NDLI: Activation of ß-catenin signaling is critical for doxorubicin-induced epithelial-mesenchymal transition in BGC-823 gastric cancer cell line.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Han, Rongfei Xiong, Jie Xiao, Ruijing Altaf, Ehtisham Wang, Jin Liu, Yanping Xu, Hui Ding, Qianshan Zhang, Qiuping
Description	Author Affiliation: Han R ( Department of Immunology, Wuhan University School of Basic Medical Science, Dong Hu Road 185, Wuchang, Wuhan, Hubei, 430071, People's Republic of China.)
Abstract	The epithelial-mesenchymal transition (EMT) is a fundamental process governing morphogenesis in multicellular organisms and has recently been implicated in promoting carcinoma invasion and metastasis. Besides their therapeutic effects, accumulating evidences suggest that chemotherapeutic agents also induced EMT and enhanced the malignancy of treated cancer cells; however, the mechanism(s) still remains unclear. Here, we investigated the role of ß-catenin signaling in doxorubicin (Dox)-induced EMT in human gastric cancer cell line BGC-823. We found that the transient treatment of Dox induced EMT and enhanced the in vitro migration ability of cancer cells. We also found that ß-catenin signaling was activated upon Dox treatment. Inhibition of ß-catenin by indomethacin (Indo) or siRNA suppressed Dox-induced EMT and decreased cancer cell migration ability. Our results showed that ß-catenin signaling was critical to Dox-induced EMT. Indo and other ß-catenin inhibitors may have a potential implication in prevention of gastric cancer metastasis.
File Format	HTM / HTML
ISSN	10104283
Issue Number	1
Volume Number	34
e-ISSN	14230380
Journal	Tumor Biology
Language	English
Publisher	Springer
Publisher Date	2013-02-01
Publisher Place	Netherlands
Access Restriction	Subscribed
Subject Keyword	Discipline Medicine__semicolon__oncology Cell Movement Drug Effects Doxorubicin Pharmacology Epithelial-mesenchymal Transition Signal Transduction Stomach Neoplasms Metabolism Pathology Beta Catenin Cell Line, Tumor Enzyme Activation Humans Indomethacin Neoplasm Metastasis Rna Interference Rna, Small Interfering Antagonists & Inhibitors Genetics Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Medicine 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