Co-treatment with alpelisib and chloroquine (CQ) further suppressed tumor cell growth, viability, migration, and colony formation more effectively than alpelisib alone, owing to increased apoptosis, elevated early and late apoptotic populations, and increased levels of cleaved PARP and caspase-3. These findings suggest that combining alpelisib with autophagy inhibition significantly enhances its antitumor activity in PI3K-mutated NSCLC, highlighting a promising therapeutic strategy to address unmet clinical needs in this molecular subset. This discovery opens new possibilities for developing innovative targeted therapies for challenging NSCLC.

This study demonstrates that SIP1 is effective in inducing apoptosis and promotes cisplatin-induced apoptosis by repressing cisplatin-induced autophagy in MDA-MB-231 cells.

Our data suggests that one of the possible mechanisms by which PV-10 triggers ICD is by inducing endoplasmic reticulum stress, autophagy, and apoptosis. Our findings contribute to further understanding of the underlying mechanisms of PV-10 induced cytotoxicity and to develop future clinical trials in locally recurrent HNSCC.

Our findings reveal a mechanism by which TNFα disrupts hemostasis through autophagy inhibition, highlighting TNFα as a critical regulator of platelet metabolism and function. This study provides new insights into inflammation-associated pathologies and suggests autophagy-targeting strategies as potential therapeutic avenues to restore hemostatic balance.

P=N/A, N=40, Completed, Sichuan Provincial People's Hospital; Sichuan Provincial People's Hospital

P=N/A, N=29, Completed, Hospices Civils de Lyon | Unknown status --> Completed

Dinutuximab beta also triggers autophagy in NB cells, and inhibition of the VEGFR pathway with anlotinib amplifies dinutuximab beta-induced autophagy. Furthermore, autophagy inhibition by CQ enhances CXCL9 expression and anti-tumor T cell responses of single anti-GD2 therapy in vitro and in vivo. Collectively, this study suggests autophagy inhibitors may be a promising strategy for enhancing therapeutic efficacy in NB in conjunction with anti-GD2 immunotherapy.

Mechanistic analyses included co-immunoprecipitation to validate the GLUT1-EGFR interaction, chloroquine to inhibit autophagy, and cycloheximide/MG132 to evaluate EGFR protein stability. In vivo, GLUT1 knockdown suppressed tumor growth and lung metastasis, and clinical samples revealed a positive correlation between GLUT1 and EGFR expression, linked to advanced TNM stages and poor survival. Collectively, these findings demonstrate that GLUT1 preserves esophageal CSC-like characteristics by stabilizing EGFR to inhibit autophagy-dependent ferroptosis, highlighting targeting GLUT1 as a potential therapeutic strategy to eliminate CSCs and combat esophageal cancer progression.

Importantly, MCGH exhibits catalase (CAT)-like activity in normal tissues, effectively detoxifying H2O2 through its decomposition. By engineering a single material platform to execute different catalytic cascades, this work provides a new perspective for precision nanomedicine design.

Gong et al. conducted a phase 1b/2 trial, demonstrating that autophagy inhibitors combined with high-dose CDK4/6is are well tolerated and effective in patients with advanced HR+/HER2- breast cancer resistant to first-line CDK4/6i therapy.1.

Mechanistically, autophagy inhibition increases the binding of T-DM1 to lysosomes, potentially facilitating the release of emtansine from the conjugate. These results present a novel strategy that combines T-DM1 with autophagy inhibitors to effectively treat HER2-low gastric cancer, thereby broadening the therapeutic scope of T-DM1 to encompass previously challenging cancer types.

P=N/A, N=90, Recruiting, Ningbo Medical Centre Lihuili Hospital; Ningbo Medical Centre Lihuili Hospital