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  1. 原著論文

Effect of gap junctional intercellular communication on radiation responses in neoplastic human cells

https://repo.qst.go.jp/records/44840
https://repo.qst.go.jp/records/44840
89ba90bd-a3a6-4b61-a9cb-2ec737136a18
Item type 学術雑誌論文 / Journal Article(1)
公開日 2007-05-02
タイトル
タイトル Effect of gap junctional intercellular communication on radiation responses in neoplastic human cells
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
著者 Shao, Chunlin

× Shao, Chunlin

WEKO 445312

Shao, Chunlin

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Furusawa, Yoshiya

× Furusawa, Yoshiya

WEKO 445313

Furusawa, Yoshiya

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Matsumoto, Yoshitaka

× Matsumoto, Yoshitaka

WEKO 445314

Matsumoto, Yoshitaka

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Pan, Yan

× Pan, Yan

WEKO 445315

Pan, Yan

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Xu, Ping

× Xu, Ping

WEKO 445316

Xu, Ping

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Chen, Honghong

× Chen, Honghong

WEKO 445317

Chen, Honghong

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古澤 佳也

× 古澤 佳也

WEKO 445318

en 古澤 佳也

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松本 孔貴

× 松本 孔貴

WEKO 445319

en 松本 孔貴

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抄録
内容記述タイプ Abstract
内容記述 Gap junctional intercellular communication (GJIC) is an important function of metazoan cells and is believed to have beneficial effects in anti-tumor therapy. In this study, we found that, when neoplastic human salivary gland (HSG) cells were irradiated with a 100 keV/mum carbon-ion beam, micronuclei, G(2)/M-phase arrest, and cell killing were induced and that their induction increased with dose. Treatment of confluent HSG cells with 8-Br-cAMP increased GJIC between cells. After release from this treatment, the cell cycle progress and the formation of binucleated cells were still similar to those of untreated cells. However, radiation-induced cellular damage, including micronucleus (MN) formation and G(2)/M-phase arrest of that cAMP-treated population, was less than that of the untreated population and that the surviving fraction was slightly enhanced by cAMP treatment, suggesting that increased GJIC protects HSG cells from lethal radiation damage. Moreover, when confluent HSG cells were treated with 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide (PTIO), a scavenger of nitric oxide (NO) free radical, MN induction and cell killing in the irradiated population were increased. Our results indicate that NO may be involved in GJIC-mediated radioprotection of HSG cells, which may have implications for radiotherapy.
書誌情報 Radiation Research

巻 167, 号 3, p. 283-288, 発行日 2007-03
ISSN
収録物識別子タイプ ISSN
収録物識別子 0033-7587
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