Opsin Gene 3 (opn3) A Preliminary Study Of Human Lung Cancer A549 Cells Paclitaxel Resistance Mechanisms

As one of the most popular fetal diseases all around the world, lung cancer was mainly treated by chemotherapy. Resistance to chemotherapy frequently occurs and represents a major obstacle to successful cancer treatment. Understanding the basis of resistance is a principal goal of molecular oncology. But the mechanisms of drug resistance are polygenetic and incompletely defined. Elucidating the molecular mechanisms of this complex process may lead to the identification of novel molecules that in turn may serve as targets for therapeutic, diagnostic tests or alternatively predictive markers.In the previous study, we found that 0PN3, the protein component of visual pigment molecules, participated in paclitaxel resistance of the non-small cell lung cancer (NSCLC) cell line (A549).In the present study, GPCR Signaling PathwayFinder genechips were used to detect the affection of OPN3 to A549 and A549_PTX cell lines with it's GPCR activity. The results showed that 0PN3 downregulated the expression of c-Jun, resulted in the depressed transcription of downstream genes, and inhibited cell proliferation and sensitivity of tumor cells to drugs. We analyzed the cell apoptosis by annexin V / propidium iodide (PI) staining detected by flow cytometry and fluorescence microscopy, suggesting that 0PN3 may upregulated the cell apoptosis signal pathway.The negative regulation of paclitaxel resistance suggested that 0PN3 could be the potential target of tumor therapy. And the data in this work could improve the research of opsins in tumor drug resistance.