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Please use this identifier to cite or link to this item: http://hdl.handle.net/10564/2762

Title: Depression of p53-independent Akt survival signals in human oral cancer cells bearing mutated p53 gene after exposure to high-LET radiation.
Other Titles: p53 変異型ヒト口腔がん細胞における高LET 放射線によるp53 非依存Akt 生存シグナルの抑制
Authors: Nakagawa, Yosuke
Takahashi, Akihisa
Kajihara, Atsuhisa
Yamakawa, Nobuhiro
Imai, Yuichiro
Ota, Ichiro
Okamoto, Noritomo
Mori, Eiichiro
Noda, Taichi
Furusawa, Yoshiya
Kirita, Tadaaki
Ohnishi, Takeo
Keywords: High LET
Cell cycle
Issue Date: 13-Jul-2012
Publisher: Elsevier / Academic Press
Citation: Biochemical and biophysical research communications Vol.423 No.4 p.654-660
Abstract: Although mutations and deletions in the p53 tumor suppressor gene lead to resistance to low linear energy transfer (LET) radiation, high-LET radiation efficiently induces cell lethality and apoptosis regardless of the p53 gene status in cancer cells. Recently, it has been suggested that the induction of p53-independent apoptosis takes place through the activation of Caspase-9 which results in the cleavage of Caspase-3 and poly (ADP-ribose) polymerase (PARP). This study was designed to examine if high-LET radiation depresses serine/threonine protein kinase B (PKB, also known as Akt) and Akt-related proteins. Human gingival cancer cells (Ca9-22 cells) harboring a mutated p53 (mp53) gene were irradiated with 2 Gy of X-rays or Fe-ion beams. The cellular contents of Akt-related proteins participating in cell survival signaling were analyzed with Western Blotting 1, 2, 3 and 6h after irradiation. Cell cycle distributions after irradiation were assayed with flow cytometric analysis. Akt-related protein levels decreased when cells were irradiated with high-LET radiation. High-LET radiation increased G(2)/M phase arrests and suppressed the progression of the cell cycle much more efficiently when compared to low-LET radiation. These results suggest that high-LET radiation enhances apoptosis through the activation of Caspase-3 and Caspase-9, and suppresses cell growth by suppressing Akt-related signaling, even in mp53 bearing cancer cells.
Description: 博士(医学)・甲第598号・平成25年3月15日
Copyright © 2012 Elsevier Inc. All rights reserved
URI: http://hdl.handle.net/10564/2762
ISSN: 0006291X
Appears in Collections:2012年度

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