Cell Death Dis: E2F1 Mediated DDX11 Transcription Activation Promotes hepatocellular Carcinoma Development through PI3K/AKT/mTOR Pathway
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Last Update: 2020-05-29
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Source: Internet
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Author: User
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Hepatocellular carcinoma (HCC) is a primary liver malignant tumor, which is the third leading cause of cancer-related deathOften when curative treatment is not possible, patients are diagnosed with advanced stages, and these patients have low resection rates, high recurrence rates, and poor response to treatment, which also lead to poor prognosis in HCC patientsTherefore, it is urgent to find new biomarkers and new therapeutic targets to control HCC metastasis and recurrencereported that DDX11, a member of the DEAD/DEAH box decyclone asse family, is essential for the clotting of chromosome armsWhen cells that lack DDX1 enter the middle of division, the copied chromosomes cannot be separated, eventually leading to filament division failureDDX11 plays a key role in regulating the initiation of DNA replication, and previous studies have shown that DDX11 may also play a key role in tumor developmentHowever, the expression pattern, function and molecular mechanism of DDX11 in liver cancer are not clearin the study, the researchers found that DDX11 was expressed in HCC tissueThe high expression level of DDX11 was positively correlated with large tumor volume, tumor diversity, late tumor lymph node metastasis (TNM) and adverse prognosis, the experimental results of functional acquisition and loss of function show that over-expression DDX11 can promote the proliferation, migration, invasive action and inhibitapopaaa of HCC cells in exogenous cultureOverexpression DDX11 also enhances the carcinogenicity of HCC in the bodyIn addition, chromatin immunoprecipitation (Ch-IP) and fluoroline enzyme reporting gene experiments confirmed that DDX11 is subject to transcription almothenosination of the transcription factor E2F1 in liver cancerThe mechanism study found that the E2F1/DDX11 pathway can promote the proliferation, migration and invasion of HCC cells in part by activating the PI3K/AKT/mTOR signaling pathwayin summary, the study shows that the expression of E2F1 uplifts in DDX1 further promotes the development of HCC through the PI3K/AKT/mTOR signaling pathway, and that DDX11 may be a potential treatment and prognostic target for liver cancer treatment
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