title: Effect of EphA7 Silencing on Proliferation, Invasion and Apoptosis in Human Laryngeal Cancer Cell Lines Hep-2 and AMC-HN-8.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Head and Neck Surgery, the Third Affiliated Hospital of Harbin Medical University, Harbin, China.
authors.forename: Cheng
authors.initials: C
authors.lastname: Xiang
authors.forename: Yuanjing
authors.initials: Y
authors.lastname: Lv
authors.forename: Yanjie
authors.initials: Y
authors.lastname: Wei
authors.forename: Jing
authors.initials: J
authors.lastname: Wei
authors.forename: Susheng
authors.initials: S
authors.lastname: Miao
authors.forename: Xionghui
authors.initials: X
authors.lastname: Mao
authors.forename: Xin
authors.initials: X
authors.lastname: Gu
authors.forename: Kaibin
authors.initials: K
authors.lastname: Song
authors.forename: Shenshan
authors.initials: S
authors.lastname: Jia
mesh_terms: D017209:Apoptosis; D002294:Carcinoma, Squamous Cell / Q000235:genetics* / Q000473:pathology / Q000628:therapy; D002453:Cell Cycle; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007822:Laryngeal Neoplasms / Q000235:genetics* / Q000473:pathology / Q000628:therapy; D007830:Larynx / Q000378:metabolism / Q000473:pathology*; D009361:Neoplasm Invasiveness / Q000235:genetics* / Q000473:pathology / Q000517:prevention & control; D034622:RNA Interference; D034741:RNA, Small Interfering / Q000235:genetics / Q000627:therapeutic use; D000067492:RNAi Therapeutics; D036141:Receptor, EphA7 / Q000235:genetics*; D015854:Up-Regulation
chemical_list: D034741:RNA, Small Interfering; D036141:Receptor, EphA7