Down-regulation of caspase 3 in breast cancer: a possible mechanism for chemoresistance View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2002-12

AUTHORS

Eswaran Devarajan, Aysegul A Sahin, Jack S Chen, Raghu R Krishnamurthy, Neeraj Aggarwal, Anne-Marie Brun, Anna Sapino, Fan Zhang, Dhawal Sharma, Xiao-He Yang, Ann D Tora, Kapil Mehta

ABSTRACT

Caspase-3 is a member of the cysteine protease family, which plays a crucial role in apoptotic pathways by cleaving a variety of key cellular proteins. Caspase-3 can be activated by diverse death-inducing signals, including the chemotherapeutic agents. The purpose of this study was to determine the levels of caspase-3 expression in breast tumor samples and to determine whether alterations in its expression can affect their ability to undergo apoptosis. Primary breast tumor and normal breast parenchyma samples were obtained from patients undergoing breast surgery and the expression of caspases-3 was studied. Similarly, normal mammary epithelial cells and several established mammary cancer cell lines were studied for caspases-3 expression by reverse transcriptase-polymerase chain reaction, Northern blot analysis, and Western blot analysis. Approximately 75% of the tumor as well as morphologically normal peritumoral tissue samples lacked the caspase-3 transcript and caspase-3 protein expression. In addition, the caspases-3 mRNA levels in commercially available total RNA samples from breast, ovarian, and cervical tumors were either undetectable (breast and cervical) or substantially decreased (ovarian). Despite the complete loss of caspase-3, the expression levels of other caspases, such as caspase-8 and caspase-9, were normal in all of the tumor samples studied. The sensitivity of caspase-3-deficient breast cancer (MCF-7) cells to undergo apoptosis in response to doxorubicin and other apoptotic stimuli could be augmented by reconstituting caspase-3 expression. These results suggest that the loss of caspases-3 expression may represent an important cell survival mechanism in breast cancer patients. More... »

PAGES

1206044

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.onc.1206044

DOI

http://dx.doi.org/10.1038/sj.onc.1206044

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1008365660

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/12483536


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Download the RDF metadata as:  json-ld nt turtle xml License info

HOW TO GET THIS DATA PROGRAMMATICALLY:

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Turtle is a human-readable linked data format.

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RDF/XML is a standard XML format for linked data.

curl -H 'Accept: application/rdf+xml' 'https://scigraph.springernature.com/pub.10.1038/sj.onc.1206044'


 

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