Document Detail


Role of PP2Calpha in cell growth, in radio- and chemosensitivity, and in tumorigenicity.
MedLine Citation:
PMID:  17941990     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: PP2Calpha is the representative member of the type 2C family of protein phosphatases, and it has recently been implicated in the regulation of p53-, TGFbeta-, cyclin-dependent kinase- and apoptosis-signaling. To investigate the role of PP2Calpha in cell growth and in radio- and chemosensitivity, wild type and PP2Calpha siRNA-expressing MCF7 cells were subjected to several different viability and cell cycle analyses, both under basal conditions and upon treatment with radio- and chemotherapy. By comparing the growth of tumors established from both types of cells, we also evaluated the involvement of PP2Calpha in tumorigenesis.
RESULTS: It was found that knockdown of PP2Calpha did not affect the proliferation, the clonogenic survival and the membrane integrity of MCF7 cells. In addition, it did not alter their radio- and chemosensitivity. For PP2Calpha siRNA-expressing MCF7 cells, the number of cells in the G0/G1 phase of the cell cycle was reduced, the induction of the G1 block was attenuated, the number of cells in G2/M was increased, and the induction of the G2 block was enhanced. The tumorigenic potential of PP2Calpha siRNA-expressing MCF7 cells was found to be higher than that of wild type MCF7 cells, and the in vivo proliferation of these cells was found to be increased.
CONCLUSION: Based on these findings, we conclude that PP2Calpha is not involved in controlling cell growth and radio- and chemosensitivity in vitro. It does, however, play a role in the regulation of the cell cycle, in the induction of cell cycle checkpoints and in tumorigenesis. The latter notion implies that PP2Calpha may possess tumor-suppressing properties, and it thereby sets the stage for more elaborate analyses on its involvement in the development and progression of cancer.
Authors:
Twan Lammers; Peter Peschke; Volker Ehemann; Jürgen Debus; Boris Slobodin; Sara Lavi; Peter Huber
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-10-17
Journal Detail:
Title:  Molecular cancer     Volume:  6     ISSN:  1476-4598     ISO Abbreviation:  Mol. Cancer     Publication Date:  2007  
Date Detail:
Created Date:  2007-12-06     Completed Date:  2008-02-22     Revised Date:  2013-06-06    
Medline Journal Info:
Nlm Unique ID:  101147698     Medline TA:  Mol Cancer     Country:  England    
Other Details:
Languages:  eng     Pagination:  65     Citation Subset:  IM    
Affiliation:
Department of Innovative Cancer Diagnosis and Therapy, Clinical Cooperation Unit Radiotherapeutic Oncology, German Cancer Research Center, Im Neuenheimer Feld 280, 69120 Heidelberg, Germany. t.lammers@dkfz.de
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MeSH Terms
Descriptor/Qualifier:
Breast Neoplasms
Cell Cycle / drug effects,  physiology*,  radiation effects
Cell Division / drug effects,  radiation effects
Cell Line, Tumor
Cobalt Radioisotopes
Doxorubicin / pharmacology
Female
Gene Deletion
Humans
Phosphoprotein Phosphatases / deficiency,  genetics*
RNA, Neoplasm / genetics
RNA, Small Interfering / genetics
Chemical
Reg. No./Substance:
0/Cobalt Radioisotopes; 0/RNA, Neoplasm; 0/RNA, Small Interfering; 23214-92-8/Doxorubicin; EC 3.1.3.16/Phosphoprotein Phosphatases; EC 3.1.3.16/protein phosphatase 2C
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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