ArticleAging2012
Ribonucleotide reductase and thymidylate synthase or exogenous deoxyribonucleosides reduce DNA damage and senescence caused by C-MYC depletion.
Article in Aging, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 29 citations in OpenAlex.
- Deletion of ENO1 sensitizes pancreatic cancer cells to gemcitabine via MYC/RRM1-mediated glycolysis.Scientific reports · 2025Article
- Article
- Indirect targeting of MYC and direct targeting in combination with chemotherapies are more effective than direct mono-targeting in triple negative breast cancer.Translational oncology · 2025Article
- Understanding the interplay between dNTP metabolism and genome stability in cancer.Disease models & mechanisms · 2024Review
- Unveiling the oncogenic significance of thymidylate synthase in human cancers.American journal of translational research · 2024Article
- dTMP imbalance through thymidylate 5'-phosphohydrolase activity induces apoptosis in triple-negative breast cancers.Scientific reports · 2022Article
- Improved tumor control with antiangiogenic therapy after treatment with gemcitabine and nab-paclitaxel in pancreatic cancer.Clinical and translational medicine · 2021Article
- The lncRNA lincNMR regulates nucleotide metabolism via a YBX1 - RRM2 axis in cancer.Nature communications · 2020Article
- Inhibition of the aryl hydrocarbon receptor/polyamine biosynthesis axis suppresses multiple myeloma.The Journal of clinical investigation · 2018Article
- Control of Nucleotide Metabolism Enables Mutant p53's Oncogenic Gain-of-Function Activity.International journal of molecular sciences · 2017Review
- Long-distance interaction of the integrated HPV fragment with MYC gene and 8q24.22 region upregulating the allele-specific MYC expression in HeLa cells.International journal of cancer · 2017Article
- Detection of Nucleotide Disbalance in Cells Undergoing Oncogene-Induced Senescence.Methods in molecular biology (Clifton, N.J.) · 2017Article
- The Immortal Senescence.Methods in molecular biology (Clifton, N.J.) · 2017Review
- CREB1 directly activates the transcription of ribonucleotide reductase small subunit M2 and promotes the aggressiveness of human colorectal cancer.Oncotarget · 2016Article
- 14-3-3σ regulation of and interaction with YAP1 in acquired gemcitabine resistance via promoting ribonucleotide reductase expression.Oncotarget · 2016Article
- Slowing down theMolecular & cellular oncology · 2016Article
- Deoxyribonucleotide metabolism, mutagenesis and cancer.Nature reviews. Cancer · 2015Review
- Review
- Nucleotide metabolism, oncogene-induced senescence and cancer.Cancer letters · 2015Review
- Deoxyribonucleotides as genetic and metabolic regulators.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
The down-regulation of dominant oncogenes, including C-MYC, in tumor cells often leads to the induction of senescence via mechanisms that are not completely identified. In the current study, we demonstrate that MYC-depleted melanoma cells undergo extensive DNA damage that is caused by the underexpression of thymidylate synthase (TS) and ribonucleotide reductase (RR) and subsequent depletion of deoxyribonucleoside triphosphate pools. Simultaneous genetic inhibition of TS and RR in melanoma cells induced DNA damage and senescence phenotypes very similar to the ones caused by MYC-depletion. Reciprocally, overexpression of TS and RR in melanoma cells or addition of deoxyribo-nucleosides to culture media substantially inhibited DNA damage and senescence-associated phenotypes caused by C-MYC depletion. Our data demonstrate the essential role of TS and RR in C-MYC-dependent suppression of senescence in melanoma 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.