Involvement of the aldo-keto reductase, AKR1B10, in mitomycin-c resistance through reactive oxygen species-dependent mechanisms

Toshiyuki Matsunaga; Yumi Yamane; Lida Keiko; Satoshi Endo; Yoshiko Banno; Ossama El-Kabbani; Akira Hara

doi:10.1097/CAD.0b013e3283448df0

Involvement of the aldo-keto reductase, AKR1B10, in mitomycin-c resistance through reactive oxygen species-dependent mechanisms

Toshiyuki Matsunaga, Yumi Yamane, Lida Keiko, Satoshi Endo, Yoshiko Banno, Ossama El-Kabbani, Akira Hara

Medicinal Chemistry

Research output: Contribution to journal › Article › Research › peer-review

31 Citations (Scopus)

Abstract

The human aldo-keto reductase (AKR) 1B10 is suggested as a tumor marker in various solid tumors. Using colon cancer cells, we found that AKR1B10 was induced with acquisition of resistance to the anticancer drug mitomycin-c (MMC). In the resistant cells, treatment with an AKR1B10 inhibitor decreased their MMC tolerance. In the nonresistant cells, overexpression and silencing of AKR1B10 decreased and increased, respectively, susceptibility to cytotoxic effects of MMC and 4-hydroxy-2-nonenal, which was formed as a product of lipid peroxidation by MMC treatment. These results suggest a role of AKR1B10 in the development of MMC resistance, which may be mediated by its ability to detoxify cytotoxic aldehydes including 4-hydroxy-2-nonenal. Anti-Cancer Drugs 22:402-408 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams Wilkins.

Original language	English
Pages (from-to)	402 - 408
Number of pages	7
Journal	Anti-Cancer Drugs
Volume	22
Issue number	5
DOIs	https://doi.org/10.1097/CAD.0b013e3283448df0
Publication status	Published - 2011

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1097/CAD.0b013e3283448df0

Cite this

@article{cc1d7cbd43c847c2970b98d2bd43443a,

title = "Involvement of the aldo-keto reductase, AKR1B10, in mitomycin-c resistance through reactive oxygen species-dependent mechanisms",

abstract = "The human aldo-keto reductase (AKR) 1B10 is suggested as a tumor marker in various solid tumors. Using colon cancer cells, we found that AKR1B10 was induced with acquisition of resistance to the anticancer drug mitomycin-c (MMC). In the resistant cells, treatment with an AKR1B10 inhibitor decreased their MMC tolerance. In the nonresistant cells, overexpression and silencing of AKR1B10 decreased and increased, respectively, susceptibility to cytotoxic effects of MMC and 4-hydroxy-2-nonenal, which was formed as a product of lipid peroxidation by MMC treatment. These results suggest a role of AKR1B10 in the development of MMC resistance, which may be mediated by its ability to detoxify cytotoxic aldehydes including 4-hydroxy-2-nonenal. Anti-Cancer Drugs 22:402-408 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams Wilkins.",

author = "Toshiyuki Matsunaga and Yumi Yamane and Lida Keiko and Satoshi Endo and Yoshiko Banno and Ossama El-Kabbani and Akira Hara",

year = "2011",

doi = "10.1097/CAD.0b013e3283448df0",

language = "English",

volume = "22",

pages = "402 -- 408",

journal = "Anti-Cancer Drugs",

issn = "0959-4973",

publisher = "Lippincott Williams & Wilkins",

number = "5",

}

Involvement of the aldo-keto reductase, AKR1B10, in mitomycin-c resistance through reactive oxygen species-dependent mechanisms. / Matsunaga, Toshiyuki; Yamane, Yumi; Keiko, Lida; Endo, Satoshi; Banno, Yoshiko; El-Kabbani, Ossama; Hara, Akira.

In: Anti-Cancer Drugs, Vol. 22, No. 5, 2011, p. 402 - 408.

Research output: Contribution to journal › Article › Research › peer-review

TY - JOUR

T1 - Involvement of the aldo-keto reductase, AKR1B10, in mitomycin-c resistance through reactive oxygen species-dependent mechanisms

AU - Matsunaga, Toshiyuki

AU - Yamane, Yumi

AU - Keiko, Lida

AU - Endo, Satoshi

AU - Banno, Yoshiko

AU - El-Kabbani, Ossama

AU - Hara, Akira

PY - 2011

Y1 - 2011

N2 - The human aldo-keto reductase (AKR) 1B10 is suggested as a tumor marker in various solid tumors. Using colon cancer cells, we found that AKR1B10 was induced with acquisition of resistance to the anticancer drug mitomycin-c (MMC). In the resistant cells, treatment with an AKR1B10 inhibitor decreased their MMC tolerance. In the nonresistant cells, overexpression and silencing of AKR1B10 decreased and increased, respectively, susceptibility to cytotoxic effects of MMC and 4-hydroxy-2-nonenal, which was formed as a product of lipid peroxidation by MMC treatment. These results suggest a role of AKR1B10 in the development of MMC resistance, which may be mediated by its ability to detoxify cytotoxic aldehydes including 4-hydroxy-2-nonenal. Anti-Cancer Drugs 22:402-408 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams Wilkins.

AB - The human aldo-keto reductase (AKR) 1B10 is suggested as a tumor marker in various solid tumors. Using colon cancer cells, we found that AKR1B10 was induced with acquisition of resistance to the anticancer drug mitomycin-c (MMC). In the resistant cells, treatment with an AKR1B10 inhibitor decreased their MMC tolerance. In the nonresistant cells, overexpression and silencing of AKR1B10 decreased and increased, respectively, susceptibility to cytotoxic effects of MMC and 4-hydroxy-2-nonenal, which was formed as a product of lipid peroxidation by MMC treatment. These results suggest a role of AKR1B10 in the development of MMC resistance, which may be mediated by its ability to detoxify cytotoxic aldehydes including 4-hydroxy-2-nonenal. Anti-Cancer Drugs 22:402-408 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams Wilkins.

UR - http://www.ncbi.nlm.nih.gov/pubmed/21317765

U2 - 10.1097/CAD.0b013e3283448df0

DO - 10.1097/CAD.0b013e3283448df0

M3 - Article

VL - 22

SP - 402

EP - 408

JO - Anti-Cancer Drugs

JF - Anti-Cancer Drugs

SN - 0959-4973

IS - 5

ER -

Involvement of the aldo-keto reductase, AKR1B10, in mitomycin-c resistance through reactive oxygen species-dependent mechanisms

Abstract

UN SDGs

Access to Document

Other files and links

Cite this