ArticleThe Journal of clinical investigation2024
Liver cancer initiation requires translational activation by an oncofetal regulon involving LIN28 proteins.
Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- SPACE-seq integrates spatial transcriptomics and lineage tracing in native tissues.Cell stem cell · 2026Article
- Targeting the Lin28/let-7 Axis with Compounds to Regulate Transcriptional Control in Cancer.Anti-cancer agents in medicinal chemistry · 2026Review
- A Mouse in vivo Model Mimicking MASH-Related HCC Pathogenesis.Journal of hepatocellular carcinoma · 2026Article
- STAT3 sustains tumorigenicity following mutant KRAS ablation.EMBO reports · 2025Article
- Exploring RNA binding proteins in hepatocellular carcinoma: insights into mechanisms and therapeutic potential.Journal of experimental & clinical cancer research : CR · 2025Review
- UBE2V1 Promotes Hepatocellular Carcinoma Progression by Forming a Positive Feedback Loop with HIF-1α.Research (Washington, D.C.) · 2025Article
- A Multimodal Energy-Depletion Strategy for Cooperative Tumor Metabolism Regulation in Enhanced Cancer Therapy.Biomaterials research · 2025Article
- Solute carrier family 2 member 2 (glucose transporter 2): a common factor of hepatocyte and hepatocellular carcinoma differentiation.PloS one · 2025Article
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Authors and funding
14 authors.
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Abstract
It is unknown which posttranscriptional regulatory mechanisms are required for oncogenic competence. Here, we show that the LIN28 family of RNA-binding proteins (RBPs), which facilitate posttranscriptional RNA metabolism within ribonucleoprotein networks, is essential for the initiation of diverse oncotypes of hepatocellular carcinoma (HCC). In HCC models driven by NRASG12V/Tp53, CTNNB1/YAP/Tp53, or AKT/Tp53, mice without Lin28a and Lin28b were markedly impaired in cancer initiation. We biochemically defined an oncofetal regulon of 15 factors connected to LIN28 through direct mRNA and protein interactions. Interestingly, all were RBPs and only 1 of 15 was a Let-7 target. Polysome profiling and reporter assays showed that LIN28B directly increased the translation of 8 of these 15 RBPs. As expected, overexpression of LIN28B and IGFBP1-3 was able to genetically rescue cancer initiation. Using this platform to probe components downstream of LIN28, we found that 8 target RBPs were able to restore NRASG12V/Tp53 cancer formation in Lin28a/Lin28b-deficient mice. Furthermore, these LIN28B targets promote cancer initiation through an increase in protein synthesis. LIN28B, central to an RNP regulon that increases translation of RBPs, is important for tumor initiation in the liver.
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