Nutritional Sensor REDD1 in Cancer and Inflammation: Friend or Foe?

Autor: Zhidkova EM; Department of Chemical Carcinogenesis, N.N. Blokhin NMRCO, 115478 Moscow, Russia., Lylova ES; Department of Chemical Carcinogenesis, N.N. Blokhin NMRCO, 115478 Moscow, Russia., Grigoreva DD; Department of Chemical Carcinogenesis, N.N. Blokhin NMRCO, 115478 Moscow, Russia., Kirsanov KI; Department of Chemical Carcinogenesis, N.N. Blokhin NMRCO, 115478 Moscow, Russia.; Faculty of General Medical Practice, Russian University of People's Friendship (RUDN), 117198 Moscow, Russia., Osipova AV; Department of Chemical Carcinogenesis, N.N. Blokhin NMRCO, 115478 Moscow, Russia., Kulikov EP; Faculty of Oncology, I.P. Pavlov Ryazan State Medical University, 390026 Ryazan, Russia., Mertsalov SA; Faculty of Oncology, I.P. Pavlov Ryazan State Medical University, 390026 Ryazan, Russia., Belitsky GA; Department of Chemical Carcinogenesis, N.N. Blokhin NMRCO, 115478 Moscow, Russia., Budunova I; Department of Dermatology, Northwestern University, Chicago, IL 60611, USA., Yakubovskaya MG; Department of Chemical Carcinogenesis, N.N. Blokhin NMRCO, 115478 Moscow, Russia., Lesovaya EA; Department of Chemical Carcinogenesis, N.N. Blokhin NMRCO, 115478 Moscow, Russia.; Faculty of Oncology, I.P. Pavlov Ryazan State Medical University, 390026 Ryazan, Russia.
Jazyk: angličtina
Zdroj: International journal of molecular sciences [Int J Mol Sci] 2022 Aug 26; Vol. 23 (17). Date of Electronic Publication: 2022 Aug 26.
DOI: 10.3390/ijms23179686
Abstrakt: Regulated in Development and DNA Damage Response 1 (REDD1)/DNA Damage-Induced Transcript 4 (DDIT4) is an immediate early response gene activated by different stress conditions, including growth factor depletion, hypoxia, DNA damage, and stress hormones, i.e., glucocorticoids. The most known functions of REDD1 are the inhibition of proliferative signaling and the regulation of metabolism via the repression of the central regulator of these processes, the mammalian target of rapamycin (mTOR). The involvement of REDD1 in cell growth, apoptosis, metabolism, and oxidative stress implies its role in various pathological conditions, including cancer and inflammatory diseases. Recently, REDD1 was identified as one of the central genes mechanistically involved in undesirable atrophic effects induced by chronic topical and systemic glucocorticoids widely used for the treatment of blood cancer and inflammatory diseases. In this review, we discuss the role of REDD1 in the regulation of cell signaling and processes in normal and cancer cells, its involvement in the pathogenesis of different diseases, and the approach to safer glucocorticoid receptor (GR)-targeted therapies via a combination of glucocorticoids and REDD1 inhibitors to decrease the adverse atrophogenic effects of these steroids.
Competing Interests: The authors declare no conflict of interest.
Databáze: MEDLINE
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