ABSTRACT
Objective To evaluate the effect of GOLPH3 on the proliferation, apoptosis and radiosensitivity of OE33 esophageal cancer cell line. Methods The expression levels of GOLPH3 mRNA and protein in the esophageal cancer cells and normal esophageal epithelial cells were detected by qRT-PCR and Western blot, respectively. The OE33 esophageal cancer cells were transfected with GOLPH3 siRNA and subject to irradiation treatment simultaneously. The cell proliferation was detected by MTT assay. The cell apoptosis was detected by flow cytometry. The radiosensitivity was assessed by cell cloning test. The expression levels of cleaved Caspase-3, Bax and cleaved Caspase-9 protein levels were quantitatively measured by Western blot. Results The expression levels of GOLPH3 mRNA and protein in the esophageal cancer cells were significantly higher than those in the normal esophageal epithelial cells ( both P<0.05) . GOLPH3 siRNA could obviously down-regulate the expression levels of GOLPH3 mRNA and protein in the OE33 esophageal cancer cells. The proliferation activity of esophageal cancer cells was decreased, whereas the apoptosis rate was increased and the expression levels of cleaved Caspase-3, Bax and cleaved Caspase-9 were up-regulated after down-regulating the expression of GOLPH3 or irradiation treatment ( all P<0.05) . After down-regulating the expression of GOLPH3 in the esophageal cancer cells treated with irradiation, the cell proliferation activity was more significantly decreased, whereas the apoptosis rate was elevated and the expression levels of cleaved Caspase-3, Bax and cleaved Caspase-9 were more evidently up-regulated ( all P<0.05) . In the irradiated OE33 esophageal cancer cells after down-regulating the expression of GOLPH3, the radiosensitization ratio of the cells was 1.673. Conclusions GOLPH3 is highly expressed in the esophageal cancer cells. Down-regulating the expression of GOLPH3 can increase the radiosensitivity, induce the apoptosis and inhibit the proliferation of OE33 esophageal cancer cells.
ABSTRACT
Objective To investigate the interrelationship between Golgi phosphoprotein 3 ( GOLPH3 ) expression with vasculoar endothelial growth factor( VEGF) expression in the progression of human gastric cancer by detecting the expression level of GOLPH3 and VEGF. Methods Immunohistochemistry ( IHC) was used to detect the ex-pression of GOLPH3 and VEGF in 55 cases of gastric cancerous and carcinoma-adjacent tissues. Pearson correlation analysis was used to discuss the association between GOLPH3 expression with VEGF expression. Results The im-munohistochemical detection showed that the positive expression rates of GOLPH3 and VEGF were 67. 27%, 58. 18% respectively, which were significantly higher than the positive expression rates in carcinoma-adjacent tis-sues ( P<0. 05 ) . A statistical analysis revealed that the positive expression rate of GOLPH3 and VEGF in the gas-tric cancer tissues were strongly correlated with depth of invasion ( P<0. 05 ) , distant metastasis ( P<0. 01 ) and TNM stages (P<0. 01), whereas it did not significantly correlate with age or gender or size of tumor. Compared with the negative for the GOLPH3 expression, the VEGF expression in gastric cancer tissues positive for the GOL-PH3 expression was significantly higher. The protein level of GOLPH3 expression was positively correlated with VEGF expression (r=0. 508,P<0. 01). Conclusion GOLPH3 overexpression may regulate gastric angiogenesis by upregulating the expression of VEGF, which affects the invasion and metastasis of gastric cancer.
ABSTRACT
Objective:To investigate the correlation between the expression of Golgi phosphoprotein 3 (GOLPH3) and the occurrence of apoptosis in colorectal cancer cells (CRC). Methods:Immunohistochemical assays of GOLPH3 and caspase-3 were performed on the paraffin-embedded sections of 62 CRC samples using the standard streptavidin-peroxidase technique. The apoptotic index of the CRCs was examined using the in situ terminal deoxynucleotidyl transferase nick-end labeling technique. The relationship of the GOLPH3 expression, the cell apoptosis, and the clinicopathologic parameters was analyzed. Results:The positive rates of GOLPH3 expression were significantly higher in the CRC tissues (53.2%) than in the normal colorectal mucosa (37.2%;P0.05). The caspase-3 expression and apoptotic index were significantly lower in the GOLPH3-positive CRC tissue than in the GOLPH3-negative tissue (P<0.05). GOLPH3 expression was negatively correlated with the apoptotic index of CRCs based on the Spearman correlation (r=-0.320, P<0.05). Conclusion:GOLPH3 overexpression in CRC tissue is negatively correlated with apoptotic index.