ArticleOncogene2014
Cystathionase mediates senescence evasion in melanocytes and melanoma cells.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 34 citations in OpenAlex.
- Hydrogen Sulfide Metabolism in the Skin: From Physiology to Malignancy.International journal of molecular sciences · 2025Review
- The metabolism of melanin synthesis-From melanocytes to melanoma.Pigment cell & melanoma research · 2024Review
- Thiol starvation triggers melanoma state switching in an ATF4 and NRF2-dependent manner.Redox biology · 2024Article
- Validity of Xiphophorus fish as models for human disease.Disease models & mechanisms · 2024Review
- Protooncogene MYC drives human melanocyte melanogenesis and senescence.Cancer gene therapy · 2022Article
- Emerging roles of cystathionine β-synthase in various forms of cancer.Redox biology · 2022Review
- Induction of CTH expression in response to amino acid starvation confers resistance to anti-LAT1 therapy in MDA-MB-231 cells.Scientific reports · 2022Article
- Amino Acid Metabolic Vulnerabilities in Acute and Chronic Myeloid Leukemias.Frontiers in oncology · 2021Review
- Hydrogen Sulfide in Skin Diseases: A Novel Mediator and Therapeutic Target.Oxidative medicine and cellular longevity · 2021Review
- Cysteine Deprivation Targets Ovarian Clear Cell CarcinomaAntioxidants & redox signaling · 2020Article
- The transcription factor NRF2 enhances melanoma malignancy by blocking differentiation and inducing COX2 expression.Oncogene · 2020Article
- "Mitotic Slippage" and Extranuclear DNA in Cancer Chemoresistance: A Focus on Telomeres.International journal of molecular sciences · 2020Article
- Hydrogen sulfide and dermatological diseases.British journal of pharmacology · 2020Review
- Cysteine Depletion, a Key Action to Challenge Cancer Cells to Ferroptotic Cell Death.Frontiers in oncology · 2020Review
- Review
- BRAF inhibition causes resilience of melanoma cell lines by inducing the secretion of FGF1.Oncogenesis · 2018Article
- ΔNp63 targets cytoglobin to inhibit oxidative stress-induced apoptosis in keratinocytes and lung cancer.Oncogene · 2016Article
- Article
- In vitro evidence for senescent multinucleated melanocytes as a source for tumor-initiating cells.Cell death & disease · 2015Article
- Hypoxia-independent drivers of melanoma angiogenesis.Frontiers in oncology · 2015Review
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The development of malignant melanoma is a highly complex process, which is still poorly understood. A majority of human melanomas are found to express a few oncogenic proteins, such as mutant RAS and BRAF variants. However, these oncogenes are also found in nevi, and it is now a well-accepted fact that their expression alone leads to senescence. This renders the understanding of senescence escape mechanisms an important point to understand tumor development. Here, we approached the question of senescence evasion by expressing the transcription factor v-myc myelocytomatosis viral oncogene homolog (c-MYC), which is known to act synergistically with many oncogenes, in melanocytes. We observed that MYC drives the evasion of reactive-oxygen stress-induced melanocyte senescence, caused by activated receptor tyrosine kinase signaling. Conversely, MIZ1, the growth suppressing interaction partner of MYC, is involved in mediating melanocyte senescence. Both, MYC overexpression and Miz1 knockdown led to a strong reduction of endogenous reactive-oxygen species (ROS), DNA damage and senescence. We identified the cystathionase (CTH) gene product as mediator of the ROS-related MYC and MIZ1 effects. Blocking CTH enzymatic activity in MYC-overexpressing and Miz1 knockdown cells increased intracellular stress and senescence. Importantly, pharmacological inhibition of CTH in human melanoma cells also reconstituted senescence in the majority of cell lines, and CTH knockdown reduced tumorigenic effects such as proliferation, H2O2 resistance and soft agar growth. Thus, we identified CTH as new MYC target gene with an important function in senescence evasion.
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.