CTSS (Cathepsin S)

We demonstrate that our model can predict a spheroid's long-term invasive fate with high accuracy using only partial image sets from early time-points, rather than the complete time-course images. Our work presents an in vivo -like, scalable 3D platform integrated with a quantitative high-throughput pipeline to elucidate GBM invasion mechanisms and to evaluate anti-invasive compounds.

This review integrates foundational principles with recent discoveries to map the molecular architects and regulators of the matrix in health and disease, emphasising how composition and mechanics interact with protease-driven turnover and receptor-mediated sensing. Finally, we outline emerging therapeutic strategies that restore matrix balance through targeted modulation of protease activity, engineering of ECM-mimetic scaffolds with programmable mechanics and degradability, and tuning of CD-mediated signalling to promote regeneration and resolution.

In this review, we summarize how lysosomes control ferroptosis, focusing on the regulation through lysosomal contents, pH, degradation processes, and exocytosis. We also discuss possible therapeutics that target lysosomes to modulate ferroptosis-associated diseases.

CTSs are critical players in PCa progression and therapy resistance. Targeting CTSs may improve therapeutic outcomes, though further research is needed to better understand their mechanisms and clinical applicability.

MCP1 and FABP4 concentrations were elevated in early pregnancy among women with PCOS, largely reflecting maternal adiposity. These markers did not modify associations between PCOS and pregnancy outcomes. Larger longitudinal studies are needed to clarify underlying inflammatory and metabolic pathways.

Importantly, MMPs and cathepsins also drive osteolytic activity that supports tumor colonization and growth in the bone microenvironment by activating osteoclasts, releasing matrix-bound growth factors, and perpetuating a vicious cycle of bone destruction. Given their multifaceted roles, MMPs and cathepsins represent promising therapeutic targets in bone-metastatic breast and prostate cancers.

Simultaneous depletion of both inhibitors revealed synergistic effects and remodeled the immune microenvironment to favor tumor suppression. These results suggest previously unknown roles for stefin B and cystatin C in tumor development and progression, which encourage further investigation of the cancer metabolic mechanisms underlying tumor behavior and their dynamic interplay with the microenvironment.

This pathway conceptually bridges environmental toxicology and neuro-oncology and highlights S100A4 and associated lipid disturbances as potential targets for preventive intervention. However, the proposed mechanistic links remain inferential, and definitive confirmation will require future in vitro and in vivo experiments to directly test the impact of DEHP on S100A4 expression, function, and downstream metabolic reprogramming in GBM models.

This inhibitory action involved modulating the phosphorylation of extracellular signal-regulated kinase and c-Jun N-terminal kinase, as well as suppressing proteins associated with epithelial-mesenchymal transition. Furthermore, jaceidin reduced the expression of extracellular matrix degradation proteins MMP-2 and cathepsins A. These compelling findings suggest that jaceidin warrants further investigation as a potential therapeutic agent for melanoma.

Currently, plerixafor (AMD3100) is the only approved CXCR4 antagonist used to mobilize hematopoietic stem cells into the peripheral blood for transplantation therapy...One interesting compound is the endogenous peptide inhibitor for CXCR4 (EPI-X4), recently discovered in the hemofiltrate of dialysis patients. It was traced back to human serum albumin, from where it was generated by the proteolytic activity of cathepsins E and D. Based on its implications for cancer therapy, this review describes its recent evaluations, which include sequence optimization, in vivo efficacy, toxicity, and bioavailability studies.

Our findings highlight the potential of another M-GB-ADC as a targeted therapy for overcoming rituximab resistance and treatment failure in DLBCL. This strategy enhances therapeutic efficacy and represents a preclinical proof-of-concept treatment option by directing a cathepsin-inhibitor payload specifically to malignant B cells.

This study suggests that eupatolitin suppresses, at least partially, the migration and invasion of oral cancer cells by promoting p38 phosphorylation and downregulating cathepsin S and cathepsin B expression. The findings provide experimental evidence supporting the antimetastatic potential of eupatolitin. Nonetheless, further studies are required to confirm its translational relevance.