BECN1 (Beclin 1)

Mechanistic verification was carried out by using the AMPK inhibitor BML-275 and the PGC-1α inhibitor SR-18292...Its protective effect may be related to the activation of the AMPK/PGC-1α signaling pathway and the subsequent enhancement of autophagy. This study reveals for the first time the potential value of Gf1 in the treatment of NAFLD and its molecular mechanism, providing new experimental evidence for the development of NAFLD drugs targeting the AMPK/PGC-1α/autophagy axis.

Pharmacological activation of the p38 MAPK/MK2 pathway abolished the cardioprotective effects mediated by DUSP4 overexpression. Collectively, these findings demonstrate that DUSP4 alleviates DOX-induced cardiotoxicity by suppressing the p38 MAPK/MK2 signaling cascade, highlighting the DUSP4 axis as a potential therapeutic target to improve cardiac safety during DOX-based chemotherapy.

The study demonstrated that COL11A1 exerts its oncogenic effects by suppressing autophagy via the AKT/Beclin 1 pathway, consequently inhibiting ferroptosis in pancreatic cancer cells. These findings reveal a novel molecular mechanism through which COL11A1 promotes tumor progression and provide a potential therapeutic target for pancreatic cancer treatment.

In conclusion, PO selectively inhibits HDAC6, promotes histone acetylation at H3K9, upregulates BECN1 expression, and induces autophagy-dependent cell death in CRC cells. These findings position PO as a promising candidate for the development of HDAC6-targeted therapies in CRC.

Inhibition of PGK1 initiates autophagy in T315I-mutant chronic myeloid leukemia (CML) cells, thereby enhancing their sensitivity to first-generation Tyrosine Kinase Inhibitor (TKI) imatinib and third-generation TKI ponatinib. Notably, CPU-216 induces autophagy via VCP and Beclin 1 in CML-T315I cells, enhancing their responsiveness to TKIs. These discoveries propose a novel therapeutic strategy for T315I-mutant CML, underscoring the potential to develop targeted treatments that leverage the kinase functions of PGK1.

Autophagy activators preserve cardiac function without affecting the antineoplastic effects of DOX in mice with cancer. Boosting autophagic flux is a suitable therapeutic approach to prevent cardiotoxicity induced by anthracyclines.

These findings demonstrate that silver(I) and gold(I) NHC complexes induce ROS-dependent autophagic cell death in this kind of cancer cells. The ability of these compounds to trigger non-apoptotic cell death mechanisms highlights their potential as promising candidates for overcoming apoptosis resistance in HCC therapy, warranting further in vivo investigations.

Collectively, these findings indicate that JI-CJ001 enhances the therapeutic impact of PTX in gastric cancer cell lines through regulation of HER2/mTOR signaling and autophagy. These results highlight JI-CJ001 as a promising natural adjuvant for improving the efficacy of conventional chemotherapy in gastric cancer.

Our work presents the largest UK cohort of DA with long-term follow-up making it an excellent resource for future biomarker studies. Validation studies in prospective clinical studies are required for clinical application.

Mechanistically, VIP-mediated autophagy was associated with sirtuin 3 (SIRT3) downregulation and increased Ac-FOXO1 levels, with SIRT3 overexpression effectively counteracting the VIP-induced autophagic effects. Our findings demonstrate that VIP induces both cytotoxic effects and autophagy in VPAC1-expressing RCC cells through modulation of the SIRT3/FOXO1 signaling pathway, highlighting its potential therapeutic value for renal cell carcinoma.

In conclusion, PrP knockdown may sensitize resistant SCLC cells to doxorubicin and promote autophagy. These findings support PrP silencing as a promising strategy to reverse chemoresistance in SCLC.

Overall, natural products targeting autophagy-related kinases hold great promise as leads for novel anticancer agents, warranting further in vivo validation, pharmacological optimization, and synergistic studies as adjuncts.