title: HAX-1 promotes the chemoresistance, invasion, and tumorigenicity of esophageal squamous carcinoma cells.
abstract: BACKGROUND
  HAX-1 is an anti-apoptotic factor and regulates the expression of DNA pol β. Interestingly, DNA polymerase pol β is overexpressed in esophageal squamous cell carcinoma (ESCC). However, the functional role of HAX-1 in ESCC remains unclear.
  
  
  OBJECTIVE
  To investigate the role of HAX-1 in chemoresistance, invasion, and tumorigenicity of ESCC.
  
  
  METHODS
  Lentivirus-mediated overexpression or knockdown of HAX-1 was employed to establish ESCC EC9706 cell lines that expressed HAX-1 at different levels. The biological behaviors of these engineered cells were characterized in vitro and in vivo using a xenograft nude mice model. In addition, HAX-1 and pol β expression in the tumor tissues was detected by RT-PCR and immunohistochemistry.
  
  
  RESULTS
  HAX-1 overexpression promoted cell proliferation and resistance against cisplatin, increased cell invasion and suppressed apoptosis along with increased pol β expression. Conversely, HAX-1 knockdown inhibited the malignant phenotypes of EC9706 cells. The xenograft nude mice model demonstrated that HAX-1 overexpression or depletion led to increased or decreased tumor growth in vivo, respectively. Furthermore, a positive correlation of HAX-1 and pol β expression in the tumor tissues was observed.
  
  
  CONCLUSIONS
  HAX-1 promotes the proliferation, chemoresistance, invasion, and tumorigenicity of ESCC, and this is correlated with increased poly β expression. HAX-1 may represent a potential target to overcome the resistance and metastasis of ESCC.
authors.affiliation: Department of Pathophysiology, College of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, People's Republic of China. sajia_sun2010@yahoo.com.cn
authors.forename: Sa-jia
authors.initials: SJ
authors.lastname: Sun
authors.forename: Long
authors.initials: L
authors.lastname: Feng
authors.forename: Guo-qiang
authors.initials: GQ
authors.lastname: Zhao
authors.forename: Zi-ming
authors.initials: ZM
authors.lastname: Dong
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000187:drug effects / Q000235:genetics / Q000502:physiology*; D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology / Q000627:therapeutic use; D002294:Carcinoma, Squamous Cell / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects / Q000502:physiology; D002471:Cell Transformation, Neoplastic / Q000473:pathology*; D002945:Cisplatin / Q000494:pharmacology / Q000627:therapeutic use; D004195:Disease Models, Animal; D019008:Drug Resistance, Neoplasm / Q000502:physiology*; D004938:Esophageal Neoplasms / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology*; D005260:Female; D057809:HEK293 Cells; D006801:Humans; D066298:In Vitro Techniques; D051379:Mice; D008819:Mice, Nude; D009361:Neoplasm Invasiveness / Q000503:physiopathology; D034741:RNA, Small Interfering / Q000494:pharmacology; D014183:Transplantation, Heterologous
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D000970:Antineoplastic Agents; C104759:HAX1 protein, human; D034741:RNA, Small Interfering; D002945:Cisplatin