The impact of lncRNA MG3 on laryngeal cancer cell growth, cycle, and apoptosis related factors

Laryngeal cancer is a common head and neck malignant tumor. Long non-coding RNA (lncRNA) is a kind of RNA at the length more than 200 nucleotides that cannot code protein. They widely exist in the human genome. Maternally expressed gene 3 (MG3) is a kind of lncRNA that is associated with various mal...

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Veröffentlicht in:International journal of clinical and experimental pathology 2017-01, Vol.10 (7), p.7475-7480
Hauptverfasser: Li, Yuan, Zhou, Xuehua, Tao, Chenjuan, Chen, Chaohui, Cui, Caixia, Dai, Lili, Wu, Honglin, Wei, Qingyu, Luo, Song
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Sprache:eng
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Zusammenfassung:Laryngeal cancer is a common head and neck malignant tumor. Long non-coding RNA (lncRNA) is a kind of RNA at the length more than 200 nucleotides that cannot code protein. They widely exist in the human genome. Maternally expressed gene 3 (MG3) is a kind of lncRNA that is associated with various malignant tumors development. This study explores the influence of MG3 on laryngeal cancer Hep-2 cell growth, cycle, and apoptosis related factors. Hep2 cells transfected by MG3 were treated as experimental group, while untransfected Hep2 cells were treated as control. MG3 expression was tested by real time PCR. Cell proliferation was evaluated by MTT assay. Cell cycle was determined by flow cytometry. Bcl-2, Bax, and survivin protein levels were detected by Western blot. MG3 expression significantly increased in Hep2 cells compared with control (P < 0.05). Hep2 cell OD value and cell percentage in S phase were obviously declined, while cell apoptosis were markedly enhanced (P < 0.05). OD value and cell percentage in S phase apparently reduced in 12 h, 24 h, and 48 h from experimental group (P < 0.05). Bcl-2 and survivin protein downregulated, while Bax protein elevated in experimental group following time extension (P < 0.05). MG3 overexpression inhibited laryngeal cancer Hep2 cell proliferation and arrested cell cycle with time dependence, which may achieve by suppressing Bcl-2 and survivin protein, and facilitating Bax protein expression.
ISSN:1936-2625