ArticleGenes & development2013
LIN28B promotes growth and tumorigenesis of the intestinal epithelium via Let-7.
Article in Genes & development, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
89 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.
- RNA-Binding Protein Polymorphisms as Novel Biomarkers to Predict Outcomes of Metastatic Colorectal Cancer: A Meta-analysis from TRIBE, FIRE-3, and MAVERICC.Molecular cancer therapeutics · 2021Pooled it
- Investigating Dietary microRNA Stability and Function Using a Transgenic Milk Model With Unique microRNA Sequences.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Wdr4 regulates ribosome biogenesis and intestinal homeostasis via let-7.EMBO reports · 2026Article
- Targeting the Lin28/let-7 Axis with Compounds to Regulate Transcriptional Control in Cancer.Anti-cancer agents in medicinal chemistry · 2026Review
- Ribosomal protein control of hematopoietic stem cell transformation through regulation of metabolism.Cell reports · 2025Article
- Milk-Derived Extracellular Vesicles and microRNAs: Potential Modulators of Intestinal Homeostasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- LIN28B-mediated PI3K/AKT pathway activation promotes metastasis in colorectal cancer models.The Journal of clinical investigation · 2025Article
- Review
- The lncRNA LINC01605 promotes the progression of pancreatic ductal adenocarcinoma by activating the mTOR signaling pathway.Cancer cell international · 2024Article
- Origins of cancer: ain't it just mature cells misbehaving?The EMBO journal · 2024Review
- RNA-binding proteins and exoribonucleases modulating miRNA in cancer: the enemy within.Experimental & molecular medicine · 2024Review
- Cell-based assay to detect small molecules restoring levels of let-7 miRNAs.American journal of cancer research · 2024Article
- The oncogenic function of PLAGL2 is mediated via ASCL2 and IGF2 and a Wnt-independent mechanism in colorectal cancer.American journal of physiology. Gastrointestinal and liver physiology · 2023Article
- LIN28B promotes cell invasion and colorectal cancer metastasis via CLDN1 and NOTCH3.JCI insight · 2023Article
- A novel tumour enhancer function of Insulin-like growth factor II mRNA-binding protein 3 in colorectal cancer.Cell death & disease · 2023Article
- Enhanced protein synthesis is a defining requirement for neonatal B cell development.Frontiers in immunology · 2023Article
- HucMSC-Exo Promote Mucosal Healing in Experimental Colitis by Accelerating Intestinal Stem Cells and Epithelium Regeneration via Wnt Signaling Pathway.International journal of nanomedicine · 2023Article
- Effects of Let-7c on the processing of hepatitis B virus associated liver diseases.Infectious agents and cancer · 2022Article
- LIN28B alters ribosomal dynamics to promote metastasis in MYCN-driven malignancy.The Journal of clinical investigation · 2021Article
- Article
29 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
The RNA-binding proteins LIN28A and LIN28B have diverse functions in embryonic stem cells, cellular reprogramming, growth, and oncogenesis. Many of these effects occur via direct inhibition of Let-7 microRNAs (miRNAs), although Let-7-independent effects have been surmised. We report that intestine targeted expression of LIN28B causes intestinal hypertrophy, crypt expansion, and Paneth cell loss. Furthermore, LIN28B fosters intestinal polyp and adenocarcinoma formation. To examine potential Let-7-independent functions of LIN28B, we pursued ribonucleoprotein cross-linking, immunoprecipitation, and high-throughput sequencing (CLIP-seq) to identify direct RNA targets. This revealed that LIN28B bound a substantial number of mRNAs and modestly augmented protein levels of these target mRNAs in vivo. Conversely, Let-7 had a profound effect; modulation of Let-7 levels via deletion of the mirLet7c2/mirLet7b genes recapitulated effects of Lin28b overexpression. Furthermore, intestine-specific Let-7 expression could reverse hypertrophy and Paneth cell depletion caused by Lin28b. This was independent of effects on insulin-PI3K-mTOR signaling. Our study reveals that Let-7 miRNAs are critical for repressing intestinal tissue growth and promoting Paneth cell differentiation. Let-7-dependent effects of LIN28B may supersede Let-7-independent effects on intestinal tissue growth. In summary, LIN28B can definitively act as an oncogene in the absence of canonical genetic alterations.
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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.