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

Hiromasa Tanaka, Masaaki Mizuno, Kenji Ishikawa, Kae Nakamura, Fumi Utsumi, Hiroaki Kajiyama, Hiroyuki Kano, Shoichi Maruyama, Fumitaka Kikkawa, Masaru Hori

研究成果: Article査読

53 被引用数 (Scopus)

抄録

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.

本文言語English
ページ(範囲)207-220
ページ数14
ジャーナルPlasma Medicine
2
4
DOI
出版ステータスPublished - 2012
外部発表はい

All Science Journal Classification (ASJC) codes

  • Biomedical Engineering
  • Physics and Astronomy(all)

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