Proteostasis, also known as protein homeostasis, is critical for cell survival. Autophagy is a cellular process that degrades and recycles damaged or long-lived proteins, misfolded proteins, and damaged or abnormal organelles in order to preserve homeostasis. Among the three forms of autophagy, chaperone-mediated autophagy (CMA) is distinct from macroautophagy and microautophagy; it does not require the formation of vacuoles and only degrades selected individual proteins. CMA helps to maintain cellular homeostasis by regulating protein quality, bioenergetics, and substrate-associated cellular processes at the right moment. This pathway’s dysfunction has been linked to several diseases and disorders. Neurodegenerative diseases and cancer have received the most attention. In various neurodegenerative disorders, especially in their later stages, CMA activity declines. CMA has been shown to act as a tumor suppressor in cancer by destroying specific tumor promoters. Once a tumor has grown, it also helps tumor survival and the metastatic cascade. The presence of changes in CMA in these diseases disorders raises the idea of targeting CMA to restore cellular homeostasis as a potential therapeutic method. Manipulation of CMA activity may be effective therapeutic strategies for treating these diseases. Therefore, in this paper; we introduce the basic processes, regulatory mechanisms, and physiological functions of CMA; evidences supporting the role of impaired CMA function in neurodegeneration and cancer; and the potential of how targeting CMA could be a promising therapeutic method for the two diseases.

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Phytochemical profiles, antioxidant, and anti-inflammatory activities were assessed in methanolic extracts of Moringa oleifera (L.) Lam. and Moringa stenopetala (Bak.) Cufod. leaves, using a workflow from plant collection to lab assays.

The transfer of molecular cargo in exosomes plays a crucial role in cancer progression, influencing metabolic processes, angiogenesis, immune interactions, and invasive capabilities. This review synthesizes current evidence on how exosomes modulate tumor metabolism and drive drug resistance, and outlines therapeutic opportunities. We searched PubMed, Scopus, Web of Science, and Google Scholar for English-language studies using terms related to exosomes/extracellular vesicles, glycolysis, oxidative phosphorylation (OXPHOS), lipid metabolism, and drug resistance/chemoresistance, and integrated the literature qualitatively. Evidence indicates that exosomes reprogram tumor and stromal metabolism by delivering enzymes and non-coding RNAs that boost glycolysis and dampen OXPHOS, activate cancer-associated fibroblasts and extracellular matrix (ECM) remodeling, and modulate ferroptosis. They stimulate angiogenesis (e.g., via vascular endothelial growth factor (VEGF)/Wnt pathways) and promote immune escape through programmed death-ligand 1 (PD-L1), transforming growth factor beta (TGF-β), and macrophage reprogramming. Exosomal integrins and proteases contribute to epithelial–mesenchymal transition (EMT), organotropism, and pre-metastatic niche formation. Critically, exosomes propagate chemoresistance by exporting drugs and spreading determinants—including P-gp/BCRP/MRP-1, anti-apoptotic proteins, and regulatory RNAs—to previously sensitive cells; adipose-derived vesicles and lipid cargos further reinforce metabolic plasticity and therapy resistance. Given their stability, nanoscale dimensions, and ability to cross the blood–brain barrier, exosomes are promising vectors for targeted delivery; engineered vesicles can enhance chemotherapy responsiveness and counteract resistance, particularly alongside immunotherapy. In summary, interventions that disrupt exosome biogenesis, cargo loading, or uptake—paired with engineered exosomes for precision delivery—could mitigate drug resistance, metastasis, and immune evasion and advance more effective cancer treatment.

Natural compounds possess anti-tumor capabilities for a wide range of cancers. The present study aims to analyze and compare the antiproliferative activity of Moringa oleifera and Moringa stenopetala leaf extracts against anaplastic thyroid carcinoma and lung adenocarcinoma cells in primary cell culture. Samples were collected from Arba Minch, Ethiopia. Water-soluble tetrazolium salt-1 assay was used to assess the antiproliferative activity of these samples against anaplastic thyroid carcinoma and lung adenocarcinoma cells in primary cell culture. Cell number counting was another method used to confirm cell proliferation. The results showed that, in comparison to the control, both Moringa species significantly lowered cancer cell proliferation in a dose-responsive manner. Although Moringa oleifera showed a stronger inhibitory effect compared to Moringa stenopetala , there was no statistically significant difference ( p > 0.05) in the proliferation of anaplastic thyroid carcinoma and lung adenocarcinoma cells between the two species. Moringa oleifera extract had a lower IC ₅₀ value in anaplastic thyroid carcinoma cells, 84.2 µg/ml, than Moringa stenopetala leaf extract, 90.6 µg/ml. Moringa oleifera leaf extract has a lower IC ₅₀ value in lung adenocarcinoma cells, 64.7 µg/ml, than Moringa stenopetala leaf extract, 75.3 µg/ml. In conclusion, the two species have antiproliferative activity on anaplastic thyroid carcinoma and lung adenocarcinoma cells in primary cell culture. These findings indicated that both extracts may serve as a basis for future cancer therapeutic applications.