TY - JOUR
T1 - Adenomatous polyposis coli- mediated accumulation of abasic dna lesions lead to cigarette smoke condensate- induced neoplastic transformation of normal breast epithelial cells
AU - Jaiswal, Aruna S.
AU - Panda, Harekrushna
AU - Pampo, Christine A.
AU - Siemann, Dietmar W.
AU - Gary Gairola, C.
AU - Hromas, Robert
AU - Narayan, Satya
N1 - Funding Information:
Abbreviations: APC, adenomatous polyposis coli; AP, apurinic/apyrimidinic; B[α]P, benzo[α]pyrene; CSC, cigarette smoke condensate; Fen1, 5′-flap endonuclease 1; LP-BER, long-patch base excision repair; SP-BER, short-patch base excision repair; Pol-β, DNA polymerase β Address all correspondence to: Dr Satya Narayan, Department of Anatomy and Cell Biology, Basic Science Building, Room B1-016, 1333 Center Drive, Gainesville, FL 32610. E-mail: [email protected] 1The financial support for this study was provided by Flight Attendant Medical Research Institute (Miami, FL) to S.N. The authors declare no potential conflicts of interest with respect to the authorship and/or publication of this article. Received 9 January 2013; Revised 6 February 2013; Accepted 8 February 2013 Copyright © 2013 Neoplasia Press, Inc. All rights reserved 1522-8002/13/$25.00 DOI 10.1593/neo.13176
PY - 2013/4
Y1 - 2013/4
N2 - 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.
AB - 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.
UR - https://www.scopus.com/pages/publications/84875637193
UR - https://www.scopus.com/pages/publications/84875637193#tab=citedBy
U2 - 10.1593/neo.13176
DO - 10.1593/neo.13176
M3 - Article
C2 - 23555190
AN - SCOPUS:84875637193
SN - 1522-8002
VL - 15
SP - 454
EP - 460
JO - Neoplasia (United States)
JF - Neoplasia (United States)
IS - 4
ER -