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摘要
The aim of the present study was to explore the function of response gene to complement 32 (RGC-32) in hypoxia-induced epithelial-mesenchymal transition (EMT) in pancreatic cancer. Three kinds of hypoxia-inducible factor 1 alpha (HIF-1 alpha) small interfering (si) RNA were synthesized and the different effects on the expression of HIF-1 alpha were detected by western blotting. In human pancreatic cancer BxPC-3 cells, HIF-1 alpha levels were diminished using siRNA transfection or HIF-1 alpha inhibitor pretreatment, and the expression levels of RGC-32 and EMT-associated proteins were analyzed using reverse transcription-quantitative polymerase chain reaction and western blotting. Subsequently, the protein levels of epithelial marker, E-cadherin, and mesenchymal marker, vimentin, were determined by western blotting. Results demonstrated that HIF-1 alpha-Homo-488 siRNA and HIF-1 alpha-Homo-1216 siRNA diminished the protein level of HIF-1 alpha. Compared with normoxia, hypoxia induced the levels of HIF-1 alpha, RGC-32, N-cadherin and vimentin, but suppressed the expression of E-cadherin and cytokeratins. The inhibition of HIF-1 alpha by HIF-1 alpha-Homo-1216 siRNA transfection or HIF-1 alpha inhibitor repressed hypoxia-induced HIF-1 alpha, RGC-32, N-cadherin and vimentin, but increased the expression of E-cadherin and cytokeratins. When RGC-32 was knocked down, hypoxia-induced vimentin was suppressed; however, hypoxia-suppressed N-cadherin was released. In conclusion, the present results demonstrated that hypoxia induced the expression of HIF-1 alpha to activate the levels of RGC-32, in turn to regulate the expression EMT-associated proteins for EMT. These findings revealed the function of RGC-32 in hypoxia-induced EMT and may have identified a novel link between HIF-1 alpha and EMT for pancreatic cancer therapy.
