PRMT1 Affects The Biological Function Of Liver Cancer Cells By Regulating S100A6

Hepatocellular Carcinoma(HCC)is the third largest malignancy in the world,and its morbidity and mortality rates constantly rise.The etiology and pathogenesis of HCC are extremely complex and have not yet been fully elucidated.Protein Arginine Methyltransferase 1(PRMT1)is highly expressed in a variety of cancers,but has been rarely studied in HCC.The purpose of this study is to explore the potential mechanism of PRMT1 in the occurrence and development of HCC through proteomics and experimental methods of cell and molecular biology.To clarify the mechanism of PRMT1 in HCC,we first analyzed the TCGA Cancer Genome Mapping Database,and the results showed that PRMT1 was up-regulated in human liver cancer tissue.At the same time,we found that PRMT1 was highly expressed in Huh7 of liver cancer in human.To explore the potential biological function of PRMT1 in the development and metastasis of HCC,PRMT1 was knocked down in the Huh7,which showed PRMT1 inhibited cell proliferation,arrested cell cycle in G2/M phase,reduced cell migration and invasiveness,and promoted the apoptosis of cells.Meanwhile,proteomic sequencing was performed on Huh7 knocking down PRMT1.The results showed that the down-regulation of PRMT1 was correlated with metabolism,cycle and proliferation,and analysis of differential expression protein revealed that calcium binding protein S100A6 was significantly reduced.In order to prove the relationship between PRMT1 and S100A6,we knocked down or overexpressed PRMT1 in the Huh7,and found that the expression of S100A6 changed accordingly.However,there was no significant change in PRMT1 expression after siRNA interference with S100A6.The biological character experiment of Huh7 after S100A6 interference was texted,and the results showed that cell proliferation was inhibited,cell cycle was blocked at G2/M,cell migration and invasion were reduced,and cell apoptosis was promoted,which was consistent with the functional phenotypic trend of the knockdown of PRMT1.This suggests that S100A6 may be a potential downstream target protein of PRMT1.At the same time,proteomic sequencing analysis also found that S100A6 had a protein interaction with P53.Interfering the expression of S100A6 in Huh7,we found that P53 was significantly up-regulated.Simultaneously,the expression of P53 target protein P21 was up-regulated,and the expression of P53 antagonist MDM2 was down-regulated.These results indicate that PRMT1 may regulate S100A6 through the P53 pathway.In this study,we explored the potential role of PRMT1 in Huh7 cells,and provided a theoretical basis for the study of hepatocellular carcinoma,suggesting that PRMT1 is a promising new target for hepatocellular carcinoma.