RBP1 (Retinol Binding Protein 1)

RT-qPCR results further confirmed differential expression patterns of the 8 genes between normal and GBM cells, supporting their involvement in GBM pathogenesis. This 8-gene risk model effectively predicts glioma prognosis and supports personalized treatment strategies by highlighting immune microenvironment differences and drug sensitivities between risk groups.

Conclusively, our study demonstrates that circSPINT2 possesses tumor-suppressive functions; the restoration of circSPINT2 expression level confers sensitivity to osimertinib treatment via miR-1296-3p/RBP1 axis. The secreted circSPINT2 may serve as a monitoring biomarker for osimertinib resistance status in LUAD.

Using the genetic dependencies of PDAR, we identify clinically used drugs that owe their lethality to a PDAR-dependent mechanism. Our findings unveil an apoptotic signaling response that contributes to the efficacy of a wide array of anti-cancer therapies.

According to the results, POU3F3 acts as a protective regulator against sorafenib-induced ferroptosis in HCC cells by enhancing the transcription of multiple retinoic acid metabolism genes and promoting retinoic acid production. The POU3F3 inhibitor, rosarin, shows potential as an ideal candidate for overcoming sorafenib resistance in HCC.

In conclusion, the project investigated the prognosis and classification value of nitrogen metabolism-related genes in GBM from multiple perspectives, predicting the sensitivity of different subtypes of patients to immunotherapy response and drug sensitivity. These findings are expected to show new research directions for further exploration in these fields.

We knocked out retinoic acid receptor beta (RAR-β) selectively in pancreatic cells by tamoxifen treatment after crossing these adult RAR-βfl/fl mice with Pdx1/CreER (PCer) and lox-stop-lox KRasG12D transgenic mice...Expression of SOX9, a key protein required for formation and maintenance of PDAC, was higher in PCer;RAR-βD/wt and PCer;RAR-βD pancreata compared to wild-type, indicating that deletion of RAR-β increases SOX9 levels even without the KRas activating mutation. In summary, lack of RAR-β in pancreatic acinar cells reduced cell proliferation and increased SOX9 protein levels in this transgenic model.

Methodological advancements in quantifying ATRA and its metabolites are reviewed, alongside the challenges inherent in studying retinoid dynamics. Future research directions are proposed to further elucidate the role of ATRA in health and disease, with the aim of identifying therapeutic targets for conditions linked to retinoid signaling dysregulation.

RBP1 is overexpressed and associated with poor patient prognosis in head and neck squamous cell carcinoma.

This nomogram was validated and demonstrated good predictive performance, with area under the curve (AUC) values for 1-year, 3-year, and 5-year OS being 0.848, 0.807, and 0.759, respectively. Our findings highlight the profound impact of prognostic-related genes on BC immune response and prognostic outcomes, suggesting that modulation of the m6A-immune pathway could offer new avenues for personalized BC treatment and potentially improve clinical outcomes.

In situ evaluation of the RBP1 gene mRNA shows differential expression in HSIL compared to LSIL and healthy cervical tissue, confirming the finding found in the previously performed gene profile. The differential expression of TMEM45A between normal cervix and HSIL favours a possible role of this gene in the carcinogenesis of well-differentiated epithelial lesions. Additional studies are being performed to detect the expression of these genes at the protein level and determine if there is a correlation with these findings.

Here, two LX-2 culture methods were applied as models of hepatic retinoid metabolism to demonstrate the effects of activation status and dose-dependent cytokine exposure on the expression of genes involved in retinoid metabolism. This study suggests that compared to quiescent cells, activated HSC are hypermetabolic, have reduced apparent formation of retinoic acid which may alter downstream retinoic acid signaling.

High infiltration of anti-tumor immune cells in both tumors and margins results in good prognosis, while in patients with minimal infiltration in tumors in spite of high infiltration in margins results in poor prognosis. Targeted CD73 immune-checkpoint inhibition may improve clinical outcome.