| BackgroundThe incidence and mortality of malignant tumors in the liver are high.According to new research reports,liver cancer ranks fourth in the mortality rate of all malignant tumors and is also the sixth most common cancer in the world.In China,liver cancer patients account for 50 percent of the world's liver cancer patients due to the high incidence of hepatitis B.Early liver cancer did not have obvious symptoms,but our medical examination is not as popular as other countries.Most patients were diagnosed at the late stage of cancer and had a poor prognosis.In terms of chemotherapy,HCC does not have several good therapeutic targets and chemotherapy drugs like breast cancer and lung cancer.Therefore,it is urgent to explore the carcinogenic molecular mechanism of HCC in order to find new prognostic biomarkers and therapeutic targets.Long-chain non-coding RNA(LncRNA)is RNA that is more than 200 units in length and does not encode proteins.FOXD2-AS1 in LncRNA has been reported to have a pro-cancer effect in colorectal cancer and gastric cancer,but the specific role and mechanism of action in HCC have not been described.The objective of this study is to investigate how FOXD2-AS1 regulates the occurrence and mechanism of hepatocellular carcinoma.MethodsTo collect 105 cases of clinical patients with hepatocellular carcinoma and their corresponding peripheral tissues,and to determine the level of expression of FOXD2-AS1 in hepatocellular carcinoma patients with hepatocellular carcinoma by RT-PCR.SPSS 19.0 software was used to analyze the relationship between FOXD2-AS1 expression level and prognosis of patients.Design and construct FOXD2-AS1 knock low cell line.Using cck8 experiment,cloning experiment,EdU experiment and cell cycle experiment to detect the effect of knock low FOXD2-AS1 on cell proliferation.At the same time,protein printing technology,RNA Pull-down and CHIP experiments were used to explore the signal path changes of FOXD2-AS1.Finally,CDKN1B was knocked down for rescue experiments to verify the correlation between FOXD2-AS1 and hepatocellular carcinoma.Results:The RT-PCR method showed that FOXD2-AS1 was significantly higher in hepatocellular carcinoma tissues than in normal tissues of the paraplastic liver,and FOXD2-AS1 patients with high expression were lower than the lower expression group(P&It;0.05).In vitro related experiments using HCCLM3 and Huh7 cell lines,the proliferation function of FOXD2-AS1 knocked low interference group was significantly lower than that of the control group,and the cell g0/g1 block after FOXD2-AS1 knocked low.In the naked mice in vivo experiment,the tumor growth ability of the low-knock group was lower than that of the control group,indicating that the low-knock FOXD2-AS1 in the body could also significantly reduce the proliferation and tumor growth ability of liver cancer cells.In the mechanism exploration experiment,FOXD2-AS1 interacts directly with EZH2 and is negatively related to the related cyclin CDKN1B.Conclusion:FOXD2-AS1 has a high expression in liver cancer tissue,and FOXD2-AS1 expression is closely related to the overall survival time of hepatocellular carcinoma patients.FOXD2-AS1 affects cell proliferation by regulating cell cycle transformation.In the mechanism,FOXD2-AS1 silences CDKN1B by directly binding EZH2 to reduce the development of liver cancer cells.FOXD2-AS1 is expected to be a new biomarker for assisted clinical diagnosis and targeted treatment of hepatocellular carcinoma. |
PDF Full Text Request