PMID- 25968442 OWN - NLM STAT- MEDLINE DCOM- 20160225 LR - 20220408 IS - 1421-9778 (Electronic) IS - 1015-8987 (Linking) VI - 36 IP - 2 DP - 2015 TI - Effect of EphA7 Silencing on Proliferation, Invasion and Apoptosis in Human Laryngeal Cancer Cell Lines Hep-2 and AMC-HN-8. PG - 435-45 LID - 10.1159/000430110 [doi] AB - AIMS: This study aimed to investigate the expression of EphA7 in human laryngeal squamous cell carcinoma (LSCC) tissues and disclose the potential roles and molecular mechanisms of EphA7 in LSCC. METHODS: In the present study, we examined EphA7 expression and its function and mechanism in LSCC. EphA7 expression levels were investigated by quantitative real-time PCR (qRT-PCR), western blotting, and immunohistochemistry in a panel of 35 LSCC patient cases. To investigate the potential mechanism of EphA7 in human laryngeal cancer, we employed EphA7 siRNA to knockdown EphA7 expression in LSCC cell line Hep-2 and AMC-HN-8. Subsequently, MTT, TUNEL, qRT-PCR, and western blotting were performed to disclose the roles of EphA7 on proliferation, invasion and migration, and apoptosis in LSCC cell line Hep-2 and AMC-HN-8. RESULTS: Depletion of EphA7 remarkably inhibited the proliferation and invasion of Hep-2 and AMC-HN-8 cells in comparison to control and EphA7 siRNA negative control (NC)-transfected cells. TUNEL staining assay demonstrated that, compared with the control group, the rate of apoptosis in the EphA7 siRNA group was significantly increased. In addition, knockdown of EphA7 in Hep-2 or AMC-HN-8 cells markedly decreased the expression of EphA7 and PTEN, which could contribute to apoptosis. However, the bpV(phen), a PTEN inhibitor, could attenuate anti-proliferation and pro-apoptotic effects of EphA7 siRNA in Hep-2 and AMC-HN-8 cells. CONCLUSION: Up-regulation of EphA7 was observed in human LSCC samples and down-regulation of EphA7 effectively suppressed laryngeal carcinoma cell growth and promoted its apoptosis. Thus, EphA7 has a critical role in modulating cell growth and apoptosis, which serves as a potential therapeutic target in human LSCC. CI - (c) 2015 S. Karger AG, Basel. FAU - Xiang, Cheng AU - Xiang C AD - Department of Head and Neck Surgery, the Third Affiliated Hospital of Harbin Medical University, Harbin, China. FAU - Lv, Yuanjing AU - Lv Y FAU - Wei, Yanjie AU - Wei Y FAU - Wei, Jing AU - Wei J FAU - Miao, Susheng AU - Miao S FAU - Mao, Xionghui AU - Mao X FAU - Gu, Xin AU - Gu X FAU - Song, Kaibin AU - Song K FAU - Jia, Shenshan AU - Jia S LA - eng PT - Journal Article DEP - 20150511 PL - Germany TA - Cell Physiol Biochem JT - Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology JID - 9113221 RN - 0 (RNA, Small Interfering) RN - EC 2.7.10.1 (Receptor, EphA7) SB - IM EIN - Cell Physiol Biochem. 2015;36(5):2084 MH - Apoptosis MH - Carcinoma, Squamous Cell/*genetics/pathology/therapy MH - Cell Cycle MH - Cell Line, Tumor MH - Cell Proliferation MH - *Gene Expression Regulation, Neoplastic MH - Humans MH - Laryngeal Neoplasms/*genetics/pathology/therapy MH - Larynx/metabolism/*pathology MH - Neoplasm Invasiveness/*genetics/pathology/prevention & control MH - RNA Interference MH - RNA, Small Interfering/genetics/therapeutic use MH - *RNAi Therapeutics MH - Receptor, EphA7/*genetics MH - Up-Regulation EDAT- 2015/05/15 06:00 MHDA- 2016/02/26 06:00 CRDT- 2015/05/14 06:00 PHST- 2015/02/20 00:00 [accepted] PHST- 2015/05/14 06:00 [entrez] PHST- 2015/05/15 06:00 [pubmed] PHST- 2016/02/26 06:00 [medline] AID - 000430110 [pii] AID - 10.1159/000430110 [doi] PST - ppublish SO - Cell Physiol Biochem. 2015;36(2):435-45. doi: 10.1159/000430110. Epub 2015 May 11.