Font Size: a A A

The Role Of UPR In Human Cholangiocarcinoma QBC939 Cells

Posted on:2009-02-16Degree:MasterType:Thesis
Country:ChinaCandidate:P GuoFull Text:PDF
GTID:2144360245998408Subject:Surgery
Abstract/Summary:
Backgroud Primary gallbladder carcinoma shows an ascensus tendency in recent years. It's incidence ranks 5th in digestive system. Cholangiocarcinoma is a kind of carcinoma with poor prognosis because its lately symptom emergence, hardly early diagnosis, low radical cure rate and poor insensitivity chemotherapy drugs. In the last few years, researchers have shown how another cancer cell survival mechanism—the unfolded protein response, or UPR. Several groups have shown that blocking the UPR makes tumor cells more sensitive to chemotherapy, both in vitro and in vivo. The cancer– UPR link has already found clinical application, thanks to bortezomib. The drug could work against solid tumors, not just multiple myeloma. Evidence is growing that bortezomib kills tumors at least partly by inhibiting the UPR. Several academic groups are now looking for drugs that target the UPR. That is to say, UPR will become the anti-tumor to treat a new target spot. So, Studies UPR and the cholangiocarcinoma relations has the significance extremely to us.Objective To study the role of UPR in human cholangiocarcinoma cell(QBC939)and to provide new ideas to cure cholangiocarcinoma in clinic. Methods QBC939 cells were treated by low concentration of H2O2 and DDP.The growth curves of QBC939 cells were detected by MTT assay.The expression of IRE1αand BiP in defferent groups was detected by western-blot assay. Results Low concentration of H2O2 induced the proliferation of QBC939 cells,while DDP produced a growth inhibiting effect on QBC939 cells.The IRE1αand BiP protein was high expression in cells that induced by H2O2. Conclusion Low concentration of H2O2 induced UPR in QBC939 cells.These results reveal a critical role for UPR activation for tumor cell resistance to oxidative stress and tumor growth promotion.Less susceptibility to cell death upon activation of the UPR may contribute to tumor progression and drug resistance of solid tumors and suggest that the UPR may be an attractive target for anti-tumor modalities.
Keywords/Search Tags:UPR, QBC939, Cholangiocarcinoma, BiP
Related items