Neoplasma Vol.65, No.5, p.745-752, 2018
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Title: Over-expression of MEOX2 promotes apoptosis through inhibiting the PI3K/Akt pathway in laryngeal cancer cells |
Author: L. TIAN, Z.Z. TAO, H.P. YE, G.Y. LI, Z.F. ZHAN, H.W. TUO |
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Abstract: Early-stage diagnosis and treatment for the recurrence of carcinoma of the larynx requires further investigation. Mesenchyme homeobox 2 (MEOX2) was speculated as a novel suppressor gene in laryngeal carcinoma and the molecular mechanism was studied. Real-time quantitative PCR (RT-qPCR) and Western blot detected MEOX2 mRNA and protein levels in laryngeal cancer tissues and cells (Hep-2, TU212, AMC-NH-8 and TU686 cells), and also apoptosis and phosphoinositide 3-kinase (PI3K)/protein kinase (Akt) related factors in TU212 cells transfected with MEOX2. Cell counting kit-8 (CCK8) assay and Annexin-Ⅴ/PI staining assay respectively determined the cell viability and apoptosis rates in the 46 laryngeal carcinoma patients in this study. The expression of MEOX2 was lower in larynx carcinoma tissues than normal tissues, and it correlated with the clinical stage, differentiated degree and survival time. The expression of MEOX2 was the lowest in those laryngeal cancer cells, so it was chosen for transfection in the following study. Over-expression of MEOX2 inhibited cell viability and promoted apoptosis of TU212 cells by increasing the expression levels of Caspase-3, and decreasing the levels of C-Myc, XIAP, PI3K p110α, PI3K p110β, PI3K class III and p-Akt. In summary, the expression levels of MEOX2 were inhibited in laryngeal carcinoma compared to normal laryngeal tissue and it correlated with cancer progression. Over-expression of MEOX2 in laryngeal cancer cells inhibited cell viability and promoted apoptosis by regulating apoptosis and PI3K/Akt pathway-related factors. This provides excellent evidence for MEOX2 use as a therapeutic gene in laryngeal carcinoma.
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Keywords: MEOX2, cell apoptosis, laryngeal cancer, PI3K/Akt pathway |
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Published online: 24-Sep-2018
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Year: 2018, Volume: 65, Issue: 5 |
Page From: 745, Page To: 752 |
doi:10.4149/neo_2018_171218N824
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