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Background and purpose:Gemcitabine-based chemotherapy has been shown to have signiifcant activity and favourable safety in metastatic breast cancer patients, but the effectiveness is limited due to drug resistance. MicroRNAs are a family of small non-coding RNA molecules, acting as oncogenes or tumor suppressors. Although various mechanisms of chemoresistance have been uncovered, the aberrant microRNA expression and its relationship with drug resistance of breast cancer are still unclear. This study explored the potential role and underlying mechanism of microRNA-21 in gemcitabine resistant breast cancer. Methods:MDA-MB-231 cells were continuously exposed to the increasing concentrations of gemcitabine to induce drug resistance to gemcitabine, which was 10 times more resis-tant. Then multiple methods were used including real-time PCR (RT-PCR), CCK-8, Western blot, transfection, wound healing and Transwell assay to observe the effect of microRNA-21 on epithelial-mesenchymal transition (EMT) and chemosensitivity. Results:The expression of microRNA-21 was up-regulated in gemcitabine resistant breast cancer cell line and inversely correlated with gemcitabine sensitivity. Manipulation of microRNA-21 status could change microR-NA-21 level, and could result in corresponding changes in EMT status and drug sensitivity. Conclusion:MicroRNA-21 induces gemcitabine resistance possibly via EMT process in breast cancer.
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Objective To investigate the possible mechanism of gemcitabine resistance in pancreatic cancer chemotherapy. Methods Recent literatures about the genes and signal pathways those play key roles in mediating gemcitabine chemotherapy resistance of pancreatic cancer were collected and reviewed.Results Oncogenes like c-Src and bcl-X-L, inflammation pathway of NF-?B, cytokines like IL-1? and NO are closely related with the chemoresistance; the relationship between multiple drug resistance relevant genes like MDR1/P-gP and the resistance to gemcitabine remains to be clarified. Conclusion Genes and pathways like c-Src, bcl-X-L, NF-?B, etc. might become new targets to increase the chemotherapeutic sensitivity of pancreatic cancer, however, the mechanism of pancreatic cancer chemotherapy resistance still needs further to be studied.