SQSTM1 (Sequestosome 1)

Drug sensitivity analysis based on oncoPredict revealed compounds with differential efficacy between risk groups, and the model also predicted response to PD-1 blockade in an external immunotherapy cohort. In summary, polyamine metabolism is closely linked to the immune microenvironment and prognosis of ESCA, providing a potential biomarker for patient stratification and treatment optimization.

Beclin1 knockdown and DHODH overexpression can reduce DOX-induced liver injury by preventing ferroptosis and autophagy.

In summary, this study elucidates the biological functions of DDX60 in CRC and provides novel experimental evidence supporting its potential as a therapeutic biomarker.

In this study, we hypothesize that SB-216 and Veru-111 (related novel compounds) inhibit cell growth via suppression of oncogenic βIII- and βIVb-tubulin subtypes and mitochondria function via suppression of BRD4, the most active BET protein...Our data demonstrates that SB-216 effectively inhibits PDAC cell growth through inhibiting oncogenic microtubules and mitochondrial function. This novel approach simultaneously targets two hallmarks of cancer and patient demise.

In contrast, this review focuses specifically on mammalian lipophagy by synthesizing the latest mechanistic insights into receptor-mediated recognition, transcriptional regulation, and signaling integration. We also outline unresolved questions and conceptual gaps - such as how lipophagy is selectively activated, how it coordinates with lipolysis, and whether distinct receptor codes exist in tissue- and disease-specific contexts - that remain unanswered in the current literature.

Mechanistically, regorafenib acts as a molecular glue, directly promoting the interaction between CD274 and the selective autophagy receptor SQSTM1/p62, leading to SQSTM1-mediated autophagic degradation of CD274 and restoration of T cell-mediated cytotoxicity. In summary, these findings identify a previously unrecognized role of regorafenib in modulating tumor immune evasion and provide a mechanistic rationale for its combination with PDCD1 inhibitors in CRC treatment.

Pyroptosis is involved in the pathogenesis of ICIs-related myocarditis, and Myd88 and Sqstm1 may serve as potential biomarkers for future clinical application.

Additionally, farnesol impaired mitochondrial ATP synthesis by reducing mitochondrial membrane potential (MMP) to 66% and elevated ROS levels to 54% creating a disturbance in mitochondrial stability. Overall, Farnesol significantly disrupts anaerobic glycolysis in A549 cells promoting cell death through mitochondrial dysfunction, oxidative stress, apoptosis and reducing cellular acidosis.

Collectively, our findings demonstrate that NaF activates the PINK1/Parkin-mediated mitophagy pathway; however, incomplete autophagic degradation leads to mitochondrial dysfunction and neuronal apoptosis, contributing to developmental neurotoxicity. Importantly, melatonin mitigates these adverse effects, suggesting its potential as a therapeutic agent for preventing fluoride-induced neurodevelopmental impairment through modulation of the PINK1/Parkin signaling axis.

In patients with PDB and spinal involvement, a rapid increase in ALP, especially in the context of specific genetic mutations like SQSTM1 and ZNF687, may be a critical indicator of malignancy. This case highlights the need for heightened clinical vigilance, enhanced genetic monitoring, and consideration of early biopsy to enable timely intervention and improve patient outcomes in this rare but devastating complication.

This led to the downregulation of key oncogenic effectors including Slug, FN1, CDH2, F2RL1, CDK6, CCND1, MMP9, CDKN2A, and SQSTM1, while upregulating tumor suppressors CDKN1B, CDKN1A, and DDIT3. In conclusion, COPB2 acts as an oncogene in GC, driving tumor progression through modulation of the cell cycle and key signaling pathways, highlighting its potential as a therapeutic target.