Cancer stem cells(CSCs) play a key role in regulating tumorigenesis, progression, as well as recurrence, and possess typical metabolic characteristics. Autophagy is a catabolic process that can aid cells to survive under stressful conditions such as nutrient deficiency and hypoxia. Although the role of autophagy in cancer cells has been extensively studied, CSCs possess unique stemness, and their potential relationship with autophagy has not been fully analyzed. This study summarizes the possible role of autophagy in the renewal, proliferation, differentiation, survival, metastasis, invasion, and treatment resistance of CSCs. It has been found that autophagy can contribute to the maintenance of CSC stemness, facilitate the tumor cells adapt to changes in the microenvironment, and promote tumor survival, whereas in some other cases autophagy acts as an important process involved in the deprivation of CSC stemness thus leading to tumor death. Mitophagy, which has emerged as another popular research area in recent years, has a great scope when explored together with stem cells. In this study, we have aimed to elaborate on the mechanism of action of autophagy in regulating the functions of CSCs to provide deeper insights for future cancer treatment.
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http://dx.doi.org/10.1038/s41419-023-05929-3 | DOI Listing |
Anim Cells Syst (Seoul)
December 2024
Yunkang School of Medicine and Health, Nanfang College, Guangzhou, People's Republic of China.
Diabetic cardiomyopathy (DCM) is a major complication of type 2 diabetes mellitus (T2DM), but its effective prevention and treatment are still limited. We investigated the effects of GYY4137, a slow-releasing hydrogen sulfide donor, and its downstream mediator forkhead box protein O1 (FOXO1) on T2DM-associated DCM. , T2DM mice were induced by a high-fat diet coupled with streptozotocin injection.
View Article and Find Full Text PDFFront Cell Infect Microbiol
December 2024
Department of Molecular Pathology and Biology, Military Faculty of Medicine, University of Defence, Hradec Kralove, Czechia.
Many pathogens have evolved sophisticated strategies to evade autophagy, a crucial cellular defense mechanism that typically targets and degrades invading microorganisms. By subverting or inhibiting autophagy, these pathogens can create a more favorable environment for their replication and survival within the host. For instance, some bacteria secrete factors that block autophagosome formation, while others might escape from autophagosomes before degradation.
View Article and Find Full Text PDFBrain Behav
January 2025
Faculty of Medicine, Department of Neurology, Sakarya University, Sakarya, Türkiye.
Introduction: Restless legs syndrome (RLS) is a frequently encountered neurological illness that has no effective treatment and imposes an enormous socioeconomic burden. Autophagy is essential for the maintenance of healthy cellular physiology, cell viability, and defense against pathogenic conditions. However, there is no study investigating the possible role of autophagy-related proteins (ATGs) in RLS patients.
View Article and Find Full Text PDFClin Rheumatol
January 2025
Department of Rheumatology and Immunology, Arthritis Research Institute, The First Affiliated Hospital of Anhui Medical University, Hefei, 230000, China.
Objective: Nuclear transcription factor-κB (NF-κB) activation is a pivotal event in the pathogenesis of osteoarthritis (OA). OA patients frequently exhibit vitamin D (VD) deficiency, which is commonly associated with NF-κB activation. Our study aimed to investigate whether VD could protect against OA by modulating NF-κB pathway and to explore the underlying mechanisms.
View Article and Find Full Text PDFInflamm Res
January 2025
Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, School of Pharmacy, Anhui Medical University, Hefei, 230032, Anhui Province, China.
Objective: Fibroblast-like synoviocytes (FLS) are key players in rheumatoid arthritis (RA) by resisting apoptosis via increased autophagy. Elevated synovial aquaporin 1 (AQP1) affects RA FLS behaviors, but its relationship with FLS autophagy is unclear. We aim to clarify that silencing AQP1 inhibits autophagy to exert its anti-RA effects.
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