NDLI: STAT5b as Molecular Target in Pancreatic Cancer—Inhibition of Tumor Growth, Angiogenesis, and Metastases1 2

Content Provider	PubMed Central
Author	Moser, Christian Petra, Ruemmele Sebastian, Gehmert Schenk, Hedwig Kreutz, Marina P. Mycielska, Maria E. Hackl, Christina Kroemer, Alexander Schnitzbauer, Andreas A. Stoeltzing, Oliver Schlitt, Hans J. Geissler, Edward K. Lang, Sven A.
Copyright Year	2012
Abstract	The prognosis of patients suffering from pancreatic cancer is still poor and novel therapeutic options are urgently needed. Recently, the transcription factor signal transducer and activator of transcription 5b (STAT5b) was associated with tumor progression in human solid cancer. Hence, we assessed whether STAT5b might serve as an anticancer target in ductal pancreatic adenocarcinoma (DPAC). We found that nuclear expression of STAT5b can be detected in approximately 50% of DPAC. Blockade of STAT5b by stable shRNA-mediated knockdown showed no effects on tumor cell growth in vitro. However, inhibition of tumor cell motility was found even in response to stimulation with epidermal growth factor or interleukin-6. These findings were paralleled by a reduction of prometastatic and proangiogenic factors in vitro. Subsequent in vivo experiments revealed a strong growth inhibition on STAT5b blockade in subcutaneous and orthotopic models. These findings were paralleled by impaired tumor angiogenesis in vivo. In contrast to the subcutaneous model, the orthotopic model revealed a strong reduction of tumor cell proliferation that emphasizes the meaning of assessing targets in an appropriate microenvironment. Taken together, our results suggest that STAT5b might be a potential novel target for human DPAC.
Starting Page	915
File Format	PDF
ISSN	14765586
e-ISSN	14765586
Journal	Neoplasia (New York, N.Y.)
Issue Number	10
Volume Number	14
Language	English
Publisher	Neoplasia Press Inc.
Publisher Date	2012-10-01
Access Restriction	Open
Rights Holder	Neoplasia Press Inc.
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cancer Research

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Tight Junction Proteins Claudin-3 and Claudin-4 Control Tumor Growth and Metastases1 2

Celastrol Suppresses Angiogenesis-Mediated Tumor Growth through Inhibition of AKT/Mammalian Target of Rapamycin Pathway

Effect of Src kinase inhibition on metastasis and tumor angiogenesis in human pancreatic cancer

Inhibition of Tumor Growth and Angiogenesis by Soluble EphB41

Inhibition of Tumor Angiogenesis and Tumor Growth by the DSL Domain of Human Delta-Like 1 Targeted to Vascular Endothelial Cells1 2

Foretinib inhibits angiogenesis, lymphangiogenesis and tumor growth of pancreatic cancer in vivo by decreasing VEGFR-2/3 and TIE-2 signaling

Inhibition of Tumor Angiogenesis and Growth by Nanoparticle-Mediated p53 Gene Therapy in Mice

MiR-145 functions as a tumor suppressor via regulating angiopoietin-2 in pancreatic cancer cells

IL10-modified Human Mesenchymal Stem Cells inhibit Pancreatic Cancer growth through Angiogenesis Inhibition

STAT5b as Molecular Target in Pancreatic Cancer—Inhibition of Tumor Growth, Angiogenesis, and Metastases1 2

Similar Documents

Tight Junction Proteins Claudin-3 and Claudin-4 Control Tumor Growth and Metastases1 2

Celastrol Suppresses Angiogenesis-Mediated Tumor Growth through Inhibition of AKT/Mammalian Target of Rapamycin Pathway

Effect of Src kinase inhibition on metastasis and tumor angiogenesis in human pancreatic cancer

Inhibition of Tumor Growth and Angiogenesis by Soluble EphB41

Inhibition of Tumor Angiogenesis and Tumor Growth by the DSL Domain of Human Delta-Like 1 Targeted to Vascular Endothelial Cells1 2

Foretinib inhibits angiogenesis, lymphangiogenesis and tumor growth of pancreatic cancer in vivo by decreasing VEGFR-2/3 and TIE-2 signaling

Inhibition of Tumor Angiogenesis and Growth by Nanoparticle-Mediated p53 Gene Therapy in Mice

MiR-145 functions as a tumor suppressor via regulating angiopoietin-2 in pancreatic cancer cells

IL10-modified Human Mesenchymal Stem Cells inhibit Pancreatic Cancer growth through Angiogenesis Inhibition

STAT5b as Molecular Target in Pancreatic Cancer—Inhibition of Tumor Growth, Angiogenesis, and Metastases1 2