ArticleOncogene2009
MITOSTATIN, a putative tumor suppressor on chromosome 12q24.1, is downregulated in human bladder and breast cancer.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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Who cites it
33 citing papers in PubMed, 48 citations in OpenAlex.
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- Decorin evokes reversible mitochondrial depolarization in carcinoma and vascular endothelial cells.American journal of physiology. Cell physiology · 2022Article
- Telomere Dysfunction Is Associated with Altered DNA Organization in Trichoplein/Tchp/Mitostatin (TpMs) Depleted Cells.Biomedicines · 2022Article
- The Role of Decorin Proteoglycan in Mitophagy.Cancers · 2022Review
- Progranulin/EphA2 axis: A novel oncogenic mechanism in bladder cancer.Matrix biology : journal of the International Society for Matrix Biology · 2020Article
- Proteoglycan-driven Autophagy: A Nutrient-independent Mechanism to Control Intracellular Catabolism.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020Review
- Trichoplein binds PCM1 and controls endothelial cell function by regulating autophagy.EMBO reports · 2020Article
- Split-TurboID enables contact-dependent proximity labeling in cells.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Discoidin Domain Receptor 1 functionally interacts with the IGF-I system in bladder cancer.Matrix biology plus · 2020Article
- Depletion of Trichoplein (TpMs) Causes Chromosome Mis-Segregation, DNA Damage and Chromosome Instability in Cancer Cells.Cancers · 2020Article
- Decorin is a devouring proteoglycan: Remodeling of intracellular catabolism via autophagy and mitophagy.Matrix biology : journal of the International Society for Matrix Biology · 2019Review
- Endorepellin remodels the endothelial transcriptome toward a pro-autophagic and pro-mitophagic gene signature.The Journal of biological chemistry · 2018Article
- Wolfram syndrome: MAMs' connection?Cell death & disease · 2018Review
- Abnormal spermatogenesis and male infertility in testicular zinc finger protein Zfp318-knockout mice.Development, growth & differentiation · 2016Article
- Molecular Functions of Glycoconjugates in Autophagy.Journal of molecular biology · 2016Review
- Decorin as a multivalent therapeutic agent against cancer.Advanced drug delivery reviews · 2016Review
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
Abstract
Allelic deletions on human chromosome 12q24 are frequently reported in a variety of malignant neoplasms, indicating the presence of a tumor suppressor gene(s) in this chromosomal region. However, no reasonable candidate has been identified so far. In this study, we report the cloning and functional characterization of a novel mitochondrial protein with tumor suppressor activity, henceforth designated MITOSTATIN. Human MITOSTATIN was found within a 3.2-kb transcript, which encoded a approximately 62 kDa, ubiquitously expressed protein with little homology to any known protein. We found homozygous deletions and mutations of MITOSTATIN gene in approximately 5 and approximately 11% of various cancer-derived cells and solid tumors, respectively. When transiently overexpressed, MITOSTATIN inhibited colony formation, tumor cell growth and was proapoptotic, all features shared by established tumor suppressor genes. We discovered a specific link between MITOSTATIN overexpression and downregulation of Hsp27. Conversely, MITOSTATIN knockdown cells showed an increase in cell growth and cell survival rates. Finally, MITOSTATIN expression was significantly reduced in primary bladder and breast tumors, and its reduction was associated with advanced tumor stages. Our findings support the hypothesis that MITOSTATIN has many hallmarks of a classical tumor suppressor in solid tumors and may play an important role in cancer development and progression.
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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.