ArticleThe Journal of biological chemistry2010
p27Kip1 mediates addiction of ovarian cancer cells to MYCC (c-MYC) and their dependence on MYC paralogs.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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
18 citing papers in PubMed, 24 citations in OpenAlex.
- Regulation of cellular senescence in tumor progression and therapeutic targeting: mechanisms and pathways.Molecular cancer · 2025Review
- CUDC-907 exhibits potent antitumor effects against ovarian cancer through multiple in vivo and in vitro mechanisms.Cancer chemotherapy and pharmacology · 2024Article
- Amplified therapeutic targets in high-grade serous ovarian carcinoma - a review of the literature with quantitative appraisal.Cancer gene therapy · 2023Review
- c-MYC-Driven Polyamine Metabolism in Ovarian Cancer: From Pathogenesis to Early Detection and Therapy.Cancers · 2023Review
- Review
- MicroRNAs as the critical regulators of Cisplatin resistance in ovarian cancer cells.Journal of ovarian research · 2021Review
- An RGDKGE-Containing Cryptic Collagen Fragment Regulates Phosphorylation of Large Tumor Suppressor Kinase-1 and Controls Ovarian Tumor Growth by a Yes-Associated Protein-Dependent Mechanism.The American journal of pathology · 2021Article
- c-MYC and Epithelial Ovarian Cancer.Frontiers in oncology · 2021Review
- Inhibition of the MYC-Regulated Glutaminase Metabolic Axis Is an Effective Synthetic Lethal Approach for Treating Chemoresistant Ovarian Cancers.Cancer research · 2020Article
- Bioinformatic analysis reveals MIR502 as a potential tumour suppressor in ovarian cancer.Journal of ovarian research · 2020Article
- Overexpression of PRC1 indicates a poor prognosis in ovarian cancer.International journal of oncology · 2020Article
- miR-137 mediates the functional link between c-Myc and EZH2 that regulates cisplatin resistance in ovarian cancer.Oncogene · 2019Article
- Clinical Importance of Myc Family Oncogene Aberrations in Epithelial Ovarian Cancer.JNCI cancer spectrum · 2018Article
- Time-Dependent Effects of POT1 Knockdown on Proliferation, Tumorigenicity, and HDACi Response of SK-OV3 Ovarian Cancer Cells.BioMed research international · 2018Article
- Overexpression of KLF4 promotes cell senescence through microRNA-203-survivin-p21 pathway.Oncotarget · 2016Article
- Altered glutamine metabolism in platinum resistant ovarian cancer.Oncotarget · 2016Article
- Targeting c-MYC in Platinum-Resistant Ovarian Cancer.Molecular cancer therapeutics · 2015Article
- Molecular requirements for transformation of fallopian tube epithelial cells into serous carcinoma.Neoplasia (New York, N.Y.) · 2011Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The MYCC (c-MYC) gene is amplified in 30-60% of human ovarian cancers. We assessed the functional significance of MYCC amplification by siRNA inhibition of MYCC or MYC paralogs in a panel of ovarian cancer cell lines expressing varying levels of MYCC. Inactivation of MYCC inhibited cell proliferation and induced replicative senescence only in lines with amplified MYCC, indicating that these cells are addicted to continued MYCC overexpression. In contrast, siRNA knockdown of all three MYC isoforms inhibited proliferation of MYCC non-amplified ovarian cancer cells without inducing replicative senescence, and did not inhibit the proliferation of telomerase-immortalized ovarian surface epithelial cells. The arrest induced by MYCC knockdown was accompanied by an increase in the level of the Cdk inhibitor p27(Kip1) and a decrease in cyclin A expression and Cdk2 activity, and could be reversed by RNAi knockdown of p27(Kip1) or Rb, or by overexpression of cyclin A/Cdk2. The arrest induced by knockdown of all three MYC isoforms could similarly be reversed by p27(Kip1) knockdown. Our findings indicate that the addiction of MYCC-amplified ovarian cancer cells to MYCC differs from the dependence of MYCC non-amplified cancer cells on MYC paralogs, but both are mediated, at least in part, by p27(Kip1). They also suggest that growth of ovarian cancers may be blocked by inhibition of MYCC or MYC paralogs.
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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.