POTEE (POTE Ankyrin Domain Family Member E)

Independent risk factors including cancer location, response to therapy and ANKRD20A4 and EVC mutational status were identified and were used in the establishment of a Nomogram model for patient prognosis prediction.

Cycloheximide (CHX) chase experiments revealed that LINC00667 overexpression accelerated POTEE degradation, while treatment with the proteasome inhibitor MG132 stabilized POTEE levels...Collectively, our findings demonstrate that LINC00667 inhibits breast cancer progression by promoting TRIM33-mediated ubiquitination and subsequent degradation of POTEE, thereby regulating mitochondrial OXPHOS activity. These results highlight the critical role of LINC00667 in the posttranslational regulation of protein stability and mitochondrial function in BC, and suggest that targeting the LINC00667-POTEE axis may represent a potential therapeutic strategy for this disease.

In patient TILs, increases in cytokine production and tetramer-positive populations identified antigen-specific CD8 T cell responses, which were dependent on antigen presentation by HLA class I. Antigen-specific T cells triggered cancer cell killing of antigen-pulsed OC cells. These findings suggest that TTLL8, POTEE, and PKMYT1 are potential targets for the development of antigen-targeted immunotherapy in OC.

Overexpressing MARK1 suppressed sorafenib-induced proliferation in resistant cells, while co-overexpression of MARK1 and POTEE reversed this effect. MARK1 potentially restrains HCC progression and enhances sorafenib resistance by negatively modulating POTEE expression, highlighting its significance as a therapeutic target in HCC treatment.

To establish the effects of protein hyperacetylation, treatment with suberoylanilide hydroxamic acid (SAHA), a lysine deacetylase inhibitor, was conducted, and this served as an independent model...The molecular linkage between protein hyperacetylation and the AKT/GSK3β/Snail pathway was demonstrated. This study highlighted the importance of protein acetylation in CCA progression, suggesting that ACC1 and KDAC are potential targets for CCA treatment.

We found that the co-localization of POTEE with Rac1 is correlated with more aggressive breast cancer subtypes. Given its role in tumour dissemination, the leading cause of cancer-related deaths, POTEE could represent a potential therapeutic target for these types of cancer.

The use of a blocking antibody targeting MHC class I demonstrated that the T cell-induced killing was dependent on CD8 T cell recognition of antigen. Conclusions These results suggest that TTLL8, POTEE, and PKMYT1 are good targets for the development of antigen-targeted immunotherapy in OC.

Our results indicate that POTEE mutation could serve as a potential predictive biomarker for ICIs in LUAD. However, prospective cohort studies are still needed for further validation.