Type I insulin-like growth factor receptor expression on colorectal adenocarcinoma cell lines is decreased in response to the chemopreventive agent N-acetyl-L-cysteine

Typeset version

 

TY  - JOUR
  - Kelly, R. G.,Nally, K.,Shanahan, F.,O'Connell, J.
  - 2002
  - Type I insulin-like growth factor receptor expression on colorectal adenocarcinoma cell lines is decreased in response to the chemopreventive agent N-acetyl-L-cysteine
  - Validated
  - ()
  - 973
  - 555
  - 558555
  - Increased expression of the type I insulin-like growth factor receptor (IGF-IR) is associated with colon cancer, while the antioxidant N-acetyl-L-cysteine (NAC) is known to suppress colonic proliferation. We demonstrate that NAC down-regulates the expression of IGF-IR on three colorectal adenocarcinoma cell lines (HT29, SW480, and LoVo). NAC also abrogates the proliferative effect of IGF-I on HT29 cells. This indicates a novel mechanism for the therapeutic effects of NAC.Increased expression of the type I insulin-like growth factor receptor (IGF-IR) is associated with colon cancer, while the antioxidant N-acetyl-L-cysteine (NAC) is known to suppress colonic proliferation. We demonstrate that NAC down-regulates the expression of IGF-IR on three colorectal adenocarcinoma cell lines (HT29, SW480, and LoVo). NAC also abrogates the proliferative effect of IGF-I on HT29 cells. This indicates a novel mechanism for the therapeutic effects of NAC.
  - 0077-89230077-8923
  - ://WOS:000179853000106://WOS:000179853000106
DA  - 2002/NaN
ER  - 
@article{V235379592,
   = {Kelly,  R. G. and Nally,  K. and Shanahan,  F. and O'Connell,  J. },
   = {2002},
   = {Type I insulin-like growth factor receptor expression on colorectal adenocarcinoma cell lines is decreased in response to the chemopreventive agent N-acetyl-L-cysteine},
   = {Validated},
   = {()},
   = {973},
  pages = {555--558555},
   = {{Increased expression of the type I insulin-like growth factor receptor (IGF-IR) is associated with colon cancer, while the antioxidant N-acetyl-L-cysteine (NAC) is known to suppress colonic proliferation. We demonstrate that NAC down-regulates the expression of IGF-IR on three colorectal adenocarcinoma cell lines (HT29, SW480, and LoVo). NAC also abrogates the proliferative effect of IGF-I on HT29 cells. This indicates a novel mechanism for the therapeutic effects of NAC.Increased expression of the type I insulin-like growth factor receptor (IGF-IR) is associated with colon cancer, while the antioxidant N-acetyl-L-cysteine (NAC) is known to suppress colonic proliferation. We demonstrate that NAC down-regulates the expression of IGF-IR on three colorectal adenocarcinoma cell lines (HT29, SW480, and LoVo). NAC also abrogates the proliferative effect of IGF-I on HT29 cells. This indicates a novel mechanism for the therapeutic effects of NAC.}},
  issn = {0077-89230077-8923},
   = {://WOS:000179853000106://WOS:000179853000106},
  source = {IRIS}
}
AUTHORSKelly, R. G.,Nally, K.,Shanahan, F.,O'Connell, J.
YEAR2002
MONTH
JOURNAL_CODE
TITLEType I insulin-like growth factor receptor expression on colorectal adenocarcinoma cell lines is decreased in response to the chemopreventive agent N-acetyl-L-cysteine
STATUSValidated
TIMES_CITED()
SEARCH_KEYWORD
VOLUME973
ISSUE
START_PAGE555
END_PAGE558555
ABSTRACTIncreased expression of the type I insulin-like growth factor receptor (IGF-IR) is associated with colon cancer, while the antioxidant N-acetyl-L-cysteine (NAC) is known to suppress colonic proliferation. We demonstrate that NAC down-regulates the expression of IGF-IR on three colorectal adenocarcinoma cell lines (HT29, SW480, and LoVo). NAC also abrogates the proliferative effect of IGF-I on HT29 cells. This indicates a novel mechanism for the therapeutic effects of NAC.Increased expression of the type I insulin-like growth factor receptor (IGF-IR) is associated with colon cancer, while the antioxidant N-acetyl-L-cysteine (NAC) is known to suppress colonic proliferation. We demonstrate that NAC down-regulates the expression of IGF-IR on three colorectal adenocarcinoma cell lines (HT29, SW480, and LoVo). NAC also abrogates the proliferative effect of IGF-I on HT29 cells. This indicates a novel mechanism for the therapeutic effects of NAC.
PUBLISHER_LOCATION
ISBN_ISSN0077-89230077-8923
EDITION
URL://WOS:000179853000106://WOS:000179853000106
DOI_LINK
FUNDING_BODY
GRANT_DETAILS