miR-363-3p
- Journal Article