ArticleCell death discovery2022
LINC01468 drives NAFLD-HCC progression through CUL4A-linked degradation of SHIP2.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The trial behind it
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- mInternational journal of molecular medicine · 2026Review
- OCTN2 Activates a Non-Canonical Carnitine Metabolic Pathway to Promote MASH-HCC Progression and Immunotherapy Resistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Recent advances in m6A RNA modification in hepatocellular carcinoma: from mechanisms to therapeutic potential.Frontiers in molecular biosciences · 2026Review
- Long non-coding RNA in hepatocellular carcinoma: mechanistic insights and therapeutic perspectives.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- RNA modifications in health and disease: from mechanistic insights to therapeutic applications.Precision clinical medicine · 2025Review
- Resistance of first-line targeted drugs in hepatocellular carcinoma: the epigenetic regulation mechanisms.Cell death & disease · 2025Review
- Reciprocal regulation between m6 A modifications and non-coding RNAs: emerging roles in cancer therapeutic resistance.Discover oncology · 2025Review
- Long Non-Coding RNAs in Non-Alcoholic Fatty Liver Disease; Friends or Foes?Cell biochemistry and biophysics · 2025Review
- LncRNAs, RNA Therapeutics, and Emerging Technologies in Liver Pathobiology.Seminars in liver disease · 2025Review
- Role of the mInternational journal of molecular medicine · 2025Review
- The role of ubiquitination and deubiquitination in the pathogenesis of non-alcoholic fatty liver disease.Frontiers in immunology · 2025Review
- Role and mechanisms of m6A demethylases in digestive system tumors.American journal of cancer research · 2025Review
- RNA modifications in the progression of liver diseases: from fatty liver to cancer.Science China. Life sciences · 2024Review
- Review
- RNA modifications in cellular metabolism: implications for metabolism-targeted therapy and immunotherapy.Signal transduction and targeted therapy · 2024Review
- Article
- PHB2 promotes SHIP2 ubiquitination via the E3 ligase NEDD4 to regulate AKT signaling in gastric cancer.Journal of experimental & clinical cancer research : CR · 2024Article
- The essential roles of lncRNAs/PI3K/AKT axis in gastrointestinal tumors.Frontiers in cell and developmental biology · 2024Review
- Advances in the Pathogenesis of Metabolic Liver Disease-Related Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2024Review
- LncRNAs-circRNAs as Rising Epigenetic Binary Superstars in Regulating Lipid Metabolic Reprogramming of Cancers.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Accumulating evidence suggests that long noncoding RNAs (lncRNAs) are deregulated in hepatocellular carcinoma (HCC) and play a role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). However, the current understanding of the role of lncRNAs in NAFLD-associated HCC is limited. In this study, transcriptomic profiling analysis of three paired human liver samples from patients with NAFLD-driven HCC and adjacent samples showed that LINC01468 expression was significantly upregulated. In vitro and in vivo gain- and loss-of-function experiments showed that LINC01468 promotes the proliferation of HCC cells through lipogenesis. Mechanistically, LINC01468 binds SHIP2 and promotes cullin 4 A (CUL4A)-linked ubiquitin degradation, thereby activating the PI3K/AKT/mTOR signaling pathway, resulting in the promotion of de novo lipid biosynthesis and HCC progression. Importantly, the SHIP2 inhibitor reversed the sorafenib resistance induced by LINC01468 overexpression. Moreover, ALKBH5-mediated N
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Registered trials
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.