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HIF-1 antagonizes p53-mediated apoptosis through a secreted neuronal tyrosinase (2010)

A. Sendoel ; I. Kohler ; C. Fellmann ; [et al.]

Nature Publishing Group (NPG)

In: Nature. 465(7298): 577-83. doi: 10.1038/nature09141.

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Publication Date: 2010-06-04

Description: Hypoxia-inducible factor (HIF) is a transcription factor that regulates fundamental cellular processes in response to changes in oxygen concentration. HIFalpha protein levels are increased in most solid tumours and correlate with patient prognosis. The link between HIF and apoptosis, a major determinant of cancer progression and treatment outcome, is poorly understood. Here we show that Caenorhabditis elegans HIF-1 protects against DNA-damage-induced germ cell apoptosis by antagonizing the function of CEP-1, the homologue of the tumour suppressor p53. The antiapoptotic property of HIF-1 is mediated by means of transcriptional upregulation of the tyrosinase family member TYR-2 in the ASJ sensory neurons. TYR-2 is secreted by ASJ sensory neurons to antagonize CEP-1-dependent germline apoptosis. Knock down of the TYR-2 homologue TRP2 (also called DCT) in human melanoma cells similarly increases apoptosis, indicating an evolutionarily conserved function. Our findings identify a novel link between hypoxia and programmed cell death, and provide a paradigm for HIF-1 dictating apoptotic cell fate at a distance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3328299/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉 〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3328299/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sendoel, Ataman -- Kohler, Ines -- Fellmann, Christof -- Lowe, Scott W -- Hengartner, Michael O -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Jun 3;465(7298):577-83. doi: 10.1038/nature09141.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Life Sciences, University of Zurich, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20520707" target="_blank"〉PubMed〈/a〉

Keywords: Animals ; *Apoptosis/radiation effects ; Caenorhabditis elegans/cytology/enzymology/*metabolism ; Caenorhabditis elegans Proteins/antagonists & inhibitors/metabolism/secretion ; Cell Hypoxia ; DNA Damage ; Germ Cells/metabolism/pathology ; Humans ; Hypoxia-Inducible Factor 1/*metabolism ; Intramolecular Oxidoreductases/deficiency/genetics/metabolism ; Melanoma/metabolism/pathology ; Monophenol Monooxygenase/deficiency/*metabolism/*secretion ; Sensory Receptor Cells/*enzymology/secretion ; Tumor Suppressor Protein p53/*antagonists & inhibitors/metabolism

Print ISSN: 0028-0836

Electronic ISSN: 1476-4687

Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics

Published by Nature Publishing Group (NPG)

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Direct in vivo RNAi screen unveils myosin IIa as a tumor suppressor of squamous cell carcinomas (2014)

D. Schramek ; A. Sendoel ; J. P. Segal ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 343(6168): 309-13. doi: 10.1126/science.1248627.

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Publication Date: 2014-01-18

Description: Mining modern genomics for cancer therapies is predicated on weeding out "bystander" alterations (nonconsequential mutations) and identifying "driver" mutations responsible for tumorigenesis and/or metastasis. We used a direct in vivo RNA interference (RNAi) strategy to screen for genes that upon repression predispose mice to squamous cell carcinomas (SCCs). Seven of our top hits-including Myh9, which encodes nonmuscle myosin IIa-have not been linked to tumor development, yet tissue-specific Myh9 RNAi and Myh9 knockout trigger invasive SCC formation on tumor-susceptible backgrounds. In human and mouse keratinocytes, myosin IIa's function is manifested not only in conventional actin-related processes but also in regulating posttranscriptional p53 stabilization. Myosin IIa is diminished in human SCCs with poor survival, which suggests that in vivo RNAi technology might be useful for identifying potent but low-penetrance tumor suppressors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159249/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉 〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159249/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schramek, Daniel -- Sendoel, Ataman -- Segal, Jeremy P -- Beronja, Slobodan -- Heller, Evan -- Oristian, Daniel -- Reva, Boris -- Fuchs, Elaine -- R37 AR027883/AR/NIAMS NIH HHS/ -- R37-AR27883/AR/NIAMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Jan 17;343(6168):309-13. doi: 10.1126/science.1248627.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Laboratory of Mammalian Cell Biology and Development, The Rockefeller University, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24436421" target="_blank"〉PubMed〈/a〉

Keywords: Animals ; Carcinoma, Squamous Cell/*genetics/*pathology ; Genetic Testing ; Head and Neck Neoplasms/genetics/pathology ; Humans ; Lung Neoplasms/secondary ; Mice ; Mice, Knockout ; Molecular Motor Proteins/genetics/*physiology ; Mutation ; Myosin Heavy Chains/genetics/*physiology ; Nonmuscle Myosin Type IIA/genetics/*physiology ; RNA Interference ; Transcription, Genetic ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Proteins/genetics/*physiology

Print ISSN: 0036-8075

Electronic ISSN: 1095-9203

Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics