Transcriptional Induction of Periostin by a Sulfatase 2-TGFb1-SMAD Signaling Axis Mediates Tumor Angiogenesis in Hepatocellular Carcinoma

Autores: Chen, Gang; Nakamura, Ikuo; Dhanasekaran, Renumathy; Iguchi, Eriko; Tolosa, Ezequiel Julian; Romecin, Paola A.; Vera, Renzo Emanuel; Almada, Luciana Victoria; Miamen, Alexander G.; Chaiteerakij, Roongruedee; Zhou, Mengtao; Asiedu, Michael K.; Moser, Catherine D.; Han, Shaoshan; Hu, Chunling; Banini, Bubu A.; Oseini, Abdul M.; Chen, Yichun; Fang, Yong; Yang, Dongye; Shaleh, Hassan M.; Wang, Shaoqing; Wu, Dehai; Song, Tao; Lee, Ju-Seog; Thorgeirsson, Snorri S.; Chevet, Eric; Shah, Vijay H.; Fernandez-Zapico, Martin E.; Roberts, Lewis R.
Año de publicación: 2017
Idioma: inglés
Tipo de recurso: artículo
Estado: versión publicada
Descripción: Existing antiangiogenic approaches to treat metastatic hepatocellular carcinoma (HCC) are weakly effectual, prompting further study of tumor angiogenesis in this disease setting. Here, we report a novel role for sulfatase 2 (SULF2) in driving HCC angiogenesis. Sulf2-deficient mice (Sulf2 KO) exhibited resistance to diethylnitrosamine-induced HCC and did not develop metastases like wild-type mice (Sulf2 WT). The smaller and less numerous tumors formed in Sulf2 KO mice exhibited a markedly lower microvascular density. In human HCC cells, SULF2 overexpression increased endothelial proliferation, adhesion, chemotaxis, and tube formation in a paracrine fashion. Mechanistic analyses identified the extracellular matrix protein periostin (POSTN), a ligand of avb3/5 integrins, as an effector protein in SULF2-induced angiogenesis. POSTN silencing in HCC cells attenuated SULF2-induced angiogenesis and tumor growth in vivo. The TGFb1/SMAD pathway was identified as a critical signaling axis between SULF2 and upregulation of POSTN transcription. In clinical HCC specimens, elevated levels of SULF2 correlated with increased microvascular density, POSTN levels, and relatively poorer patient survival. Together, our findings define an important axis controlling angiogenesis in HCC and a mechanistic foundation for rational drug development.
Fil: Chen, Gang. Mayo Clinic; Estados Unidos. Wenzhou Medical University; China
Fil: Nakamura, Ikuo. Mayo Clinic; Estados Unidos
Fil: Dhanasekaran, Renumathy. Mayo Clinic; Estados Unidos. University of Stanford; Estados Unidos
Fil: Iguchi, Eriko. Schulze Center For Novel Therapeutics, Mayo Clinic; Estados Unidos
Fil: Tolosa, Ezequiel Julian. Schulze Center For Novel Therapeutics, Mayo Clinic; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones Biológicas y Tecnológicas. Universidad Nacional de Córdoba. Facultad de Ciencias Exactas, Físicas y Naturales. Instituto de Investigaciones Biológicas y Tecnológicas; Argentina
Fil: Romecin, Paola A.. Schulze Center For Novel Therapeutics, Mayo Clinic; Estados Unidos
Fil: Vera, Renzo Emanuel. Schulze Center For Novel Therapeutics, Mayo Clinic; Estados Unidos. Universidad Nacional de Río Cuarto. Facultad de Ciencias Exactas Fisicoquímicas y Naturales. Departamento de Biología Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina
Fil: Almada, Luciana Victoria. Schulze Center For Novel Therapeutics, Mayo Clinic; Estados Unidos
Fil: Miamen, Alexander G.. Mayo Clinic; Estados Unidos
Fil: Chaiteerakij, Roongruedee. Mayo Clinic; Estados Unidos
Fil: Zhou, Mengtao. Wenzhou Medical University; China
Fil: Asiedu, Michael K.. Mayo Clinic; Estados Unidos
Fil: Moser, Catherine D.. Mayo Clinic; Estados Unidos
Fil: Han, Shaoshan. Mayo Clinic; Estados Unidos
Fil: Hu, Chunling. Mayo Clinic; Estados Unidos
Fil: Banini, Bubu A.. Mayo Clinic; Estados Unidos
Fil: Oseini, Abdul M.. Mayo Clinic; Estados Unidos
Fil: Chen, Yichun. Mayo Clinic; Estados Unidos
Fil: Fang, Yong. Mayo Clinic; Estados Unidos
Fil: Yang, Dongye. Mayo Clinic; Estados Unidos
Fil: Shaleh, Hassan M.. Mayo Clinic; Estados Unidos
Fil: Wang, Shaoqing. Mayo Clinic; Estados Unidos
Fil: Wu, Dehai. Mayo Clinic; Estados Unidos
Fil: Song, Tao. Mayo Clinic; Estados Unidos
Fil: Lee, Ju-Seog. Anderson Cancer Center; Estados Unidos
Fil: Thorgeirsson, Snorri S.. National Cancer Institute; Estados Unidos
Fil: Chevet, Eric. Université Rennes; Francia
Fil: Shah, Vijay H.. Mayo Clinic; Estados Unidos
Fil: Fernandez-Zapico, Martin E.. Schulze Center For Novel Therapeutics, Mayo Clinic; Estados Unidos
Fil: Roberts, Lewis R.. Mayo Clinic; Estados Unidos
Materia: ANGIOGENESIS
HEPATOCELLULAR CARCINOMA
SULFATASE 2
Nivel de accesibilidad: acceso abierto
Condiciones de uso: https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
Institución: Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador: oai:ri.conicet.gov.ar:11336/81650

Acceder

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oai_identifier_str	oai:ri.conicet.gov.ar:11336/81650
network_acronym_str	CONICETDig
repository_id_str	3498
network_name_str	CONICET Digital (CONICET)
spelling	Transcriptional Induction of Periostin by a Sulfatase 2-TGFb1-SMAD Signaling Axis Mediates Tumor Angiogenesis in Hepatocellular CarcinomaChen, GangNakamura, IkuoDhanasekaran, RenumathyIguchi, ErikoTolosa, Ezequiel JulianRomecin, Paola A.Vera, Renzo EmanuelAlmada, Luciana VictoriaMiamen, Alexander G.Chaiteerakij, RoongruedeeZhou, MengtaoAsiedu, Michael K.Moser, Catherine D.Han, ShaoshanHu, ChunlingBanini, Bubu A.Oseini, Abdul M.Chen, YichunFang, YongYang, DongyeShaleh, Hassan M.Wang, ShaoqingWu, DehaiSong, TaoLee, Ju-SeogThorgeirsson, Snorri S.Chevet, EricShah, Vijay H.Fernandez-Zapico, Martin E.Roberts, Lewis R.ANGIOGENESISHEPATOCELLULAR CARCINOMASULFATASE 2https://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Existing antiangiogenic approaches to treat metastatic hepatocellular carcinoma (HCC) are weakly effectual, prompting further study of tumor angiogenesis in this disease setting. Here, we report a novel role for sulfatase 2 (SULF2) in driving HCC angiogenesis. Sulf2-deficient mice (Sulf2 KO) exhibited resistance to diethylnitrosamine-induced HCC and did not develop metastases like wild-type mice (Sulf2 WT). The smaller and less numerous tumors formed in Sulf2 KO mice exhibited a markedly lower microvascular density. In human HCC cells, SULF2 overexpression increased endothelial proliferation, adhesion, chemotaxis, and tube formation in a paracrine fashion. Mechanistic analyses identified the extracellular matrix protein periostin (POSTN), a ligand of avb3/5 integrins, as an effector protein in SULF2-induced angiogenesis. POSTN silencing in HCC cells attenuated SULF2-induced angiogenesis and tumor growth in vivo. The TGFb1/SMAD pathway was identified as a critical signaling axis between SULF2 and upregulation of POSTN transcription. In clinical HCC specimens, elevated levels of SULF2 correlated with increased microvascular density, POSTN levels, and relatively poorer patient survival. Together, our findings define an important axis controlling angiogenesis in HCC and a mechanistic foundation for rational drug development.Fil: Chen, Gang. Mayo Clinic; Estados Unidos. Wenzhou Medical University; ChinaFil: Nakamura, Ikuo. Mayo Clinic; Estados UnidosFil: Dhanasekaran, Renumathy. Mayo Clinic; Estados Unidos. University of Stanford; Estados UnidosFil: Iguchi, Eriko. Schulze Center For Novel Therapeutics, Mayo Clinic; Estados UnidosFil: Tolosa, Ezequiel Julian. Schulze Center For Novel Therapeutics, Mayo Clinic; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones Biológicas y Tecnológicas. Universidad Nacional de Córdoba. Facultad de Ciencias Exactas, Físicas y Naturales. Instituto de Investigaciones Biológicas y Tecnológicas; ArgentinaFil: Romecin, Paola A.. Schulze Center For Novel Therapeutics, Mayo Clinic; Estados UnidosFil: Vera, Renzo Emanuel. Schulze Center For Novel Therapeutics, Mayo Clinic; Estados Unidos. Universidad Nacional de Río Cuarto. Facultad de Ciencias Exactas Fisicoquímicas y Naturales. Departamento de Biología Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; ArgentinaFil: Almada, Luciana Victoria. Schulze Center For Novel Therapeutics, Mayo Clinic; Estados UnidosFil: Miamen, Alexander G.. Mayo Clinic; Estados UnidosFil: Chaiteerakij, Roongruedee. Mayo Clinic; Estados UnidosFil: Zhou, Mengtao. Wenzhou Medical University; ChinaFil: Asiedu, Michael K.. Mayo Clinic; Estados UnidosFil: Moser, Catherine D.. Mayo Clinic; Estados UnidosFil: Han, Shaoshan. Mayo Clinic; Estados UnidosFil: Hu, Chunling. Mayo Clinic; Estados UnidosFil: Banini, Bubu A.. Mayo Clinic; Estados UnidosFil: Oseini, Abdul M.. Mayo Clinic; Estados UnidosFil: Chen, Yichun. Mayo Clinic; Estados UnidosFil: Fang, Yong. Mayo Clinic; Estados UnidosFil: Yang, Dongye. Mayo Clinic; Estados UnidosFil: Shaleh, Hassan M.. Mayo Clinic; Estados UnidosFil: Wang, Shaoqing. Mayo Clinic; Estados UnidosFil: Wu, Dehai. Mayo Clinic; Estados UnidosFil: Song, Tao. Mayo Clinic; Estados UnidosFil: Lee, Ju-Seog. Anderson Cancer Center; Estados UnidosFil: Thorgeirsson, Snorri S.. National Cancer Institute; Estados UnidosFil: Chevet, Eric. Université Rennes; FranciaFil: Shah, Vijay H.. Mayo Clinic; Estados UnidosFil: Fernandez-Zapico, Martin E.. Schulze Center For Novel Therapeutics, Mayo Clinic; Estados UnidosFil: Roberts, Lewis R.. Mayo Clinic; Estados UnidosAmerican Association for Cancer Research2017-02info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/81650Chen, Gang; Nakamura, Ikuo; Dhanasekaran, Renumathy; Iguchi, Eriko; Tolosa, Ezequiel Julian; et al.; Transcriptional Induction of Periostin by a Sulfatase 2-TGFb1-SMAD Signaling Axis Mediates Tumor Angiogenesis in Hepatocellular Carcinoma; American Association for Cancer Research; Cancer Research; 77; 3; 2-2017; 