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Plasma Medicine
SJR: 0.198 SNIP: 0.183 CiteScore™: 0.57

ISSN Imprimir: 1947-5764
ISSN En Línea: 1947-5772

Plasma Medicine

DOI: 10.1615/PlasmaMed.2013008267
pages 207-220

Cell survival and proliferation signaling pathways are downregulated by plasma-activated medium in glioblastoma brain tumor cells

Hiromasa Tanaka
Plasma Nanotechnology Research Center, Nagoya University; Center for Advanced Medicine and Clinical Research, Nagoya University Graduate School of Medicine, Tsurumai-cho 65, Showa-ku, Nagoya 466-8550, Japan
Masaaki Mizuno
Center for Advanced Medicine and Clinical Research, Nagoya University Graduate School of Medicine, Tsurumai-cho 65, Showa-ku, Nagoya 466-8550, Japan
Kenji Ishikawa
Plasma Nanotechnology Research Center, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-8603, Japan
Kae Nakamura
Department of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Tsurumai-cho 65, Showa-ku, Nagoya 466-8550, Japan
Fumi Utsumi
Department of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Tsurumai-cho 65, Showa-ku, Nagoya 466-8550, Japan
Hiroaki Kajiyama
Department of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Tsurumai-cho 65, Showa-ku, Nagoya 466-8550, Japan
Hiroyuki Kano
NU Eco-Engineering Co., Ltd., 1237-87 Umazutsumi, Kurozasa-cho, Miyoshi-shi, Nishikamo-gun, Aichi 470-0201, Japan
Shoichi Maruyama
Department of Nephrology, Nagoya University Graduate School of Medicine, Tsurumai-cho 65, Showa-ku, Nagoya 466-8550, Japan
Fumitaka Kikkawa
Department of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Tsurumai-cho 65, Showa-ku, Nagoya 466-8550, Japan
Masaru Hori
Plasma Nanotechnology Research Center, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-8603, Japan

SINOPSIS

We previously reported that plasma-activated medium (PAM) selectively kills glioblastoma brain tumor cells by downregulating the signaling molecule, the serine-threonine kinase AKT. AKT kinase plays a key role in survival and proliferation by acting as a hub molecule in the signaling network to inhibit apoptosis. The pathways that contain AKT and that are affected by PAM are unclear. In this study of glioblastoma brain tumor cells, phosphorylation of AKT at both Ser473 and Thr308 was downregulated by PAM, suggesting that upstream signaling by the mammalian target of rapamycin complex 2 (mTORC2) and phosphatidylinositol- 3 kinase (PI3K)/ 3-phosphoinositide-dependent protein kinase-1 (PDK1) were affected by PAM. Furthermore, the extracellular regulated kinase (ERK) signaling pathway, which is parallel to the AKT signaling pathway, was downregulated by PAM, and the mTORC1 signaling pathway, which is a major downstream signaling pathway of AKT and ERK, was also downregulated by PAM. In addition, CD44, a cell membrane-bound receptor that promotes both the AKT pathway and the ERK pathway, was downregulated by PAM. Taken together, these results suggest that PAM completely downregulates the survival and proliferation signaling network in glioblastoma brain tumor cells.


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