Open AccessLong non-coding RNA MEG3 inhibits the proliferation of cervical carcinoma cells through the induction of cell cycle arrest and apoptosis
Author(s) -
Rongjun Qin,
Z Chen,
Yan Ding,
Jun Hao,
Jian Hu,
Fei Guo
Publication year - 2013
Publication title -
neoplasma
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.628
H-Index - 50
eISSN - 1338-4317
pISSN - 0028-2685
DOI - 10.4149/neo_2013_063
Subject(s) - meg3 , hela , cervical cancer , carcinogenesis , cancer research , long non coding rna , apoptosis , cell cycle , ectopic expression , gene knockdown , cell growth , biology , cervical carcinoma , cancer , cell , medicine , rna , cell culture , gene , genetics
Cervical cancer remains an important public health problem worldwide. New and effective therapeutic strategies targeting cervical cancer are urgently needed. Long non-coding RNAs (lncRNAs) are newly identified regulators in tumorigenesis and tumor progression. To investigate the role of lncRNA MEG3 in the development of cervical cancer, we examined MEG3 expression in 18 pairs of cervical cancer and matched adjacent non-neoplastic tissues. Real-time quantitative RT-PCR (qRT-PCR) results showed high expression levels of MEG3 in non-neoplastic tissues, but markedly lower levels in cancer tissues. We further investigated whether the restoration of MEG3 expression might affect the proliferation of cervical carcinoma cells. Ectopic expression of MEG3 inhibited the proliferation of human cervical carcinoma cells HeLa and C-33A in vitro. On the other hand, knockdown of MEG3 promoted the growth of well-differentiated cervical carcinoma HCC94 cells. Further investigation into the mechanisms responsible for the growth inhibitory effects revealed that overexpression of MEG3 resulted in the induction of G2/M cell cycle arrest and apoptosis. These results identified an important role of MEG3 in the molecular etiology of cervical cancer and implicated the potential application of MEG3 in cervical cancer therapy.