632-6450008-54721538-7445CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1158/0008-5472.CAN-15-2556info:eu-repo/semantics/altIdentifier/url/https://cancerres.aacrjournals.org/content/77/3/632info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:30:09Zoai:ri.conicet.gov.ar:11336/81650instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 10:30:09.568CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv	Transcriptional Induction of Periostin by a Sulfatase 2-TGFb1-SMAD Signaling Axis Mediates Tumor Angiogenesis in Hepatocellular Carcinoma
title	Transcriptional Induction of Periostin by a Sulfatase 2-TGFb1-SMAD Signaling Axis Mediates Tumor Angiogenesis in Hepatocellular Carcinoma
spellingShingle	Transcriptional Induction of Periostin by a Sulfatase 2-TGFb1-SMAD Signaling Axis Mediates Tumor Angiogenesis in Hepatocellular Carcinoma Chen, Gang ANGIOGENESIS HEPATOCELLULAR CARCINOMA SULFATASE 2
title_short	Transcriptional Induction of Periostin by a Sulfatase 2-TGFb1-SMAD Signaling Axis Mediates Tumor Angiogenesis in Hepatocellular Carcinoma
title_full	Transcriptional Induction of Periostin by a Sulfatase 2-TGFb1-SMAD Signaling Axis Mediates Tumor Angiogenesis in Hepatocellular Carcinoma
title_fullStr	Transcriptional Induction of Periostin by a Sulfatase 2-TGFb1-SMAD Signaling Axis Mediates Tumor Angiogenesis in Hepatocellular Carcinoma
title_full_unstemmed	Transcriptional Induction of Periostin by a Sulfatase 2-TGFb1-SMAD Signaling Axis Mediates Tumor Angiogenesis in Hepatocellular Carcinoma
title_sort	Transcriptional Induction of Periostin by a Sulfatase 2-TGFb1-SMAD Signaling Axis Mediates Tumor Angiogenesis in Hepatocellular Carcinoma
dc.creator.none.fl_str_mv	Chen, Gang Nakamura, Ikuo Dhanasekaran, Renumathy Iguchi, Eriko Tolosa, Ezequiel Julian Romecin, Paola A. Vera, Renzo Emanuel Almada, Luciana Victoria Miamen, Alexander G. Chaiteerakij, Roongruedee Zhou, Mengtao Asiedu, Michael K. Moser, Catherine D. Han, Shaoshan Hu, Chunling Banini, Bubu A. Oseini, Abdul M. Chen, Yichun Fang, Yong Yang, Dongye Shaleh, Hassan M. Wang, Shaoqing Wu, Dehai Song, Tao Lee, Ju-Seog Thorgeirsson, Snorri S. Chevet, Eric Shah, Vijay H. Fernandez-Zapico, Martin E. Roberts, Lewis R.
author	Chen, Gang
author_facet	Chen, Gang Nakamura, Ikuo Dhanasekaran, Renumathy Iguchi, Eriko Tolosa, Ezequiel Julian Romecin, Paola A. Vera, Renzo Emanuel Almada, Luciana Victoria Miamen, Alexander G. Chaiteerakij, Roongruedee Zhou, Mengtao Asiedu, Michael K. Moser, Catherine D. Han, Shaoshan Hu, Chunling Banini, Bubu A. Oseini, Abdul M. Chen, Yichun Fang, Yong Yang, Dongye Shaleh, Hassan M. Wang, Shaoqing Wu, Dehai Song, Tao Lee, Ju-Seog Thorgeirsson, Snorri S. Chevet, Eric Shah, Vijay H. Fernandez-Zapico, Martin E. Roberts, Lewis R.
author_role	author
author2	Nakamura, Ikuo Dhanasekaran, Renumathy Iguchi, Eriko Tolosa, Ezequiel Julian Romecin, Paola A. Vera, Renzo Emanuel Almada, Luciana Victoria Miamen, Alexander G. Chaiteerakij, Roongruedee Zhou, Mengtao Asiedu, Michael K. Moser, Catherine D. Han, Shaoshan Hu, Chunling Banini, Bubu A. Oseini, Abdul M. Chen, Yichun Fang, Yong Yang, Dongye Shaleh, Hassan M. Wang, Shaoqing Wu, Dehai Song, Tao Lee, Ju-Seog Thorgeirsson, Snorri S. Chevet, Eric Shah, Vijay H. Fernandez-Zapico, Martin E. Roberts, Lewis R.
