ArticleCancer research2014
MYC activates stem-like cell potential in hepatocarcinoma by a p53-dependent mechanism.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 84 citations in OpenAlex.
- Astaxanthin suppresses hepatocellular carcinoma via targeting Wnt/Β-catenin pathway: Experimental study on chemically induced HCC in rats.Scientific reports · 2026Article
- Strawberry Notch 1 Acts as a Transcriptional Regulator Driving Oncogenic Programs in Liver Carcinogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Integrated Bioinformatic Analyses Reveal Thioredoxin as a Putative Marker of Cancer Stem Cells and Prognosis in Prostate Cancer.Cancer informatics · 2025Article
- Role of HNF4α-cMyc Interaction in CDE Diet-Induced Liver Injury and Regeneration.The American journal of pathology · 2024Article
- Lysine-specific methyltransferase Set7/9 in stemness, differentiation, and development.Biology direct · 2024Review
- LINC00460-FUS-MYC feedback loop drives breast cancer metastasis and doxorubicin resistance.Oncogene · 2024Article
- Review
- Comprehensive Analysis of Gene Expression Profiling to Explore Predictive Markers for Eradication Therapy Efficacy againstCancers · 2023Article
- A key driver to promote HCC: Cellular crosstalk in tumor microenvironment.Frontiers in oncology · 2023Review
- Difluoromethylornithine (DFMO) Enhances the Cytotoxicity of PARP Inhibition in Ovarian Cancer Cells.Medical sciences (Basel, Switzerland) · 2022Article
- Exosomal Carboxypeptidase E (CPE) and CPE-shRNA-Loaded Exosomes Regulate Metastatic Phenotype of Tumor Cells.International journal of molecular sciences · 2022Article
- ING4 Promotes Stemness Enrichment of Human Renal Cell Carcinoma Cells Through Inhibiting DUSP4 Expression to Activate the p38 MAPK/type I IFN-Stimulated Gene Signaling Pathway.Frontiers in pharmacology · 2022Article
- Generation of combined hepatocellular-cholangiocarcinoma through transdifferentiation and dedifferentiation in p53-knockout mice.Cancer science · 2021Article
- Conflicting metabolic alterations in cancer stem cells and regulation by the stromal niche.Regenerative therapy · 2021Article
- MCM10 compensates for Myc-induced DNA replication stress in breast cancer stem-like cells.Cancer science · 2021Article
- Loss of miR-192-5p initiates a hyperglycolysis and stemness positive feedback in hepatocellular carcinoma.Journal of experimental & clinical cancer research : CR · 2020Article
- BCL11B suppresses tumor progression and stem cell traits in hepatocellular carcinoma by restoring p53 signaling activity.Cell death & disease · 2020Article
- lncRNA MALAT1 modulates cancer stem cell properties of liver cancer cells by regulating YAP1 expression via miR‑375 sponging.Molecular medicine reports · 2020Article
- Cancer stemness in hepatocellular carcinoma: mechanisms and translational potential.British journal of cancer · 2020Review
- Incomplete radiofrequency ablation provokes colorectal cancer liver metastases through heat shock response by PKCα/Fra-1 pathway.Cancer biology & medicine · 2019Article
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 2 institutions in 1 country.
Funding
Abstract
Activation of c-MYC is an oncogenic hallmark of many cancers, including liver cancer, and is associated with a variety of adverse prognostic characteristics. Despite a causative role during malignant transformation and progression in hepatocarcinogenesis, consequences of c-MYC activation for the biology of hepatic cancer stem cells (CSC) are undefined. Here, distinct levels of c-MYC overexpression were established by using two dose-dependent tetracycline-inducible systems in four hepatoma cell lines with different p53 mutational status. The CSCs were evaluated using side population (SP) approach as well as standard in vitro and in vivo assays. Functional repression of p53 was achieved by lentiviral shRNA transduction. The results show that c-MYC expression levels have a differential impact on liver CSC characteristics. At low levels, c-MYC activation led to increased proliferation and enhanced CSC properties including activation of reprogramming transcription factors and CSC marker expression (e.g., NANOG, OCT4, and EpCAM), expansion of SP, and acceleration of tumor growth upon subcutaneous transplantation into immunocompromised mice. However, when exceeding a threshold level, c-MYC induced a proapoptotic program and loss of CSC potential both in vitro and in vivo. Mechanistically, c-MYC-induced self-renewal capacity of liver cancer cells was exerted in a p53-dependent manner. Low c-MYC activation increased spheroid formation in p53-deficient tumor cells, whereas p53-dependent effects were blunted in the absence of c-MYC overexpression. Together, our results confirm the role of c-MYC as a master regulator during hepatocarcinogenesis and establish a new gatekeeper role for p53 in repressing c-MYC-induced CSC phenotype in liver cancer cells.
Indexed as
Identifiers
What OpenQuestion holds
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.