Redox-Active Iron-Induced Oxidative Stress in the Pathogenesis of Clear Cell Carcinoma of the Ovary

Yoshihiko Yamada, Yamada Y, Shigetomi H, Hiroshi Shigetomi, Onogi A, Akira Onogi, Shoji Haruta, Haruta S, Ryuji Kawaguchi, Kawaguchi R, Yoshida S, Shozo Yoshida, Furukawa N, Naoto Furukawa, Nagai A, Akira Nagai, Yasuhito Tanase, Tanase Y, Taihei Tsunemi, Tsunemi T, Hidekazu Oi, Oi H, Kobayashi H, Hiroshi Kobayashi
International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · 2011 · vol. 21(7) , pp. 1200–1207 · doi:10.1097/igc.0b013e318222cfdd · PMID:21885986 · W2088995577
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This study investigated how redox-active iron contributes to oxidative stress and the development of clear cell carcinoma in the ovary.

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Abstract

ObjectiveEpithelial ovarian cancer (EOC) is the most lethal pelvic gynecologic cancer. Clear cell carcinoma (CCC) and endometrioid adenocarcinoma (EAC) of the ovary have been associated with endometriosis, thus indicating that endometriosis has been believed to increase the risk of developing EOC. The aim of our review was to identify and synthesize the most current information on CCC with regard to molecular and pathophysiological distinctions.MethodThis article reviews the English-language literature for molecular, pathogenetic, and pathophysiological studies on endometriosis and endometriosis-associated ovarian cancer (EAOC). In this review, we focus on the functions and roles of redox-active iron in CCC carcinogenesis.ResultsThe iron-induced reactive oxygen species signals can contribute to carcinogenesis via 3 major processes: step 1, by increasing oxidative stress, which promotes DNA mutagenesis, histone modification, chromatin remodeling, and gene products activation/inactivation thus contributing to EAOC initiation; step 2, by activating detoxification and antiapoptotic pathways via the transcription factor hepatocyte nuclear factor 1β overexpression, thereby contributing to CCC promotion; and step 3, by creating an environment that supports sustained growth, angiogenesis, migration, and invasion of cancer cells via estrogen-dependent (EAC) or estrogen-independent (CCC) mechanisms, thus supporting tumor progression and metastasis.ConclusionsThese aspects of reactive oxygen species biology will be discussed in the context of its relationship to EAOC carcinogenesis.

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Condition tags

endometriosis

MeSH descriptors

Adenocarcinoma, Clear Cell Endometriosis Iron Ovarian Neoplasms Oxidative Stress Adenocarcinoma, Clear Cell Adenocarcinoma, Clear Cell Adenocarcinoma, Clear Cell Animals Cell Transformation, Neoplastic Endometriosis Endometriosis Female Humans Iron Ovarian Neoplasms Ovarian Neoplasms Ovarian Neoplasms Reactive Oxygen Species Reactive Oxygen Species

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