author2_role	author author author author author author author author author author author author author author author author author author author author author author author author author author author author author
dc.subject.none.fl_str_mv	ANGIOGENESIS HEPATOCELLULAR CARCINOMA SULFATASE 2
topic	ANGIOGENESIS HEPATOCELLULAR CARCINOMA SULFATASE 2
purl_subject.fl_str_mv	https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv	Existing antiangiogenic approaches to treat metastatic hepatocellular carcinoma (HCC) are weakly effectual, prompting further study of tumor angiogenesis in this disease setting. Here, we report a novel role for sulfatase 2 (SULF2) in driving HCC angiogenesis. Sulf2-deficient mice (Sulf2 KO) exhibited resistance to diethylnitrosamine-induced HCC and did not develop metastases like wild-type mice (Sulf2 WT). The smaller and less numerous tumors formed in Sulf2 KO mice exhibited a markedly lower microvascular density. In human HCC cells, SULF2 overexpression increased endothelial proliferation, adhesion, chemotaxis, and tube formation in a paracrine fashion. Mechanistic analyses identified the extracellular matrix protein periostin (POSTN), a ligand of avb3/5 integrins, as an effector protein in SULF2-induced angiogenesis. POSTN silencing in HCC cells attenuated SULF2-induced angiogenesis and tumor growth in vivo. The TGFb1/SMAD pathway was identified as a critical signaling axis between SULF2 and upregulation of POSTN transcription. In clinical HCC specimens, elevated levels of SULF2 correlated with increased microvascular density, POSTN levels, and relatively poorer patient survival. Together, our findings define an important axis controlling angiogenesis in HCC and a mechanistic foundation for rational drug development. Fil: Chen, Gang. Mayo Clinic; Estados Unidos. Wenzhou Medical University; China Fil: Nakamura, Ikuo. Mayo Clinic; Estados Unidos Fil: Dhanasekaran, Renumathy. Mayo Clinic; Estados Unidos. University of Stanford; Estados Unidos Fil: Iguchi, Eriko. Schulze Center For Novel Therapeutics, Mayo Clinic; Estados Unidos Fil: Tolosa, Ezequiel Julian. Schulze Center For Novel Therapeutics, Mayo Clinic; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones Biológicas y Tecnológicas. Universidad Nacional de Córdoba. Facultad de Ciencias Exactas, Físicas y Naturales. Instituto de Investigaciones Biológicas y Tecnológicas; Argentina Fil: Romecin, Paola A.. Schulze Center For Novel Therapeutics, Mayo Clinic; Estados Unidos Fil: Vera, Renzo Emanuel. Schulze Center For Novel Therapeutics, Mayo Clinic; Estados Unidos. Universidad Nacional de Río Cuarto. Facultad de Ciencias Exactas Fisicoquímicas y Naturales. Departamento de Biología Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina Fil: Almada, Luciana Victoria. Schulze Center For Novel Therapeutics, Mayo Clinic; Estados Unidos Fil: Miamen, Alexander G.. Mayo Clinic; Estados Unidos Fil: Chaiteerakij, Roongruedee. Mayo Clinic; Estados Unidos Fil: Zhou, Mengtao. Wenzhou Medical University; China Fil: Asiedu, Michael K.. Mayo Clinic; Estados Unidos Fil: Moser, Catherine D.. Mayo Clinic; Estados Unidos Fil: Han, Shaoshan. Mayo Clinic; Estados Unidos Fil: Hu, Chunling. Mayo Clinic; Estados Unidos Fil: Banini, Bubu A.. Mayo Clinic; Estados Unidos Fil: Oseini, Abdul M.. Mayo Clinic; Estados Unidos Fil: Chen, Yichun. Mayo Clinic; Estados Unidos Fil: Fang, Yong. Mayo Clinic; Estados Unidos Fil: Yang, Dongye. Mayo Clinic; Estados Unidos Fil: Shaleh, Hassan M.. Mayo Clinic; Estados Unidos Fil: Wang, Shaoqing. Mayo Clinic; Estados Unidos Fil: Wu, Dehai. Mayo Clinic; Estados Unidos Fil: Song, Tao. Mayo Clinic; Estados Unidos Fil: Lee, Ju-Seog. Anderson Cancer Center; Estados Unidos Fil: Thorgeirsson, Snorri S.. National Cancer Institute; Estados Unidos Fil: Chevet, Eric. Université Rennes; Francia Fil: Shah, Vijay H.. Mayo Clinic; Estados Unidos Fil: Fernandez-Zapico, Martin E.. Schulze Center For Novel Therapeutics, Mayo Clinic; Estados Unidos Fil: Roberts, Lewis R.. Mayo Clinic; Estados Unidos
