TFEB Signalling-Related MicroRNAs and Autophagy.

Davide Corà, Federico Bussolino, Gabriella Doronzo

Journal: Biomolecules 2021;11(7):985

PMID: 34356609

Abstract

The oncogenic Transcription Factor EB (TFEB), a member of MITF-TFE family, is known to be the most important regulator of the transcription of genes responsible for the control of lysosomal biogenesis and functions, autophagy, and vesicles flux. TFEB activation occurs in response to stress factors such as nutrient and growth factor deficiency, hypoxia, lysosomal stress, and mitochondrial damage. To reach the final functional status, TFEB is regulated in multimodal ways, including transcriptional rate, post-transcriptional regulation, and post-translational modifications. Post-transcriptional regulation is in part mediated by miRNAs. miRNAs have been linked to many cellular processes involved both in physiology and pathology, such as cell migration, proliferation, differentiation, and apoptosis. miRNAs also play a significant role in autophagy, which exerts a crucial role in cell behaviour during stress or survival responses. In particular, several miRNAs directly recognise TFEB transcript or indirectly regulate its function by targeting accessory molecules or enzymes involved in its post-translational modifications. Moreover, the transcriptional programs triggered by TFEB may be influenced by the miRNA-mediated regulation of TFEB targets. Finally, recent important studies indicate that the transcription of many miRNAs is regulated by TFEB itself. In this review, we describe the interplay between miRNAs with TFEB and focus on how these types of crosstalk affect TFEB activation and cellular functions.

Address: Department of Translational Medicine, Piemonte Orientale University, 28100 Novara, Italy.; Center for Translational Research on Autoimmune and Allergic Diseases-CAAD, 28100 Novara, Italy.; Department of Oncology, University of Torino, 10060 Candiolo, Italy.; Candiolo Cancer Institute-IRCCS-FPO, Laboratory of Vascular Oncology, 10060 Candiolo, Italy.
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