OBJECTIVE: To investigate the tumor-suppressing function of human esophageal cancer related gene 4 (ECRG4) in esophageal squamous cell carcinoma (ESCC). METHODS: The recombinant plasmid pcDNA3.1-ECRG4 with ECRG4 open reading frame was constructed. The EC9706 cell was transfected with either pcDNA3.1 or pcDNA3.1-ECRG4. And the effects of ECRG4 on tumor cell were examined by in vivo assays of cell proliferation, adhesion, migration, invasion and tumor growth. The expression levels of P53 and P21 proteins were detected in EC9706 cell with transfection of ECRG4 gene by Western blotting. RESULTS: The final tumor volume and weight in ECRG4 transfection group were (264±43) mm3 and (0.39±0.09) g, versus (464±128) mm3 and (0.76±0.13) g in control group (both P<0.05). And the capacities of tumor cells adhesion, migration and invasion decreased in ECRG4 transfection group versus that in control group (all P>0.05). Furthermore, the expression levels of P53 and P21 proteins were higher in ECRG4 transfection group than those in control group (100.00±3.87, 35.71±2.36 vs 16.6±1.92, 1.09±0.11, both P<0.05). CONCLUSION: As a novel candidate tumor suppressor in ESCC, ECRG4 may induce the up-regulation of p21 protein through p53 pathway to inhibit tumor growth in ESCC.
OBJECTIVE: To investigate the tumor-suppressing function of humanesophageal cancer related gene 4 (ECRG4) in esophageal squamous cell carcinoma (ESCC). METHODS: The recombinant plasmid pcDNA3.1-ECRG4 with ECRG4 open reading frame was constructed. The EC9706 cell was transfected with either pcDNA3.1 or pcDNA3.1-ECRG4. And the effects of ECRG4 on tumor cell were examined by in vivo assays of cell proliferation, adhesion, migration, invasion and tumor growth. The expression levels of P53 and P21 proteins were detected in EC9706 cell with transfection of ECRG4 gene by Western blotting. RESULTS: The final tumor volume and weight in ECRG4 transfection group were (264±43) mm3 and (0.39±0.09) g, versus (464±128) mm3 and (0.76±0.13) g in control group (both P<0.05). And the capacities of tumor cells adhesion, migration and invasion decreased in ECRG4 transfection group versus that in control group (all P>0.05). Furthermore, the expression levels of P53 and P21 proteins were higher in ECRG4 transfection group than those in control group (100.00±3.87, 35.71±2.36 vs 16.6±1.92, 1.09±0.11, both P<0.05). CONCLUSION: As a novel candidate tumor suppressor in ESCC, ECRG4 may induce the up-regulation of p21 protein through p53 pathway to inhibit tumor growth in ESCC.