| Both intrinsic or acquired drug resistance, or the phenomenon of multidrug resistance, has been considered involving in many molecules, and molecular mechanism of tumor drug resistance are extremely complex. The major biological mechanisms include mutations or amplifications of the target gene; altered DNA damage repair; efflux or absorption of drugs; apoptotic realated genes. Our previous study showed that FOLR1 was highly expressed in taxol-resistant cells, and it positively correlated with the resistance index. Therefore, it is importance to understand the role of FOLR1 in the process of drug resistance in nasopharyngeal carcinoma.Objectives: Inhibiting the expression of FOLR1 genes in nasopharyngeal carcinoma cells by RNA interference, and observe the changes in drug-resistant phenotype.Methods: The growth inhibition rates of cell line to paclitaxel was determined using the colony formation assay. The expression of FOLR1 genes were detected by Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and Western blot in paclitaxel-resistance cells (CNE-1/Taxol) after treated by RNA interference of FOLR1. Proliferation inhibition rate of CNE1 and CNE1/Taxol cells was assayed by colony formation assayed after treated by RNA interference of FOLR1.Results: The FOLR1- targeted siRNA can effectively reduce the expression level of FOLR1 gene mRNA and protein of nasopharyngeal carcinoma cells. The sensitivity to paclitaxel of CNE-1/Taxol was significantly increased after inhibition of FOLR1 gene expression by siRNA technology, and its IC50 value was decreased 2.47 times.Conclusions: The FOLR1-targeted siRNA can effectively reduce the expression level of FOLR1 gene of nasopharyngeal carcinoma cells, and increase the sensitivity to paclitaxel in CNE1/Taxol, and reverse the drug resistance of CNE1/Taxol. It indicated that the FOLR1 gene is one of the important target molecules in the reversion of the paclitaxel-resistance in nasopharyngeal carcinoma cells.
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