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All the therapeutic strategies for treating cancers aim at killing the cancer cells via apoptosis (programmed cell death type I). Defective apoptosis endow tumor cells with survival. The cell can respond to such defects with autophagy. Autophagy is a cellular process by which cytoplasmic material is either degraded to maintain homeostasis or recycled for energy and nutrients in starvation. A plethora of evidence has shown that the role of autophagy in tumors is complex. A lot of effort is needed to underline the functional status of autophagy in tumor progression and treatment, and elucidate how to tweak autophagy to treat cancer. Furthermore, during the treatment of cancer, the limitation for the cure rate and survival is the phenomenon of multi drug resistance (MDR). The development of MDR is an intricate process that could be regulated by drug transporters, enzymes, anti-apoptotic genes or DNA repair mechanisms. Reports have shown that autophagy has a dual role in MDR. Furthermore, it has been reported that activation of a death pathway may overcome MDR, thus pointing the importance of other death pathways to regulate tumor cell progression and growth. Therefore, in this review we will discuss the role of autophagy in MDR tumors and a possible link amongst these phenomena.
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http://dx.doi.org/10.3390/cells1030558 | DOI Listing |
Cell Biochem Biophys
March 2025
Department of Medical Laboratory Science, the Third Xiangya Hospital, Central South University, Changsha, Hunan, China.
The myosin regulatory light chain 2 (MLC2) is a crucial regulator of myosin activity. Its phosphorylation, mediated by various kinases, plays a vital role in maintaining normal physiological functions in skeletal muscle, myocardium, smooth muscle, and nonmuscle cells. Moreover, MLC2 has been implicated in the development of many cancers through its phosphorylation.
View Article and Find Full Text PDFCommun Biol
March 2025
Department of Chemical, Materials and Industrial Production Engineering, University of Naples Federico II, Naples, Italy.
Transcription Factor EB (TFEB) controls lysosomal biogenesis and autophagy in response to nutritional status and other stress factors. Although its regulation by nuclear translocation is known to involve a complex network of well-studied regulatory processes, the precise contribution of each of these mechanisms is unclear. Using microfluidics technology and real-time imaging coupled with mathematical modelling, we explored the dynamic regulation of TFEB under different conditions.
View Article and Find Full Text PDFCell Death Dis
March 2025
Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, China.
Traumatic brain injury (TBI) is a significant global health concern that often results in death or disability, and effective pharmacological treatments are lacking. G protein-coupled receptor 56 (GPR56), a potential drug target, is crucial for neuronal and glial cell function and therefore plays important roles in various neurological diseases. Here, we investigated the potential role and mechanism of GPR56 in TBI-related damage to gain new insights into the pharmacological treatment of TBI.
View Article and Find Full Text PDFMicrob Pathog
March 2025
Instituto Politécnico Nacional, Escuela Nacional de Ciencias Biológicas, Department of Microbiology, México City, México. Electronic address:
In recent years, Candida glabrata (C. glabrata) has emerged as a pathogen responsible for systemic mortal infections. C.
View Article and Find Full Text PDFExp Eye Res
March 2025
Changzhou Third People's Hospital, Changzhou Medical Center, Nanjing Medical University, Jiangsu Changzhou, 213000. Electronic address:
The objective of this study was to investigate the protective effects and related mechanisms of lactoferrin and HIF-1α on dry eye syndrome (DED) in mice. The expression levels of lactoferrin and HIF-1α in tears of DED patients and normal controls were detected. A DED mouse model received lactoferrin (50 mg/kg dissolved in 2 mL PBS) or DMOG (40 mg/kg dissolved in 2 mL PBS) orally daily for 28 days.
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