Adenomatous polyposis coli- mediated accumulation of abasic dna lesions lead to cigarette smoke condensate- induced neoplastic transformation of normal breast epithelial cells

Aruna S. Jaiswal, Harekrushna Panda, Christine A. Pampo, Dietmar W. Siemann, C. Gary Gairola, Robert Hromas, Satya Narayan

Research output: Contribution to journalArticle

8 Scopus citations

Abstract

Adenomatous polyposis coli (APC) is a multifunctional protein having diverse cellular functions including cell migration, cell-cell adhesion, cell cycle control, chromosomal segregation, and apoptosis. Recently, we found a new role of APC in base excision repair (BER) and showed that it interacts with DNA polymerase β and 5′-flap endonuclease 1 and interferes in BER. Previously, we have also reported that cigarette smoke condensate (CSC) increases expression of APC and enhances the growth of normal human breast epithelial (MCF10A) cells in vitro. In the present study, using APC overexpression and knockdown systems, we have examined the molecular mechanisms by which CSC and its major component, Benzo[α]pyrene, enhances APC-mediated accumulation of abasic DNA lesions, which is cytotoxic and mutagenic in nature, leading to enhanced neoplastic transformation of MCF10A cells in an orthotopic xenograft model.

Original languageEnglish (US)
Pages (from-to)454-460
Number of pages7
JournalNeoplasia (United States)
Volume15
Issue number4
DOIs
StatePublished - Apr 2013
Externally publishedYes

ASJC Scopus subject areas

  • Cancer Research

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