The function of miR-200 family in oxidative stress response evoked in cancer chemotherapy and radiotherapy - 14/03/20
, Katarzyna Jonak b, Ryszard Maciejewski aBienvenido a EM-consulte, la referencia de los profesionales de la salud.
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Graphical abstract |
Highlights |
• | Chemotherapy and radiotherapy influences the status of miR-200 family members. |
• | Mir-200 family might contribute to the development of resistance to anticancer therapies. |
• | Acquired cancer chemoresistance is a multifactorial phenomenon involving a variety of factors. |
• | Increasing the level of reactive oxygen species (ROS) might influence the cellular profile of miR-200 family. |
• | The crosstalk between miR-200 family and oxidative stress might shed new light on anticancer therapy resistance. |
Abstract |
Since the beginning of the discovery of microRNAs (miRs), these molecules have attracted highly progressive attention due to their powerful regulatory roles in a broad spectrum of biological processes, including proliferation, differentiation, apoptosis and carcinogenesis. With regard to carcinogenesis, the miRs regulatory potency has been associated with cancer onset, progression, metastasis, diagnosis and therapeutic response. In this review we discuss the impact of miR-200 family on drug resistance development during anti-cancer therapy. Developing resistance to chemotherapeutic drugs as well as radiotherapy are major clinical obstacles in the successful therapeutic strategies to cancer treatment. Acquired cancer chemoresistance is a multifactorial phenomenon involving such factors as tumor type, tumor stage, cellular reactive oxygen species (ROS) level or ROS-responsive miRs profile. ROS level could influence the miRs expression level, which changes the cellular profile of the content of miRs. Such significant changes in the cellular miRs profile generate subsequent biological effects through the regulation of their target genes. This review outlines the interactions between ROS and miR-200 family in different kinds of cancers in response to chemotherapy.
El texto completo de este artículo está disponible en PDF.Abbreviations : 3’UTR, 5-FU, AKR1C1 and AKRIC4, AKT, ALDH1A3, BCNU, Bmi1, CAT, CYA, EMT, eNOS, FOXO, GPxs, HGF, HIF, Keap1, MAPK, miRs, mRNA, MnSOD, MTHFD2, NF-κB, Nrf2, NQO1, PRDX2, ROS, RRM2, SAHA, SESN, SCD, SIRT1, SOD, TBK1, TrkB, Trx, TP53INP1, TUBB3, TXNDC12, YAP1, ZEB
Keywords : Reactive oxygen species, miR-200 family, Oxidative stress, Chemotherapy, Radiotherapy
Esquema
Vol 125
Artículo 110037- mai 2020 Regresar al número
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Bienvenido a EM-consulte, la referencia de los profesionales de la salud.
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Bienvenido a EM-consulte, la referencia de los profesionales de la salud.
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