Transcription Factor NFIB Is a Driver of Small Cell Lung Cancer Progression in Mice and Marks Metastatic Disease in Patients

Small cell lung cancer (SCLC) is an aggressive neuroendocrine tumor, and no effective treatment is available to date. Mouse models of SCLC based on the inactivation of Rb1 and Trp53 show frequent amplifications of the Nfib and Mycl genes. Here, we report that, although overexpression of either trans...

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Vydané v:	Cell reports (Cambridge) Ročník 16; číslo 3; s. 631 - 643
Hlavní autori:	Semenova, Ekaterina A., Kwon, Min-chul, Monkhorst, Kim, Song, Ji-Ying, Bhaskaran, Rajith, Krijgsman, Oscar, Kuilman, Thomas, Peters, Dennis, Buikhuisen, Wieneke A., Smit, Egbert F., Pritchard, Colin, Cozijnsen, Miranda, van der Vliet, Jan, Zevenhoven, John, Lambooij, Jan-Paul, Proost, Natalie, van Montfort, Erwin, Velds, Arno, Huijbers, Ivo J., Berns, Anton
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	United States Elsevier Inc 19.07.2016 Cell Press Elsevier
Predmet:	Animals Biomarkers, Tumor - metabolism Cadherins - metabolism Cell Proliferation - physiology Disease Models, Animal Disease Progression Gene Expression Regulation, Neoplastic - physiology Humans Lung Neoplasms - metabolism Lung Neoplasms - pathology Mice Neoplasm Metastasis - pathology NFI Transcription Factors - metabolism Proto-Oncogene Proteins c-myc - metabolism Retinoblastoma Protein - metabolism Small Cell Lung Carcinoma - metabolism Small Cell Lung Carcinoma - pathology Tumor Suppressor Protein p53 - metabolism
ISSN:	2211-1247, 2211-1247
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Abstract	Small cell lung cancer (SCLC) is an aggressive neuroendocrine tumor, and no effective treatment is available to date. Mouse models of SCLC based on the inactivation of Rb1 and Trp53 show frequent amplifications of the Nfib and Mycl genes. Here, we report that, although overexpression of either transcription factor accelerates tumor growth, NFIB specifically promotes metastatic spread. High NFIB levels are associated with expansive growth of a poorly differentiated and almost exclusively E-cadherin (CDH1)-negative invasive tumor cell population. Consistent with the mouse data, we find that NFIB is overexpressed in almost all tested human metastatic high-grade neuroendocrine lung tumors, warranting further assessment of NFIB as a tumor progression marker in a clinical setting. [Display omitted] •NFIB drives tumor initiation and progression in mouse models of SCLC•NFIB enhances metastasis and changes the metastatic profile•NFIB promotes dedifferentiation and invasion in SCLC•NFIB marks stage III/IV high-grade neuroendocrine carcinomas in patients SCLC is a highly malignant cancer with an unmet need for better intervention strategies. Semenova et al. report that the transcription factor NFIB drives SCLC growth and metastasis, defines an aggressive tumor compartment in mice, and marks a subgroup of high-grade pulmonary neuroendocrine tumors (pNETs) in patients.
AbstractList	Small cell lung cancer (SCLC) is an aggressive neuroendocrine tumor, and no effective treatment is available to date. Mouse models of SCLC based on the inactivation of Rb1 and Trp53 show frequent amplifications of the Nfib and Mycl genes. Here, we report that, although overexpression of either transcription factor accelerates tumor growth, NFIB specifically promotes metastatic spread. High NFIB levels are associated with expansive growth of a poorly differentiated and almost exclusively E-cadherin (CDH1)-negative invasive tumor cell population. Consistent with the mouse data, we find that NFIB is overexpressed in almost all tested human metastatic high-grade neuroendocrine lung tumors, warranting further assessment of NFIB as a tumor progression marker in a clinical setting. Small cell lung cancer (SCLC) is an aggressive neuroendocrine tumor, and no effective treatment is available to date. Mouse models of SCLC based on the inactivation of Rb1 and Trp53 show frequent amplifications of the Nfib and Mycl genes. Here, we report that, although overexpression of either transcription factor accelerates tumor growth, NFIB specifically promotes metastatic spread. High NFIB levels are associated with expansive growth of a poorly differentiated and almost exclusively E-cadherin (CDH1)-negative invasive tumor cell population. Consistent with the mouse data, we find that NFIB is overexpressed in almost all tested human metastatic high-grade neuroendocrine lung tumors, warranting further assessment of NFIB as a tumor progression marker in a clinical setting.Small cell lung cancer (SCLC) is an aggressive neuroendocrine tumor, and no effective treatment is available to date. Mouse models of SCLC based on the inactivation of Rb1 and Trp53 show frequent amplifications of the Nfib and Mycl genes. Here, we report that, although overexpression of either transcription factor accelerates tumor growth, NFIB specifically promotes metastatic spread. High NFIB levels are associated with expansive growth of a poorly differentiated and almost exclusively E-cadherin (CDH1)-negative invasive tumor cell population. Consistent with the mouse data, we find that NFIB is overexpressed in almost all tested human metastatic high-grade neuroendocrine lung tumors, warranting further assessment of NFIB as a tumor progression marker in a clinical setting. Small cell lung cancer (SCLC) is an aggressive neuroendocrine tumor, and no effective treatment is available to date. Mouse models of SCLC based on the inactivation of Rb1 and Trp53 show frequent amplifications of the Nfib and Mycl genes. Here, we report that, although overexpression of either transcription factor accelerates tumor