Skip Navigation


Carcinogenesis Advance Access originally published online on March 19, 2004
Carcinogenesis 2004 25(8):1409-1415; doi:10.1093/carcin/bgh149
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
25/8/1409    most recent
bgh149v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (19)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Smith, T. K.
Right arrow Articles by Johnson, I. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Smith, T. K.
Right arrow Articles by Johnson, I. T.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Carcinogenesis vol.25 no.8 © Oxford University Press 2004; all rights reserved.

ARTICLE

Allyl-isothiocyanate causes mitotic block, loss of cell adhesion and disrupted cytoskeletal structure in HT29 cells

Tracy K. Smith, Elizabeth K. Lund1, Mary L. Parker, Rosemary G. Clarke and Ian T. Johnson

Institute of Food Research, Norwich Research Park, Colney, Norwich NR4 7UA, UK

1 To whom correspondence should be addressed Email: liz.lund{at}bbsrc.ac

Epidemiological evidence indicates that Brassica vegetables protect against colorectal cancer. Brassicas contain glucosinolates, the breakdown products of which exert antiproliferative effects against cancer cells. We have examined the effects of allyl-isothiocyanate (AITC), a major breakdown product of the glucosinolate sinigrin, on proliferation and death of colorectal cancer cells. HT-29 colorectal cells were exposed to AITC for 24 h and the number of adherent and detached cells determined. Both populations were analysed for cell-cycle characteristics and examined by light and electron microscopy for features of apoptosis and mitosis. Evidence of apoptosis was also determined by flow cytometric analysis of Annexin V staining in the detached population of cells. AITC-treated cells were also stained for {alpha}-tubulin. Treatment caused cells to round up after 7 h of exposure and subsequently detach. At 24 h these cells were blocked in mitosis. Detached AITC-treated cells showed no signs of apoptosis as assessed by morphological features or by Annexin V staining but they did show evidence of disrupted tubulin. AITC inhibits proliferation of cancer cells by causing mitotic block associated with disruption of {alpha}-tubulin in a manner analogous to a number of chemotherapeutic agents.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
J. Pharmacol. Exp. Ther.Home page
R. Ragasa, E. Nakamura, L. Marrone, S. Yanaka, S. Hayashi, K. Takeuchi, and S. J. Hagen
Isothiocyanate Inhibits Restitution and Wound Repair after Injury in the Stomach: Ex Vivo and in Vitro Studies
J. Pharmacol. Exp. Ther., October 1, 2007; 323(1): 1 - 9.
[Abstract] [Full Text] [PDF]


Home page
J. Nutr.Home page
R. Zhang, S. Loganathan, I. Humphreys, and S. K. Srivastava
Benzyl Isothiocyanate-Induced DNA Damage Causes G2/M Cell Cycle Arrest and Apoptosis in Human Pancreatic Cancer Cells
J. Nutr., November 1, 2006; 136(11): 2728 - 2734.
[Abstract] [Full Text] [PDF]



Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.