Literature DB >> 17920061

Beta-catenin/Tcf-4 inhibition after progastrin targeting reduces growth and drives differentiation of intestinal tumors.

Julie Pannequin1, Nathalie Delaunay, Michael Buchert, Fanny Surrel, Jean-François Bourgaux, Joanne Ryan, Stéphanie Boireau, Jessica Coelho, André Pélegrin, Pomila Singh, Arthur Shulkes, Mildred Yim, Graham S Baldwin, Christine Pignodel, Gérard Lambeau, Philippe Jay, Dominique Joubert, Frédéric Hollande.   

Abstract

BACKGROUND & AIMS: Aberrant activation of the beta-catenin/Tcf-4 transcriptional complex represents an initiating event for colorectal carcinogenesis, shifting the balance from differentiation toward proliferation in colonic crypts. Here, we assessed whether endogenous progastrin, encoded by a target gene of this complex, was in turn able to regulate beta-catenin/Tcf-4 activity in adenomatous polyposis coli (APC)-mutated cells, and we analyzed the impact of topical progastrin depletion on intestinal tumor growth in vivo.
METHODS: Stable or transient RNA silencing of the GAST gene was induced in human tumor cells and in mice carrying a heterozygous Apc mutation (APCDelta14), which overexpress progastrin but not amidated or glycine-extended gastrin.
RESULTS: Depletion of endogenous progastrin production strongly decreased intestinal tumor growth in vivo through a marked inhibition of constitutive beta-catenin/Tcf-4 activity in tumor cells. This effect was mediated by the de novo expression of the inhibitor of beta-catenin and Tcf-4 (ICAT), resulting from a down-regulation of integrin-linked kinase in progastrin-depleted cells. Accordingly, ICAT down-regulation was correlated with progastrin overexpression and Tcf-4 target gene activation in human colorectal tumors, and ICAT repression was detected in the colon epithelium of tumor-prone, progastrin-overexpressing mice. In APCDelta14 mice, small interfering RNA-mediated progastrin depletion not only reduced intestinal tumor size and numbers, but also increased goblet cell lineage differentiation and cell apoptosis in the remaining adenomas.
CONCLUSIONS: Thus, depletion of endogenous progastrin inhibits the tumorigenicity of APC-mutated colorectal cancer cells in vivo by promoting ICAT expression, thereby counteracting Tcf-4 activity. Progastrin targeting strategies should provide an exciting prospect for the differentiation therapy of colorectal cancer.

Entities:  

Mesh:

Substances:

Year:  2007        PMID: 17920061     DOI: 10.1053/j.gastro.2007.08.023

Source DB:  PubMed          Journal:  Gastroenterology        ISSN: 0016-5085            Impact factor:   22.682


  18 in total

1.  P53 gene mutation increases progastrin dependent colonic proliferation and colon cancer formation in mice.

Authors:  Vigneshwaran Ramanathan; Guangchun Jin; Christoph Benedikt Westphalen; Ashley Whelan; Alexander Dubeykovskiy; Shigeo Takaishi; Timothy C Wang
Journal:  Cancer Invest       Date:  2012-04-05       Impact factor: 2.176

2.  Annexin A2 mediates up-regulation of NF-κB, β-catenin, and stem cell in response to progastrin in mice and HEK-293 cells.

Authors:  Shubhashish Sarkar; Rafal Swiercz; Carla Kantara; Katherine A Hajjar; Pomila Singh
Journal:  Gastroenterology       Date:  2010-09-06       Impact factor: 22.682

3.  Insulin-like growth factors are more effective than progastrin in reversing proapoptotic effects of curcumin: critical role of p38MAPK.

Authors:  Pomila Singh; Shubhashish Sarkar; Shahid Umar; William Rengifo-Cam; Amar P Singh; Thomas G Wood
Journal:  Am J Physiol Gastrointest Liver Physiol       Date:  2010-02-04       Impact factor: 4.052

4.  Progastrin Peptides Increase the Risk of Developing Colonic Tumors: Impact on Colonic Stem Cells.

Authors:  Pomila Singh; Shubhashish Sarkar; Carla Kantara; Carrie Maxwell
Journal:  Curr Colorectal Cancer Rep       Date:  2012-12

5.  Functional cross-talk between beta-catenin and NFkappaB signaling pathways in colonic crypts of mice in response to progastrin.

Authors:  Shahid Umar; Shubhashish Sarkar; Yu Wang; Pomila Singh
Journal:  J Biol Chem       Date:  2009-06-04       Impact factor: 5.157

6.  A gastrin precursor, gastrin-gly, upregulates VEGF expression in colonic epithelial cells through an HIF-1-independent mechanism.

Authors:  Claudine Bertrand; Aline Kowalski-Chauvel; Catherine Do; Cécile Résa; Souad Najib; Laurence Daulhac; Timothy C Wang; Audrey Ferrand; Catherine Seva
Journal:  Int J Cancer       Date:  2010-06-15       Impact factor: 7.396

7.  Inactivating cholecystokinin-2 receptor inhibits progastrin-dependent colonic crypt fission, proliferation, and colorectal cancer in mice.

Authors:  Guangchun Jin; Vigneshwaran Ramanathan; Michael Quante; Gwang Ho Baik; Xiangdong Yang; Sophie S W Wang; Shuiping Tu; Shanisha A K Gordon; David Mark Pritchard; Andrea Varro; Arthur Shulkes; Timothy C Wang
Journal:  J Clin Invest       Date:  2009-08-03       Impact factor: 14.808

8.  Expression of gastrin precursors by CD133-positive colorectal cancer cells is crucial for tumour growth.

Authors:  Audrey Ferrand; Mauro S Sandrin; Arthur Shulkes; Graham S Baldwin
Journal:  Biochim Biophys Acta       Date:  2009-01-15

9.  Progastrin stimulates colonic cell proliferation via CCK2R- and β-arrestin-dependent suppression of BMP2.

Authors:  Guangchun Jin; C Benedikt Westphalen; Yoku Hayakawa; Daniel L Worthley; Samuel Asfaha; Xiangdong Yang; Xiaowei Chen; Yiling Si; Hongshan Wang; Yagnesh Tailor; Richard A Friedman; Timothy C Wang
Journal:  Gastroenterology       Date:  2013-07-25       Impact factor: 22.682

10.  Interrelationships between circulating gastrin and iron status in mice and humans.

Authors:  Suzana Kovac; Kelly Smith; Gregory J Anderson; John R Burgess; Arthur Shulkes; Graham S Baldwin
Journal:  Am J Physiol Gastrointest Liver Physiol       Date:  2008-08-28       Impact factor: 4.052

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.