growth, NFIB specifically promotes metastatic spread. High NFIB levels are associated with expansive growth of a poorly differentiated and almost exclusively E-cadherin (CDH1)-negative invasive tumor cell population. Consistent with the mouse data, we find that NFIB is overexpressed in almost all tested human metastatic high-grade neuroendocrine lung tumors, warranting further assessment of NFIB as a tumor progression marker in a clinical setting. • NFIB drives tumor initiation and progression in mouse models of SCLC • NFIB enhances metastasis and changes the metastatic profile • NFIB promotes dedifferentiation and invasion in SCLC • NFIB marks stage III/IV high-grade neuroendocrine carcinomas in patients SCLC is a highly malignant cancer with an unmet need for better intervention strategies. Semenova et al. report that the transcription factor NFIB drives SCLC growth and metastasis, defines an aggressive tumor compartment in mice, and marks a subgroup of high-grade pulmonary neuroendocrine tumors (pNETs) in patients. Small cell lung cancer (SCLC) is an aggressive neuroendocrine tumor, and no effective treatment is available to date. Mouse models of SCLC based on the inactivation of Rb1 and Trp53 show frequent amplifications of the Nfib and Mycl genes. Here, we report that, although overexpression of either transcription factor accelerates tumor growth, NFIB specifically promotes metastatic spread. High NFIB levels are associated with expansive growth of a poorly differentiated and almost exclusively E-cadherin (CDH1)-negative invasive tumor cell population. Consistent with the mouse data, we find that NFIB is overexpressed in almost all tested human metastatic high-grade neuroendocrine lung tumors, warranting further assessment of NFIB as a tumor progression marker in a clinical setting. [Display omitted] •NFIB drives tumor initiation and progression in mouse models of SCLC•NFIB enhances metastasis and changes the metastatic profile•NFIB promotes dedifferentiation and invasion in SCLC•NFIB marks stage III/IV high-grade neuroendocrine carcinomas in patients SCLC is a highly malignant cancer with an unmet need for better intervention strategies. Semenova et al. report that the transcription factor NFIB drives SCLC growth and metastasis, defines an aggressive tumor compartment in mice, and marks a subgroup of high-grade pulmonary neuroendocrine tumors (pNETs) in patients.
Author	Pritchard, Colin Berns, Anton Proost, Natalie Krijgsman, Oscar Zevenhoven, John Bhaskaran, Rajith Velds, Arno Kuilman, Thomas Peters, Dennis Cozijnsen, Miranda Kwon, Min-chul Song, Ji-Ying Smit, Egbert F. Lambooij, Jan-Paul van der Vliet, Jan Buikhuisen, Wieneke A. Huijbers, Ivo J. Monkhorst, Kim Semenova, Ekaterina A. van Montfort, Erwin
AuthorAffiliation	3 Division of Experimental Animal Pathology, The Netherlands Cancer Institute, Amsterdam 1066 CX, the Netherlands 6 Division of Thoracic Oncology, The Netherlands Cancer Institute, Amsterdam 1066 CX, the Netherlands 9 Skolkovo Institute of Science and Technology, Moscow 143026, Russia 1 Division of Molecular Genetics, The Netherlands Cancer Institute, Amsterdam 1066 CX, the Netherlands 7 Mouse Clinic for Cancer and Aging research Transgenic Core Facility, The Netherlands Cancer Institute, Amsterdam 1066 CX, the Netherlands 4 Core Facility for Molecular Pathology and Biobanking, The Netherlands Cancer Institute, Amsterdam 1066 CX, the Netherlands 2 Division of Pathology, The Netherlands Cancer Institute, Amsterdam 1066 CX, the Netherlands 5 Division of Molecular Oncology, The Netherlands Cancer Institute, Amsterdam 1066 CX, the Netherlands 8 Genomics Core Facility, The Netherlands Cancer Institute, Amsterdam 1066 CX, the Netherlands
AuthorAffiliation_xml	– name: 2 Division of Pathology, The Netherlands Cancer Institute, Amsterdam 1066 CX, the Netherlands – name: 7 Mouse Clinic for Cancer and Aging research Transgenic Core Facility, The Netherlands Cancer Institute, Amsterdam 1066 CX, the Netherlands – name: 1 Division of Molecular Genetics, The Netherlands Cancer Institute, Amsterdam 1066 CX, the Netherlands – name: 4 Core Facility for Molecular Pathology and Biobanking, The Netherlands Cancer Institute, Amsterdam 1066 CX, the Netherlands – name: 5 Division of Molecular Oncology, The Netherlands Cancer Institute, Amsterdam 1066 CX, the Netherlands – name: 8 Genomics Core Facility, The Netherlands Cancer Institute, Amsterdam 1066 CX, the Netherlands – name: 9 Skolkovo Institute of Science and Technology, Moscow 143026, Russia – name: 3 Division of Experimental Animal Pathology, The Netherlands Cancer Institute, Amsterdam 1066 CX, the Netherlands – name: 6 Division of Thoracic Oncology, The Netherlands Cancer Institute, Amsterdam 1066 CX, the Netherlands
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Snippet	Small cell lung cancer (SCLC) is an aggressive neuroendocrine tumor, and no effective treatment is available to date. Mouse models of SCLC based on the...
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SubjectTerms	Animals Biomarkers, Tumor - metabolism Cadherins - metabolism Cell Proliferation - physiology Disease Models, Animal Disease Progression Gene Expression Regulation, Neoplastic - physiology Humans Lung Neoplasms - metabolism Lung Neoplasms - pathology Mice Neoplasm Metastasis - pathology NFI Transcription Factors - metabolism Proto-Oncogene Proteins c-myc - metabolism Retinoblastoma Protein - metabolism Small Cell Lung Carcinoma - metabolism Small Cell Lung Carcinoma - pathology Tumor Suppressor Protein p53 - metabolism
Title	Transcription Factor NFIB Is a Driver of Small Cell Lung Cancer Progression in Mice and Marks Metastatic Disease in Patients
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