CDK3 Is A Key Target Of MiR-150 In Cell Proliferation And Anti-tumor Function

Recent studies have shown that MicroRNA(miRNA)can regulate the expression of intracellular target genes,and the conservatism of miRNAs is closely related to its function.MiR-150,a member of miRNAs,has been proven to play a key role in the regulation of various types of tumors by controlling the expression of many genes,including NOTCH3,c-MYB,EGR2 and utrophin,for cancer and cancer Prognosis has an impact.In view of the fact that utrophin can relieve muscle tissue damage caused by the lack of muscular dystrophy protein in Duchenne muscular dystrophy(DMD)and is considered to be a promising therapeutic target for Duchenne muscular dystrophy(DMD)It is necessary to further study the role of miR-150 in different tissue cells.First,by using bioinformatics predictions,we found that miR-150 is highly conserved among the tissues gotten different animals.MiR-150 is capable of pairing with cyclin-dependent kinase ?(CDK3)in both human and mouse tissues.Then,through a series of molecular and cellular biology methods,we found that miR-150 can directly target the level of inhibition of CDK3,and lead to muscle and non-muscle cells in the regulation of CDK3 gene expression,mdx muscle miR-150 expression up.And CDK3 is closely related to the lower level.Transient transfection of miR-150 analogues into normal growth of C2C12 cells resulted in a rapid decrease in the level of CDK3 mRNA and a marked decrease in cell proliferation,which further confirmed that miR-150 in muscle tissue inhibited the expression of CDK3 Cell proliferation.In order to further confirm the relationship between miR-150 and CDK3 interactions,we studied its role in lung cancer tissue and lung cancer cell lines in the second part.First,we collected 16 pairs of tissues,which included non-small cell lung cancer tissue and adjacent normal lung tissue.The level of miR-150 was negatively correlated with the level of CDK3 in the lung cancer tissues by RT-PCR.The expression of miR-150 was negatively correlated with the level of CDK3.At the same time,the expression of miR-150 in lung cancer cell lines also showed low levels.By miR-150 analogue transient transfection experiments,we found that miR-150 significantly inhibited the expression of CDK3 in cells.CCK-8 and clone formation experiments showed that miR-150 overexpression could significantly inhibit the proliferation of lung cancer cells,which may contribute to the inhibition of CDK3 expression in cells.The above results show that miR-150 could effectively inhibit the level of CDK3 in muscle cells and lung cancer cells,which can inhibit the proliferation of CDK3 cells and provide new targets and new ideas for the treatment of muscular atrophy and lung cancer.