The Molecular Mechanism Of OPN3 In Regulating The Resistance Of Lung Cancer Cells To Paclitaxel

As one of the most popular fetal diseases all around the world, Lung cancer is mainly treated by chemotherapy. Rapidly development of tumor resistance to chemotherapy drugs represents a major obstacle to successful cancer treatment. Abnormal resistance-associated gene expression plays an important role in the drug-resistance to lung cancer. Elucidating the molecular mechanisms of this complex process may prevent and reverse the drug resistance, and thus may serve as targets for therapeutic, diagnostic tests or alternatively predictive markers.Our previous study suggested that OPN3, a homologene of insecticide resistance opsin gene in Cx. Pipiens pallens, participated in the paclitaxel resistance of the non-small cell lung cancer (NSCLC) cell line (A549).In this study, GPCR Signaling PathwayFinder Microarray was used to detect the effection of OPN3 to A549 and paclitaxel resistant A549_PTX cell lines. Subsequently, the real-time PCR and Western blot were used for verification and analysis. The results showed that OPN3 downregulated the expression of Ras-ERK/JNK-Jun-CCND1 signal pathway.The negative regulation of paclitaxel resistance suggested that OPN3 could be the potential target for tumor gene therapy. And this work may improve the research of molecular mechanism for lung cancer cells resistant to chemotherapy drugs.