Metabolomic analysis of uterine serous carcinoma with acquired resistance to paclitaxel

Manabu Seino; Tsuyoshi Ohta; Akiko Sugiyama; Hirotsugu Sakaki; Takeshi Sudo; Seiji Tsutsumi; Shogo Shigeta; Hideki Tokunaga; Masafumi Toyoshima; Nobuo Yaegashi; Satoru Nagase

doi:10.18632/oncotarget.25868

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This article has been corrected. Correction in: Oncotarget. 2021; 12:2321-2322.

Metabolomic analysis of uterine serous carcinoma with acquired resistance to paclitaxel

Manabu Seino _, Tsuyoshi Ohta, Akiko Sugiyama, Hirotsugu Sakaki, Takeshi Sudo, Seiji Tsutsumi, Shogo Shigeta, Hideki Tokunaga, Masafumi Toyoshima, Nobuo Yaegashi and Satoru Nagase

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Oncotarget. 2018; 9:31985-31998. https://doi.org/10.18632/oncotarget.25868

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Abstract

Manabu Seino1, Tsuyoshi Ohta1, Akiko Sugiyama1, Hirotsugu Sakaki1, Takeshi Sudo1, Seiji Tsutsumi1, Shogo Shigeta2, Hideki Tokunaga2, Masafumi Toyoshima2, Nobuo Yaegashi2 and Satoru Nagase1

1Department of Obstetrics and Gynecology, Yamagata University School of Medicine, Iidanishi, Yamagata 990-9585, Japan

2Department of Obstetrics and Gynecology, Tohoku University Graduate School of Medicine, Iidanishi, Yamagata 990-9585, Japan

Correspondence to:

Manabu Seino, email: [email protected]

Keywords: endometrial cancer; uterine serous carcinoma; metabolomic analysis; paclitaxel

Received: September 20, 2017 Accepted: July 12, 2018 Published: August 10, 2018

ABSTRACT

Introduction: Uterine serous carcinoma (USC) is more aggressive than other subtypes of endometrial carcinoma and is associated with a poor prognosis. We analyzed the metabolomic profile of USC with acquired resistance to paclitaxel.

Results: Glutathione (GSH) concentration in PTX-1 cells was higher than in USPC-1 cells. In addition, GSH concentration in the USPC-1 cells increased after treatment with paclitaxel but was unchanged in PTX-1 cells. Glucose-6-phosphate (G6P) and ribose-5-phosphate (R5P) concentrations in PTX-1 cells were higher than those in USPC-1 cells. G6P concentration in the USPC-1 cells was unchanged after treatment with paclitaxel, while it decreased in PTX-1 cells.

Conclusion: Our results indicate that increased GSH and glucose metabolism may be related to acquiring resistance to paclitaxel in USC and thus may be targets for anti-USC therapy.

Materials and Methods: We compared metabolic profiles and reactions to paclitaxel in both a wild type USC cell line (USPC-1) and PTX-1, a cell line derived from USPC-1 which acquired paclitaxel resistance, using a capillary electrophoresis CE-MS/MS system.

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Metabolomic analysis of uterine serous carcinoma with acquired resistance to paclitaxel

Abstract