Study On The Molecular Mechanism Of MiR-486-3p Targeting Erbb2 Affecting The Chemotherapy Resistance Of Lung Cancer

Lung cancer is one of the fastest growing malignancies and the most threatening malignant tumors to people’s health and life worldwide in morbidity and mortality.Drug resistance in cancer chemotherapy severely hinders the clinical treatment of lung cancer patients.Research shows that Erbb2 overexpression can be detected in many cancers,such as breast cancer,lung cancer and panc reatic cancer.The malignant degree of tumors often caused by abnormally high expression of Erbb2 is prone to relapse,and the resistance to chemotherapy drugs is relatively large,and it is easy to recur.Erbb2 has become an important target molecule for tumor immunodiagnosis and treatment.Micro RNA involves many processes,such as cell differentiation,transcription,inflammation,proliferation,cell signaling and apoptosis.In the development of lung cancer,miRNA often acts as a tumor suppressor or oncogene.The change of micro RNA expression level is related to the occurrence,progression and metastasis of tumor.In recent years,the emergence of micro RNA in cancer biology and pathogenesis has completely changed the treatment methods in this field,especially opened a new window for further understanding of tumor drug resistance.In this study,we explored the molecular mechanism of miR-486-3p targeting Erbb2 to affect lung cancer chemotherapy resistance.First of all,we explored the molecular mechanism of miR-486-3p targeting Erbb2 to affect lung cancer chemotherapy resistance.The background expression of miR-486-3p and Erbb2 genes in lung cancer cell lines A549、 H358 and H460 was analyzed.The results showed that the expressions of miR-486-3p and Erbb2 in lung cancer cells were significantly negatively correlated.Subsequently,Erbb2 3’UTR was cloned into a reporter gene vector and co-transformed with miR-486-3p mimics.Using the luciferase reporter gene,it was found that overexpression of miR-486-3p can significantly inhibit the activity of the Erbb2 reporter gene.At the same time,fluorescent quantitative PCR and Western Blot detection also proved that overexpression of miR-486-3p can significantly inhibit the expression level of Erbb2 in lung cancer cells.Combined with the results of immunofluorescence,it was finally concluded that miR-486-3p targeted regulation in lung cancer Erbb2.Later,in this study,we overexpressed miR-486-3p,at the same time,we treated lung cancer cells with a p53 agonist and a common chemotherapy drug.We found that overexpression of miR-486-3p can increase the effect of chemotherapy drugs and anticancer drugs.The stable knockdown cell line of miR-486-3p was constructed,which proved that chemotherapy drugs played a certain role by up regulating miR-486-3p.Finally,we knock down Erbb2 by sh RNA,and find that the effect of Erbb2 knockdown is the same as that of miR-486-3p overexpression on chemotherapy drugs and anticancer drugs.That is,overexpression of miR-486-3p and Erbb2 knockdown can promote the sensitivity of lung cancer cells to chemotherapy drugs.In conclusion,it is found that miR-486-3p can target Erbb2 to affect the chemotherapy resistance of lung cancer and promote the sensitivity of lung cancer cells to chemotherapy drugs,which provides new ideas and directions for the clinical treatment of lung cancer.