P53 induced by ionizing radiation mediates dna end-jointing activity, but not apoptosis of thryroid cells

ABSTRACT To understand the effects of ionizing radiation on thyroid cells, we investigated the role of p53 in mediating apoptosis and in DNA repair following _IN VIVO_ and _IN VITRO_

irradiation of thyroid cells. _IN VITRO_ exposure of human thyroid cells to ionizing radiation of up to 5 – 8 Gy failed to induce apoptosis in primary cells. The same results were obtained

when the thyroid gland was irradiated in the intact rat. To explore the mechanism of failure of the wild-type p53 in inducing apoptosis in thyroid cells, we investigated the expression of

apoptosis-related genes, _BAX_, _BCL-2_ and _FAS/APO-1_ following irradiation or induction of temperature-sensitive p53. The expression of Bax, Bcl-2 and Fas/APO-1 in human primary cultured

thyroid cells did not change after irradiation. To further confirm the results, we established a clonal cell line (tsFRO) in which a temperature sensitive p53 (Val138) expression vector was

stably transfected to a thyroid carcinoma cell line lacking endogenous p53. Incubation of tsFRO cells at the permissive temperature for three days, however, did not induce apoptosis although

G1 arrest was noted. Although enhanced expression of the _BAX_ mRNA level was observed, the expression of Bax, Bcl-2 and Fas/APO-1 protein did not change by shifting tsFRO cells to

permissive temperature as well as irradiated primary cells. Furthermore, DNA end-jointing ability was examined by transfection of linearized luciferase plasmid into tsFRO cells. Increased

luciferase activity occurred when the cells were cultured at the permissive temperature, indicating that the wild-type p53 enhances DNA end-jointing activity. Our results indicate that the

wild-type p53 does not lead to apoptosis but facilitates DNA end-jointing in thyroid cells. These results may reflect specific responses in thyroid cells following irradiation. Access

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access 21 March 2024 AUTHOR INFORMATION AUTHORS AND AFFILIATIONS * Department of Cell Physiology, Atomic Disease Institute, Nagasaki University School of Medicine, Nagasaki, 852, Japan

Ting-ting Yang, Hiroyuki Namba, Takesi Hara, Noboru Takmura & Shunichi Yamashita * Department of Pharmacology, Nagasaki University School of Medicine, Nagasaki, 852, Japan Yuji Nagayama

* Kuma Hospital, Kobe, 650, Japan Shuji Fukata & Kanji Kuma * Ito Hospital, Tokyo, 150, Japan Naofumi Ishikawa & Kunihiko Ito Authors * Ting-ting Yang View author publications You

can also search for this author inPubMed Google Scholar * Hiroyuki Namba View author publications You can also search for this author inPubMed Google Scholar * Takesi Hara View author

publications You can also search for this author inPubMed Google Scholar * Noboru Takmura View author publications You can also search for this author inPubMed Google Scholar * Yuji Nagayama

View author publications You can also search for this author inPubMed Google Scholar * Shuji Fukata View author publications You can also search for this author inPubMed Google Scholar *

Naofumi Ishikawa View author publications You can also search for this author inPubMed Google Scholar * Kanji Kuma View author publications You can also search for this author inPubMed 

Google Scholar * Kunihiko Ito View author publications You can also search for this author inPubMed Google Scholar * Shunichi Yamashita View author publications You can also search for this

author inPubMed Google Scholar RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Yang, Tt., Namba, H., Hara, T. _et al._ p53 induced by ionizing radiation

mediates DNA end-jointing activity, but not apoptosis of thryroid cells. _Oncogene_ 14, 1511–1519 (1997). https://doi.org/10.1038/sj.onc.1200979 Download citation * Received: 27 August 1996

* Revised: 22 November 1996 * Accepted: 25 November 1996 * Issue Date: 03 April 1997 * DOI: https://doi.org/10.1038/sj.onc.1200979 SHARE THIS ARTICLE Anyone you share the following link with

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content-sharing initiative KEYWORDS * ionizing radiation * p53 * DNA end-jointing * apoptosis * thyroid cell * thyroid carcinoma