Open AccessEpigenetic regulation of miR‐129‐2 and its effects on the proliferation and invasion in lung cancer cells
Author(s) -
Xiao Yingying,
Li Xiaoxia,
Wang Haoli,
Wen Ruiling,
He Juan,
Tang Jun
Publication year - 2015
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12597
Subject(s) - carcinogenesis , dna methylation , biology , cancer research , lung cancer , rna , methylation , epigenetics , microrna , microbiology and biotechnology , a549 cell , cell growth , transfection , cancer , cell , gene expression , gene , genetics , medicine , pathology
Micro RNA s (mi RNA s) play a pivotal role in carcinogenesis. Dysregulation of mi RNA s, both oncogenic mi RNA s and tumour‐suppressive mi RNA s, is closely associated with cancer development and progression. The levels of mi RNA s could be changed epigenetically by DNA methylation in the 5′ untranslated region ( UTR ) of pre‐mature mi RNA s. To investigate whether DNA methylation alters the expression of miR‐129 in lung cancer, we did DNA methylation assays and found that 5′ UTR region of miR‐129‐2 gene was absolutely methylated in both A549 and SPCA ‐1 lung cancer cells, but totally un‐methylated in 95‐D cells. The expression of miR‐129 was restored by 5‐Aza‐2'‐deoxycytidine ( DAC ), a de‐methylation agent, in both A549 and SPCA ‐1 cells, resulting in attenuated cell migration and invasion ability, and decreased protein level of NF ‐κB, which indicates the involvement of NF ‐κB pathway. To further illustrate the roles of miR‐129 in lung tumourigenesis, we overexpressed miR‐129 in lung cancer cells by transfection of miR‐129 mimics, and found arrested cell proliferation at G2/M phase of cell cycle and inhibited cell invasion. These findings strongly suggest that miR‐129 is a tumour suppressive mi RNA , playing important roles in the development and progression of human lung cancer.