SCD1, autophagy and cancer: implications for therapy

Bibliographic Details
Title: SCD1, autophagy and cancer: implications for therapy
Authors: Francesca Ascenzi, Claudia De Vitis, Marcello Maugeri-SaccĂ , Christian Napoli, Gennaro Ciliberto, Rita Mancini
Source: Journal of Experimental & Clinical Cancer Research, Vol 40, Iss 1, Pp 1-16 (2021)
Publisher Information: BMC, 2021.
Publication Year: 2021
Collection: LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens
Subject Terms: Autophagy, Lipid metabolism, cancer, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
More Details: Abstract Background Autophagy is an intracellular degradation system that removes unnecessary or dysfunctional components and recycles them for other cellular functions. Over the years, a mutual regulation between lipid metabolism and autophagy has been uncovered. Methods This is a narrative review discussing the connection between SCD1 and the autophagic process, along with the modality through which this crosstalk can be exploited for therapeutic purposes. Results Fatty acids, depending on the species, can have either activating or inhibitory roles on autophagy. In turn, autophagy regulates the mobilization of fat from cellular deposits, such as lipid droplets, and removes unnecessary lipids to prevent cellular lipotoxicity. This review describes the regulation of autophagy by lipid metabolism in cancer cells, focusing on the role of stearoyl-CoA desaturase 1 (SCD1), the key enzyme involved in the synthesis of monounsaturated fatty acids. SCD1 plays an important role in cancer, promoting cell proliferation and metastasis. The role of autophagy in cancer is more complex since it can act either by protecting against the onset of cancer or by promoting tumor growth. Mounting evidence indicates that autophagy and lipid metabolism are tightly interconnected. Conclusion Here, we discuss controversial findings of SCD1 as an autophagy inducer or inhibitor in cancer, highlighting how these activities may result in cancer promotion or inhibition depending upon the degree of cancer heterogeneity and plasticity.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 1756-9966
Relation: https://doaj.org/toc/1756-9966
DOI: 10.1186/s13046-021-02067-6
Access URL: https://doaj.org/article/68ed6951cd7943219a091c9cc07df416
Accession Number: edsdoj.68ed6951cd7943219a091c9cc07df416
Database: Directory of Open Access Journals
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More Details
ISSN:17569966
DOI:10.1186/s13046-021-02067-6
Published in:Journal of Experimental & Clinical Cancer Research
Language:English