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Please use this identifier to cite or link to this item: http://hdl.handle.net/10564/3498

Title: Expression of cytosolic malic enzyme (ME1) is associated with disease progression in human oral squamous cell carcinoma.
Other Titles: ME1発現はヒト口腔扁平上皮癌の進行と関連する
Authors: Nakashima, Chie
Yamamoto, Kazuhiko
Fujiwara‐Tani, Rina
Luo, Yi
Matsushima, Sayako
Fujii, Kiyomu
Ohmori, Hitoshi
Sasahira, Tomonori
Sasaki, Takamitsu
Kitadai, Yasuhiko
Kirita, Tadaaki
Kuniyasu, Hiroki
Keywords: cancer invasion
glutamine
malic enzyme
prognosis
stemness
Issue Date: Jun-2018
Publisher: John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association
Citation: Cancer science Vol.109 No.6 p.2036-2045 (2018 Jun)
Abstract: Malic enzyme 1 (ME1) is a multifunctional protein involved in glycolysis, the citric acid cycle, NADPH production, glutamine metabolism, and lipogenesis. It is overexpressed in various cancers. We examined the expression of ME1 in 119 oral squamous cell carcinomas (OSCCs) using immunohistochemistry. Malic enzyme 1 expression was moderate to strong in 57 (48%) OSCCs and correlated with pT, pN, clinical stage, and histological grade. In 37 cases with prognostic evaluation, moderate to strong ME1 expression indicated a worse prognosis than did weak ME1 expression. Malic enzyme 1 knockdown or inactivation by lanthanide inhibited cell proliferation and motility and suppressed the epithelial-mesenchymal transition in HSC3 human OSCC cells. Knockdown of ME1 also shifted energy metabolism from aerobic glycolysis and lactate fermentation to mitochondrial oxidative phosphorylation, and the redox status from reductive to oxidative. In a mouse tumor model, lanthanide suppressed tumor growth and increased survival time. These findings reveal that ME1 is a valid target for molecular therapy in OSCC.
Description: 博士(医学)・乙第1420号・平成30年9月26日
This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License(https://creativecommons.org/licenses/by-nc/4.0/), which permits use, distribution and repro duction in any medium, provided the original work is properly cited and is not used for commercial purposes.
©2018 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.
URI: http://hdl.handle.net/10564/3498
ISSN: 13479032
Academic Degrees and number: 24601B1420
Degree-granting date: 2018-09-26
Degree name: 博士(医学)
Degree-granting institutions: 奈良県立医科大学
Appears in Collections:2018年度

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