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Role of ROS­mediated autophagy in melanoma (Review).
Zhang, Xuebing; Li, Huaijun; Liu, Chengxiang; Yuan, Xingxing.
Afiliación
  • Zhang X; Department of Dermatology, Heilongjiang Academy of Traditional Chinese Medicine, Harbin, Heilongjiang 150001, P.R. China.
  • Li H; Department of Dermatology, Heilongjiang Academy of Traditional Chinese Medicine, Harbin, Heilongjiang 150001, P.R. China.
  • Liu C; Department of Dermatology, Heilongjiang Academy of Traditional Chinese Medicine, Harbin, Heilongjiang 150001, P.R. China.
  • Yuan X; Department of Dermatology, Heilongjiang Academy of Traditional Chinese Medicine, Harbin, Heilongjiang 150001, P.R. China.
Mol Med Rep ; 26(4)2022 Oct.
Article en En | MEDLINE | ID: mdl-35946460
ABSTRACT
Melanoma is the most aggressive form of skin cancer with the poorest prognosis and its pathogenesis has yet to be fully elucidated. As key factors that regulate cellular homeostasis, both reactive oxygen species (ROS) and autophagy are involved in the development of melanoma, from melanomagenesis to progression and drug resistance. However, the interaction between ROS and autophagy in the etiology and treatment of melanoma is not well characterized. The present review examined the production of ROS and the role of oxidative stress in melanoma, and summarized the role of ROS­mediated autophagy in melanomagenesis and melanoma cell fate decision following treatment with various anticancer drugs. The present findings may lead to a better understanding of the pathogenesis and progression of melanoma, and suggest promising treatment options for this disease.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Melanoma / Antineoplásicos Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: Mol Med Rep Año: 2022 Tipo del documento: Article

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Melanoma / Antineoplásicos Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: Mol Med Rep Año: 2022 Tipo del documento: Article
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