RESUMEN
The Editor-in-Chief has retracted this article [1] because Figure 3c appears to have been modified and reused as Figure 3d.
RESUMEN
BACKGROUND: HAX-1 is an anti-apoptotic factor and regulates the expression of DNA pol ß. Interestingly, DNA polymerase pol ß is overexpressed in esophageal squamous cell carcinoma (ESCC). However, the functional role of HAX-1 in ESCC remains unclear. AIMS: 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 ß 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 ß 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 ß 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 ß expression. HAX-1 may represent a potential target to overcome the resistance and metastasis of ESCC.
