ATG16L1 (Autophagy Related 16 Like 1)

Suboptimal expression of the autophagic protein ATG16L1 results in accelerated carcinogenesis, and an altered B cell response may be one of the aggravating factors.

Topics include anti-TNFα, integrin blockade, IL-12/23 and IL-23 inhibition, JAK inhibitors, S1P receptor modulators, microRNA modulation, senomorphics, mesenchymal cell therapy, and microbiome interventions. We endorse biomarker-guided therapy and propose future directions to break the SASP-driven inflammatory loop and mitigate long-term carcinogenic risk.

Our in vitro study demonstrates that H. pylori could alter the expression of autophagy-related genes. Further investigation could precisely uncover the mechanism whereby H. pylori dysregulates host autophagy.

In a model of transcription-associated mutagenesis, deficiency of the IBD risk gene Atg16l1 does not induce small intestinal cancer. In contrast, double deficiency of Xbp1 and Atg16l1 drives spontaneous tumor formation highlighting a cooperative role of Xbp1 and Atg16l1 in tumor suppression.

Aramchol interacted with the multi-kinase inhibitors sorafenib, regorafenib or lenvatinib, to kill GI tumor cells, with regorafenib exhibiting the greatest effect. Knock down of Beclin1 reduced the lethality of regorafenib and aramchol as single agents and when combined whereas knock down of LAMP2 or BID did not reduce killing caused by aramchol as a single agent but did reduce the lethality of regorafenib alone and regorafenib plus aramchol. In vivo using the HuH7 adult hepatoma cell line, regorafenib and aramchol interacted to suppress tumor growth without normal tissue toxicities.

RT-qPCR analysis further confirmed significant upregulation of mRNA expression levels of randomly selected BAG3, EIF2AK2, KIF5B, and RAB24 in HCC cell lines, consistent with the bioinformatics analysis findings. This study showed that the 41 obtained ARGs, such as ATG16L1, ATG4B, BAG3, KIF5B, MAPK1, RAB24, and SOGA1, these findings suggest that ARGs may serve as prognostic biomarkers for HCC, warranting further validation in clinical cohorts and functional studies.

Importantly, our results indicate that CDK12 determines the oncogenic function of UPF3B. In conclusions, these results provide basis for research on liver cancer prevention and treatment.

Moreover, the methylation of LC3B facilitates OC cell migration by inhibiting autophagy. Overall, our study defines a novel modification of LC3B and unveils a SETD5-mediated methylation-dependent regulatory mechanism controlling nuclear LC3B function in autophagy and migration in OC cells, offering potential therapeutic targets for OC.

This results in HITT sensitizing PI-103-mediated cell death both in vitro and in vivo in nude mice by attenuating protective autophagy. The data presented herein demonstrate that HITT is a newly identified RNA regulator of autophagy and that it can be used to sensitize the colon cancer response to cell death by blocking the protective autophagy.

SIRT3 overexpression activated the AMPK/mTOR pathway and triggered ATG16L1-mediated autophagy, promoting ferroptosis in SCC15 cells, and we proposed that quercetin may be a promising therapeutic drug for OSCC.

Genotypic differences highlight the correlation between the wild genotype for CD96 and ATG16L1 with unfavorable laboratory and endoscopic response to adalimumab. Finally, the more significant levels of immune complexes in the CDA group indicate an association with a worse response to adalimumab.

Abnormal skeletal muscle mitochondrial turnover and dynamics are associated with disease progression in Smn2B/- mice despite compensatory elevations in upstream factors important for organelle synthesis and recycling. Exercise and UA enhance mitochondrial health in skeletal muscle, which indicates that lifestyle-based and pharmacological interventions may be effective countermeasures targeting the organelle for therapeutic remodelling in SMA.