دورية أكاديمية
أعرض في EDS

ASCL1 represses a SOX9 + neural crest stem-like state in small cell lung cancer.

التفاصيل البيبلوغرافية
العنوان: ASCL1 represses a SOX9 + neural crest stem-like state in small cell lung cancer.
المؤلفون: Olsen RR; Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah 84112, USA., Ireland AS; Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah 84112, USA., Kastner DW; Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah 84112, USA., Groves SM; Department of Biochemistry, Vanderbilt University, Nashville, Tennessee 37212, USA., Spainhower KB; Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah 84112, USA., Pozo K; Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA., Kelenis DP; Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA., Whitney CP; Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah 84112, USA., Guthrie MR; Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah 84112, USA., Wait SJ; Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah 84112, USA., Soltero D; Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah 84112, USA., Witt BL; Department of Pathology, University of Utah, Salt Lake City, Utah 84112, USA.; ARUP Laboratories at University of Utah, Salt Lake City, Utah 84108, USA., Quaranta V; Department of Biochemistry, Vanderbilt University, Nashville, Tennessee 37212, USA., Johnson JE; Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.; Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA., Oliver TG; Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah 84112, USA.
المصدر: Genes & development [Genes Dev] 2021 Jun; Vol. 35 (11-12), pp. 847-869. Date of Electronic Publication: 2021 May 20.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Cold Spring Harbor Laboratory Press Country of Publication: United States NLM ID: 8711660 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1549-5477 (Electronic) Linking ISSN: 08909369 NLM ISO Abbreviation: Genes Dev Subsets: MEDLINE
أسماء مطبوعة: Publication: Cold Spring Harbor, NY : Cold Spring Harbor Laboratory Press
Original Publication: [Cold Spring Harbor, N.Y.] : Cold Spring Harbor Laboratory in association with the Genetical Society of Great Britain, [c1987-
مواضيع طبية MeSH: Basic Helix-Loop-Helix Transcription Factors/*genetics , Basic Helix-Loop-Helix Transcription Factors/*metabolism , SOX9 Transcription Factor/*genetics , Small Cell Lung Carcinoma/*genetics, Animals ; Animals, Genetically Modified ; Disease Models, Animal ; Gene Expression Regulation, Neoplastic/genetics ; Humans ; Mice ; Neural Crest/cytology ; Small Cell Lung Carcinoma/physiopathology ; Stem Cells/cytology
مستخلص: ASCL1 is a neuroendocrine lineage-specific oncogenic driver of small cell lung cancer (SCLC), highly expressed in a significant fraction of tumors. However, ∼25% of human SCLC are ASCL1-low and associated with low neuroendocrine fate and high MYC expression. Using genetically engineered mouse models (GEMMs), we show that alterations in Rb1/Trp53/Myc in the mouse lung induce an ASCL1 + state of SCLC in multiple cells of origin. Genetic depletion of ASCL1 in MYC-driven SCLC dramatically inhibits tumor initiation and progression to the NEUROD1 + subtype of SCLC. Surprisingly, ASCL1 loss promotes a SOX9 + mesenchymal/neural crest stem-like state and the emergence of osteosarcoma and chondroid tumors, whose propensity is impacted by cell of origin. ASCL1 is critical for expression of key lineage-related transcription factors NKX2-1, FOXA2, and INSM1 and represses genes involved in the Hippo/Wnt/Notch developmental pathways in vivo. Importantly, ASCL1 represses a SOX9/RUNX1/RUNX2 program in vivo and SOX9 expression in human SCLC cells, suggesting a conserved function for ASCL1. Together, in a MYC-driven SCLC model, ASCL1 promotes neuroendocrine fate and represses the emergence of a SOX9 + nonendodermal stem-like fate that resembles neural crest.
(© 2021 Olsen et al.; Published by Cold Spring Harbor Laboratory Press.)
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معلومات مُعتمدة: U01 CA215845 United States CA NCI NIH HHS; U24 CA213274 United States CA NCI NIH HHS; U01 CA213338 United States CA NCI NIH HHS; R21 CA216504 United States CA NCI NIH HHS; U01 CA231844 United States CA NCI NIH HHS; P30 CA042014 United States CA NCI NIH HHS
فهرسة مساهمة: Keywords: ASCL1; SCLC; cell of origin; lung cancer; mouse models; neuroendocrine; plasticity; small cell lung cancer
المشرفين على المادة: 0 (Ascl1 protein, mouse)
0 (Basic Helix-Loop-Helix Transcription Factors)
0 (SOX9 Transcription Factor)
تواريخ الأحداث: Date Created: 20210521 Date Completed: 20211022 Latest Revision: 20231006
رمز التحديث: 20231006
مُعرف محوري في PubMed: PMC8168563
DOI: 10.1101/gad.348295.121
PMID: 34016693
قاعدة البيانات: MEDLINE
الوصف
تدمد:1549-5477
DOI:10.1101/gad.348295.121