ATG4B (Autophagy Related 4B Cysteine Peptidase)

This compound activates ATG4B and induces autophagy, significantly inhibiting the proliferation and migration of TNBC cells both in vitro and in vivo. In conclusion, this study has identified the first allosteric small-molecule activator targeting ATG4B, which not only provides a powerful tool molecule for in-depth exploration of autophagy regulation in TNBC treatment, but also lays an important foundation for the development of innovative drugs based on the autophagy activation mode.

This study reveals the ATG4B-PKM2 axis as a critical regulatory node linking autophagy, metabolic reprogramming, and EMT. Targeting this axis with Curcumol provides a precise strategy to interrupt metabolism-phenotype coupling, offering a mechanistically grounded and translationally promising approach for inhibiting CRC progression and metastasis.

O-GlcNAcylation serves as a nutrient and stress sensor that dynamically regulates autophagy at multiple stages in cancer cells. It fine-tunes autophagy initiation, maturation and fusion by modifying key proteins such as ULK1, ATG4B and SNAP-29. Context-dependent O-GlcNAcylation promotes tumour adaptation and therapy resistance via autophagy remodelling. Targeting the O-GlcNAc-autophagy axis offers a promising strategy to overcome cancer drug resistance.

Using the autophagy suppressor, 3-methyladenine (3MA, 2mM), chloroquine (CQ, 10μM), and knockdown of autophagy-related protein 4 homolog B (ATG4B) gene by siRNA, it was shown that Cr (VI)-provoked mTOR was reliant on autophagy...HMGA2 mediated this effect by transcription regulation of ATG4B. These suggested that blocking the HMGA2-autophagy-mTOR axis could serve as an effective strategy to inhibit Cr (VI)-induced cell viability.

To the best of our knowledge, this is the first study exploring the clinical implications of ATG4B, LC3 and p62 in urothelial tumorigenesis. Studies are required to validate their relevances in larger cohort.

The present study demonstrates that a novel ATG4B-SESN3 regulatory circuit plays a crucial role in T cell leukemogenesis, which suggests that targeting ATG4B is a promising strategy for T-ALL treatment.

Subsequently, miRNA-34a and ATG4B initiated cyclic cleavage of the signal probes to yield distinct fluorescence for highly sensitive detection of miRNA-34a and ATG4B, thereby achieving specific autophagy pathway detection. Besides, the dynamic concentration interplay between miRNA-34a and ATG4B upon drug stimulation can also be monitored by the ZnO-DNA NSs to realize effective discrimination of drug-sensitive and -resistant cancer cells to access chemoresistance reversion, revealing the robust potential of ZnO-DNA NSs for detecting different autophagy pathways and screening potent therapeutic drugs.

Collectively, our findings demonstrate that RNF216P1 promotes malignant progression in HCC cells by acting as a competing endogenous RNA for miR-195-5p, thereby upregulating ATG4B and enhancing autophagy. This study identifies a novel ceRNA axis-RNF216P1/miR-195-5p/ATG4B-that plays a pivotal role in HCC development and may represent a potential therapeutic target.

Taken together, our results demonstrate that ATG4B is required for anabolic behavior in NSCLC, indicating that the autophagic cascade may be a required input for mTORC1 activity and cellular anabolism in lung cancer. These results have implications for the field of cancer biology more broadly, as they indicate that the far from being a simple target of mTORC1, the autophagic cascade may serve as a requisite input for anabolic signaling, casting new light on the relationship between these processes in cancer pathophysiology.

We identified key APIGs and constructed a robust APIG-based prognostic signature for HCC. CDC25C was a key target through which APs impact HCC and multiple other cancers.

In autophagy-activated MDA-MB-231 cells and tumor-bearing mice, IR780-CBT NPs exhibited 4.5-fold and 3.1-fold enhanced fluorescence signals, respectively, compared to the "RAPA + Inh."-treated controls. These findings highlight the potential of IR780-CBT NPs for precise autophagy imaging in vivo, offering a promising tool for early diagnosis and mechanistic studies of autophagy-related diseases.

Genetic knockdown or pharmacological inhibition of ATG4B in AML cells restores DNA repair capacity, activates the cell-cycle checkpoint kinase CHEK1/CHK1, attenuates malignant progression, and ultimately delays leukemia progression. These findings reveal an autophagy-independent role for nuclear ATG4B that links metabolic stress to the suppression of DNA repair and identify ATG4B as a potential therapeutic target in AML.