{"title":"黑色素瘤中的BNIP3:这不是很讽刺吗?","authors":"Mónica Vara-Pérez, Patrizia Agostinis","doi":"10.1080/23723556.2021.1947169","DOIUrl":null,"url":null,"abstract":"<p><p>Melanoma cells exploit mitophagy and hypoxia signaling to promote their growth. In a recent study, we found that loss of B-cell lymphoma 2 (BCL-2)/adenovirus E1B 19kDa protein-interacting protein 3 (BNIP3) curbed Hypoxia Inducible Factor 1 alpha (HIF-1α) levels and melanoma growth <i>in vivo</i>. Insufficient levels of BNIP3 boost iron-driven prolyl hydroxylase 2 (Phd2)-mediated degradation of HIF-1α by exacerbating nuclear receptor activator 4 (Ncoa4)-mediated ferritinophagy. Thus, BNIP3 promotes melanoma growth by controlling iron metabolism.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 4","pages":"1947169"},"PeriodicalIF":2.6000,"publicationDate":"2021-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8489953/pdf/KMCO_8_1947169.pdf","citationCount":"0","resultStr":"{\"title\":\"BNIP3 in melanoma: isn't it IRONic?\",\"authors\":\"Mónica Vara-Pérez, Patrizia Agostinis\",\"doi\":\"10.1080/23723556.2021.1947169\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Melanoma cells exploit mitophagy and hypoxia signaling to promote their growth. In a recent study, we found that loss of B-cell lymphoma 2 (BCL-2)/adenovirus E1B 19kDa protein-interacting protein 3 (BNIP3) curbed Hypoxia Inducible Factor 1 alpha (HIF-1α) levels and melanoma growth <i>in vivo</i>. Insufficient levels of BNIP3 boost iron-driven prolyl hydroxylase 2 (Phd2)-mediated degradation of HIF-1α by exacerbating nuclear receptor activator 4 (Ncoa4)-mediated ferritinophagy. Thus, BNIP3 promotes melanoma growth by controlling iron metabolism.</p>\",\"PeriodicalId\":37292,\"journal\":{\"name\":\"Molecular and Cellular Oncology\",\"volume\":\"8 4\",\"pages\":\"1947169\"},\"PeriodicalIF\":2.6000,\"publicationDate\":\"2021-08-02\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8489953/pdf/KMCO_8_1947169.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Molecular and Cellular Oncology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1080/23723556.2021.1947169\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2021/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q3\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular and Cellular Oncology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/23723556.2021.1947169","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2021/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"ONCOLOGY","Score":null,"Total":0}
Melanoma cells exploit mitophagy and hypoxia signaling to promote their growth. In a recent study, we found that loss of B-cell lymphoma 2 (BCL-2)/adenovirus E1B 19kDa protein-interacting protein 3 (BNIP3) curbed Hypoxia Inducible Factor 1 alpha (HIF-1α) levels and melanoma growth in vivo. Insufficient levels of BNIP3 boost iron-driven prolyl hydroxylase 2 (Phd2)-mediated degradation of HIF-1α by exacerbating nuclear receptor activator 4 (Ncoa4)-mediated ferritinophagy. Thus, BNIP3 promotes melanoma growth by controlling iron metabolism.
期刊介绍：
For a long time, solid neoplasms have been viewed as relatively homogeneous entities composed for the most part of malignant cells. It is now clear that tumors are highly heterogeneous structures that evolve in the context of intimate interactions between cancer cells and endothelial, stromal as well as immune cells. During the past few years, experimental and clinical oncologists have witnessed several conceptual transitions of this type. Molecular and Cellular Oncology (MCO) emerges within this conceptual framework as a high-profile forum for the publication of fundamental, translational and clinical research on cancer. The scope of MCO is broad. Submissions dealing with all aspects of oncogenesis, tumor progression and response to therapy will be welcome, irrespective of whether they focus on solid or hematological neoplasms. MCO has gathered leading scientists with expertise in multiple areas of cancer research and other fields of investigation to constitute a large, interdisciplinary, Editorial Board that will ensure the quality of articles accepted for publication. MCO will publish Original Research Articles, Brief Reports, Reviews, Short Reviews, Commentaries, Author Views (auto-commentaries) and Meeting Reports dealing with all aspects of cancer research.
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