description	Existing antiangiogenic approaches to treat metastatic hepatocellular carcinoma (HCC) are weakly effectual, prompting further study of tumor angiogenesis in this disease setting. Here, we report a novel role for sulfatase 2 (SULF2) in driving HCC angiogenesis. Sulf2-deficient mice (Sulf2 KO) exhibited resistance to diethylnitrosamine-induced HCC and did not develop metastases like wild-type mice (Sulf2 WT). The smaller and less numerous tumors formed in Sulf2 KO mice exhibited a markedly lower microvascular density. In human HCC cells, SULF2 overexpression increased endothelial proliferation, adhesion, chemotaxis, and tube formation in a paracrine fashion. Mechanistic analyses identified the extracellular matrix protein periostin (POSTN), a ligand of avb3/5 integrins, as an effector protein in SULF2-induced angiogenesis. POSTN silencing in HCC cells attenuated SULF2-induced angiogenesis and tumor growth in vivo. The TGFb1/SMAD pathway was identified as a critical signaling axis between SULF2 and upregulation of POSTN transcription. In clinical HCC specimens, elevated levels of SULF2 correlated with increased microvascular density, POSTN levels, and relatively poorer patient survival. Together, our findings define an important axis controlling angiogenesis in HCC and a mechanistic foundation for rational drug development.
publishDate	2017
dc.date.none.fl_str_mv	2017-02
dc.type.none.fl_str_mv	info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo
format	article
status_str	publishedVersion
dc.identifier.none.fl_str_mv	http://hdl.handle.net/11336/81650 Chen, Gang; Nakamura, Ikuo; Dhanasekaran, Renumathy; Iguchi, Eriko; Tolosa, Ezequiel Julian; et al.; Transcriptional Induction of Periostin by a Sulfatase 2-TGFb1-SMAD Signaling Axis Mediates Tumor Angiogenesis in Hepatocellular Carcinoma; American Association for Cancer Research; Cancer Research; 77; 3; 2-2017; 632-645 0008-5472 1538-7445 CONICET Digital CONICET
url	http://hdl.handle.net/11336/81650
identifier_str_mv	Chen, Gang; Nakamura, Ikuo; Dhanasekaran, Renumathy; Iguchi, Eriko; Tolosa, Ezequiel Julian; et al.; Transcriptional Induction of Periostin by a Sulfatase 2-TGFb1-SMAD Signaling Axis Mediates Tumor Angiogenesis in Hepatocellular Carcinoma; American Association for Cancer Research; Cancer Research; 77; 3; 2-2017; 632-645 0008-5472 1538-7445 CONICET Digital CONICET
dc.language.none.fl_str_mv	eng
language	eng
dc.relation.none.fl_str_mv	info:eu-repo/semantics/altIdentifier/doi/10.1158/0008-5472.CAN-15-2556 info:eu-repo/semantics/altIdentifier/url/https://cancerres.aacrjournals.org/content/77/3/632
dc.rights.none.fl_str_mv	info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv	openAccess
rights_invalid_str_mv	https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv	application/pdf application/pdf
dc.publisher.none.fl_str_mv	American Association for Cancer Research
publisher.none.fl_str_mv	American Association for Cancer Research
dc.source.none.fl_str_mv	reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str	CONICET Digital (CONICET)
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instname_str	Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv	CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv	dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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Transcriptional Induction of Periostin by a Sulfatase 2-TGFb1-SMAD Signaling Axis Mediates Tumor Angiogenesis in Hepatocellular Carcinoma

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