These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Down-regulation of p21Waf-1 protein facilitates IR- and UV-induced apoptosis in human squamous carcinoma cells.
    Author: Izumaru S, Arima N, Toyozumi Y, Kato S, Morimatsu M, Nakashima T.
    Journal: Int J Oncol; 2004 May; 24(5):1245-55. PubMed ID: 15067348.
    Abstract:
    DNA damage via radiation exposure and administration of chemotherapeutic agents induce apoptosis, which is a basic mechanism for non-surgical anti-cancer treatment. We analyzed ionizing radiation (IR)- or ultraviolet (UV)-induced apoptosis in human laryngeal carcinoma (HEp-2) and uterine cervical carcinoma (HeLa) cells, and found that HeLa cells were significantly more sensitive to both IR- and UV-induced apoptosis compared to HEp-2 cells, in spite of the same histological type and p53 status. The cyclin-dependent kinase (Cdk) inhibitor, p21Waf-1 was modified differently between the two cancer cell types, whereas p53 protein was induced in a similar manner after IR or UV treatment. IR steadily induced p21Waf-1 protein in HEp-2 cells, but not in HeLa cells. Additionally, p21Waf-1 protein recovered close to the basal level only in HEp-2 cells, although UV caused rapid, dramatic and caspase-independent reduction of p21Waf-1 protein in both cancer cells. Furthermore, overexpression of p21Waf-1 protein in these cells by transient transfection and in stable cell lines in a tetracycline-regulated system, rescued IR- and UV-induced apoptosis. Finally, suppression of p21Waf-1 protein using antisense oligodeoxynucleotide transfection facilitated UV-induced apoptosis in both HEp-2 and HeLa cells. We concluded that p21Waf-1 protein is modified independently of p53 and functions as an inhibitor of IR- as well as UV-induced apoptosis in squamous carcinoma cells.
    [Abstract] [Full Text] [Related] [New Search]