ArticlePloS one2011
Epigenetic modulation of miR-122 facilitates human embryonic stem cell self-renewal and hepatocellular carcinoma proliferation.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 63 citations in OpenAlex.
- The Impact of miR-122 on Cancer.Current pharmaceutical biotechnology · 2024Review
- MicroRNAs as Regulators of Cancer Cell Energy Metabolism.Journal of personalized medicine · 2022Review
- Distinct promotor methylation at tumor suppressive genes in ovarian cancer stromal progenitor cells and ovarian cancer and its clinical implication.American journal of cancer research · 2022Article
- PTBP1-targeting microRNAs regulate cancer-specific energy metabolism through the modulation of PKM1/M2 splicing.Cancer science · 2021Review
- The Epigenetic Modulation of Cancer and Immune Pathways in Hepatitis B Virus-Associated Hepatocellular Carcinoma: The Influence of HBx and miRNA Dysregulation.Frontiers in immunology · 2021Review
- LncRNA HOTAIR epigenetically suppresses miR-122 expression in hepatocellular carcinoma via DNA methylation.EBioMedicine · 2018Article
- Review
- High Fat Diet-Induced miR-122 Regulates Lipid Metabolism and Fat Deposition in Genetically Improved Farmed Tilapia (GIFT,Frontiers in physiology · 2018Article
- Aberrant Expression of miR-362 Promotes Lung Cancer Metastasis through Downregulation of Sema3A.Journal of immunology research · 2018Article
- Road to stemness in hepatocellular carcinoma.World journal of gastroenterology · 2017Review
- The long non-coding RNA TP73-AS1 modulates HCC cell proliferation through miR-200a-dependent HMGB1/RAGE regulation.Journal of experimental & clinical cancer research : CR · 2017Article
- miR-122 inhibits cancer cell malignancy by targeting PKM2 in gallbladder carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Hepatocarcinogenesis associated with hepatitis B, delta and C viruses.Current opinion in virology · 2016Review
- DDX3 Represses Stemness by Epigenetically Modulating Tumor-suppressive miRNAs in Hepatocellular Carcinoma.Scientific reports · 2016Article
- CCAT1: a pivotal oncogenic long non-coding RNA in human cancers.Cell proliferation · 2016Review
- MicroRNA Regulates Hepatocytic Differentiation of Progenitor Cells by Targeting YAP1.Stem cells (Dayton, Ohio) · 2016Article
- MicroRNA-346 functions as an oncogene in cutaneous squamous cell carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Natural compound-derived epigenetic regulators targeting epigenetic readers, writers and erasers.Current topics in medicinal chemistry · 2016Review
- MiR-146a suppresses hepatocellular carcinoma by downregulating TRAF6.American journal of cancer research · 2016Article
- A cell culture system for distinguishing hepatitis C viruses with and without liver cancer-related mutations in the viral core gene.Journal of hepatology · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The self-renewal capacity ascribed to hESCs is paralleled in cancer cell proliferation, suggesting that a common network of genes may facilitate the promotion of these traits. However, the molecular mechanisms that are involved in regulating the silencing of these genes as stem cells differentiate into quiescent cellular lineages remain poorly understood. Here, we show that a differentiated cell specific miR-122 exemplifies this regulatory attribute by suppressing the translation of a gene, Pkm2, which is commonly enriched in hESCs and liver cancer cells (HCCs), and facilitates self-renewal and proliferation. Through a series of gene expression analysis, we show that miR-122 expression is highly elevated in quiescent human primary hepatocytes (hPHs) but lost or attenuated in hESCs and HCCs, while an opposing expression pattern is observed for Pkm2. Depleting hESCs and HCCs of Pkm2, or overexpressing miR-122, leads to a common deficiency in self-renewal and proliferation. Likewise, during the differentiation process of hESCs into hepatocytes, a reciprocal expression pattern is observed between miR-122 and Pkm2. An examination of the genomic region upstream of miR-122 uncovered hyper-methylation in hESCs and HCCs, while the same region is de-methylated and occupied by a transcription initiating protein, RNA polymerase II (RNAPII), in hPHs. These findings indicate that one possible mechanism by which hESC self-renewal is modulated in quiescent hepatic derivatives of hESCs is through the regulatory activity of a differentiated cell-specific miR-122, and that a failure to properly turn "on" this miRNA is observed in uncontrollably proliferating HCCs.
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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.