Hyperthermia synergistically enhances cancer cell death by plasma-activated acetated Ringer's solution

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Hyperthermia synergistically enhances cancer cell death by plasma-activated acetated Ringer's solution

https://gifu-pu.repo.nii.ac.jp/records/14008

Item type		研究室原著論文(1)
公開日		2020-09-08
タイトル
	タイトル	Hyperthermia synergistically enhances cancer cell death by plasma-activated acetated Ringer's solution
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
抄録
	値	Applications of non-thermal plasma (NTP) discharges in medicine, particularly cancer therapy, have increased in recent years. The aim of the present study was to investigate the advantages of the combined application of NTP-irradiated acetated Ringer's solution (PAA) and hyperthermia, a heat treatment at 42 °C, on A549 cancer cell death and elucidate the underlying mechanisms. Cell death was enhanced more by the above combined treatment and was accompanied by increases in intracellular calcium ([Ca2+]i). The activation of transient receptor potential melastatin 2 (TRPM2) may enhance cell death because the addition of TRPM2 inhibitors and knockdown of TRPM2 significantly abrogated the above phenomena. TRPM2 is a temperature-sensitive, Ca2+-permeable, non-elective cation channel and hydrogen peroxide (H2O2) and ADP ribose are its main agonists. PAA functioned as a donor of reactive oxygen species, mainly H2O2, and a treatment with PAA under hyperthermia induced both mitochondrial and nuclear damage with DNA breaks. The activation of poly(ADP-ribose) polymerase-1 as the DNA repair mechanism induced TRPM2 activation because this enzyme accumulates ADP ribose. The sensitivity of fibroblasts as normal cells to PAA was less than that of A549 cells. These results suggest that hyperthermia synergistically induces the sensitivity of cancer cells to PAA.
書誌情報		en : Archives of Biochemistry and Biophysics p. 108565, 発行日 2020
DOI
	値	10.1016/j.abb.2020.108565