BECN1 (Beclin 1)

DSF-induced autophagy may mitigate its pro-apoptotic effects, while autophagy inhibition fully blocks protein degradation pathways, leading to lethal protein accumulation. This study elucidates DSF's dual regulation of autophagy through UPS suppression and the c-Fos/beclin-1 axis, and validates the synergistic efficacy of DSF combination with CQ in CRC, providing a theoretical foundation and translational potential for DSF-based combination therapies.

Meanwhile, the relative protein ratio of LC3-II/LC3-I was elevated at 0.65 μM DON, while the p62 expression was decreased in a dose-dependent manner compared to the control. In summary, DON exerts toxic effects on mouse hepatocytes, while Cu can mitigate DON-induced cellular damage at low concentrations, likely through involvement in Beclin-1/p62 related autophagic regulation.

mTOR or caloric-restriction mimetics jump-start a protective flux; chloroquine derivatives and ULK1 blockers clip tumour survival circuits; cannabinoids, photodynamic therapy and immune-checkpoint combinations exploit context-specific toggling between induction and brake. Emerging biomarkers (LC3B-II, p62, AMBRA1) promise patient-stratified interventions. By weaving together molecular detail, pre-clinical insight and clinical translation, we show why autophagy is no longer a backstage process but a star player in dermatology - and how targeting its switches could reshape future treatment algorithms.

This study provides the first evidence that CA suppresses OC progression via ROS-mediated dual mechanisms: apoptosis induction and mitophagy activation. Our results underscore the translational potential of CA as a promising therapeutic candidate and provide a robust experimental foundation for its further development against OC.

This study demonstrates that a therapeutic-grade exosome formulation can alleviate osteoarthritis by restoring the balance between autophagy and apoptosis through modulation of the BCL2-Beclin-1 signaling axis. These findings highlight the potential of exosome-based nanotherapeutics as a novel disease-modifying treatment strategy for degenerative joint disorders.

However, there was a parallel drop in p62 expression, which indicates autophagy induction. AICAR increased the influence of WJ-CM on viability, as well as the levels of biomarkers associated with autophagy, phosphorylated  AMPK, and phosphorylated  mTOR in the HT-29 cells. WJ-CM inhibits colorectal cancer cell growth via activating AMPK/mTOR-mediated autophagy.

Adjuvant chemotherapy with TMZ (Temozolomide) does not improve the survival of patients suffering from GBM (Glioblastoma)...Increased XBP-1s expression might contribute to the enhanced TMZ sensitivity. This combination therapy is promising for TMZ-resistant cancers, but it needs further investigation.

MTT assay showed that 6 and 9b were 4.5 and 2 times more potent than doxorubicin against MCF-7 cells, while 9a and 13b were 10 and 7.5 times more effective against MDA-MB-231 cells, respectively...Compound 13b exhibited comparable EGFRL858R inhibition to lapatinib and outperformed pictilisib against PI3Kα, PI3Kβ, and PI3Kδ. Compound 6 showed greater ARO inhibition than letrozole, while being slightly less potent than pictilisib against PI3Kα and PI3Kβ...Docking studies supported the in vitro enzymatic inhibition assays results. Thus, 9b and 13d are potent anti-breast cancer benzoxazoles with selective ARO and PI3kα inhibition activity, respectively, while 6, 9a, and 13b are multi-target inhibitors exhibiting other anticancer synergistic mechanisms.

This work expands our understanding of the role of ARV in regulating host cell autophagy pathways and viral replication. It also provides a new avenue for understanding viral modulation of host cellular processes in the context of oncolytic virotherapy.

The reciprocal regulation between TNF-α and autophagy may contribute to tumor progression in OSCC.

In SK-BR-3 and T47D breast cancer cell lines, piperlongumine induces apoptosis via the MAPK/NF-κB pathway and promotes autophagy. These findings suggests that piperlongumine may serve as a potential therapeutic agent against human breast cancer cells.

CRM1 also synergistically potentiated the cytotoxic efficacy of paclitaxel by co-targeting multiple cell death processes. Collectively, these results suggest CRM1 as a promising cytotoxic candidate with a multimodal mechanism of action in lung cancer cells.