ArticleHepatology (Baltimore, Md.)2019
DEAD Box Protein 5 Inhibits Liver Tumorigenesis by Stimulating Autophagy via Interaction with p62/SQSTM1.
Article in Hepatology (Baltimore, Md.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 125 citations in OpenAlex.
- SPOP-mediated nuclear ubiquitination degradation of p62/SQSTM1 contributes to HR repair.Oncogene · 2026Article
- LAMTOR5 promotes hepatoma growth in mice by disrupting LC3-p62-mediated autophagy and preventing p62 proteasome degradation.Acta pharmacologica Sinica · 2026Article
- Qushi Huoxue ointment ameliorates metabolic associated steatotic liver disease through autophagy activation and ferroptosis inhibition.World journal of hepatology · 2026Article
- Heavy moxibustion at Sanyin point ameliorates neurogenic bladder dysfunction in spinal cord injury rats through the PI3 K/mTOR pathway.The journal of spinal cord medicine · 2026Article
- TRIM39 aggravates hepatocellular carcinoma growth through targeting the p62-KEAP1-NRF2 axis.Scientific reports · 2025Article
- Deciphering the relevance of dead box RNA helicases in gliomagenesis and autophagy.Human cell · 2025Review
- Intermittent Hypoxia Impairs Cognitive Function and Promotes Mitophagy and Lysophagy in Obstructive Sleep Apnea-Hypopnea Syndrome Rat Model.Molecular biotechnology · 2025Article
- Evidence of an unprecedented cytoplasmic function of DDX11, the Warsaw breakage syndrome DNA helicase, in regulating autophagy.Autophagy · 2025Article
- Roles of the Keap1/Nrf2 pathway and mitophagy in liver diseases.Journal of Zhejiang University. Science. B · 2025Review
- METTL3 stabilizes DDX17 mRNA via IGF2BP2-mediated m6A modification to suppress endometrial cancer progression.Clinical and experimental medicine · 2025Article
- NAP1L1 degradation by FBXW7 reduces the deubiquitination of HDGF-p62 signaling to stimulate autophagy and induce primary cisplatin chemosensitivity in nasopharyngeal carcinoma.Molecular cancer · 2025Article
- DDX24 spatiotemporally orchestrates VEGF and Wnt signaling during developmental angiogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Coordination of SLC39A1 and DRP1 facilitates HCC recurrence by impairing mitochondrial quality control.Clinical and translational medicine · 2025Article
- Construction and evaluation of a prognostic model of autophagy-related genes in hepatocellular carcinoma.Biochemistry and biophysics reports · 2025Article
- Crucial roles of CircRNA-mediated autophagy in digestive cancer.Frontiers in oncology · 2025Review
- Increased PRP19 in Hepatocyte Impedes B Cell Function to Promote Hepatocarcinogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Ubiquitination regulates autophagy in cancer: simple modifications, promising targets.Journal of translational medicine · 2024Review
- Application trends and strategies of hydrogel delivery systems in intervertebral disc degeneration: A bibliometric review.Materials today. Bio · 2024Review
- DDX5 promotes esophageal squamous cell carcinoma growth through sustaining VAV3 mRNA stability.Oncogene · 2024Article
- Comprehensive Proteogenomic Profiling Reveals the Molecular Characteristics of Colorectal Cancer at Distinct Stages of Progression.Cancer research · 2024Article
9 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
In hepatocellular carcinoma (HCC), dysregulated expression of DDX5 (DEAD box protein 5) and impaired autophagy have been reported separately. However, the relationship between them has not been explored. Here we present evidence to show that, by interacting with autophagic receptor p62, DDX5 promotes autophagy and suppresses tumorigenesis. DDX5 inversely correlated with p62/sequestosome 1 (SQSTM1) expression in hepatitis B virus (HBV)-associated and non-HBV-associated HCCs. Patients with low DDX5 expression showed poor prognosis after tumor resection. We found that DDX5 overexpression induced, while DDX5 knockdown attenuated, autophagic flux in HepG2 and Huh7 cells. DDX5 promoted p62 degradation and markedly reduced the half-life of p62. Moreover, DDX5 overexpression dramatically reduced, while DDX5 knockdown promoted, cancer cell growth and tumorigenesis in vitro and in vivo. We found that DDX5 bound to p62 and interfered with p62/TRAF6 (tumor necrosis factor receptor-associated factor 6) interaction. Further findings revealed that the N-terminal domain of DDX5, involved in the interaction with p62, was sufficient to induce autophagy independent of its RNA binding and helicase activity. DDX5 overexpression decreased p62/TRAF6-mediated lysine 63-linked ubiquitination of mammalian target of rapamycin (mTOR) and subsequently inhibited the mTOR signaling pathway. Knockdown of TRAF6 blocked DDX5-induced autophagy. Furthermore, we showed that miR-17-5p downregulated DDX5 and impaired autophagy. Inhibition of miR-17-5p promoted autophagic flux and suppressed tumor growth in HCC xenograft models. Conclusion: Our findings define a noncanonical pathway that links miR-17-5p, DDX5, p62/TRAF6, autophagy, and HCC. These findings open an avenue for the treatment of HCC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.