CREB5 (CAMP Responsive Element Binding Protein 5)

Immune-related gene expression patterns are associated with response to nCRT in rectal cancer. High expression levels of S100A8, SPINK5, ANXA1, FOXJ1, and CLEC7A were indicative of favorable treatment response, and S100A8 and SPINK5 were associated with prognosis. A machine learning-based model composed of immune-related genes showed strong predictive potential. Our results support the use of immune gene signatures to guide personalized therapy in rectal cancer.

It may suppress the cell invasion and angiogenesis of endometrial cells by reducing the phosphorylation levels of PI3K and AKT mediated by increasing CREB5. This mechanistic insight provides novel pathogenic explanations for EMs.

Inhibition of CREB5 or treatment with ML221, a selective APLN receptor (APLNR) antagonist, potently suppressed lymphatic metastasis in preclinical CCa models. These findings establish CREB5 as a critical regulator of APLN-dependent lymphangiogenesis and LNM, highlighting its potential as a dual diagnostic biomarker and therapeutic target for mitigating lymphatic dissemination in CCa patients.

Mechanistically, proteomic profiling coupled with RNA immunoprecipitation identified CREB5 as a direct binding partner mediating SNHG15-dependent survival signaling under genotoxic stress. These results position the SNHG15-CREB5 axis as an important player governing genomic fidelity in lung adenocarcinoma, suggesting druggable targets for precision oncology approaches.

More importantly, alteration of NFIX expression could reverse the effect of CREB5 on NSPC proliferation. These findings highlight CREB5 as a key regulator of NSPC proliferation through its interaction with NFIX, providing a potential therapeutic target for stem cell-based treatments of CNS disorders.

We found that CREB5 is a transcription factor overexpressed in 15% of BLBCs and was upregulated in breast cancers that metastasize to the brain. In cell lines, CREB5 overexpression regulated cell phenotypes and transcriptional changes, including IL13RA2, a cell surface receptor that is currently druggable and represents a novel target in BLBC.

To the best of our knowledge, the current study underscores the non-invasive diagnostic biomarker potential of miRNA 1827 in monitoring the disease severity of PCa for the first time. Furthermore, the miRNA-mRNA interactions may be exploited for therapeutic purposes.

In summary, the diagnostic model based on the FR-related gene PTGS2 demonstrated significant and specific diagnostic value for CS and AS, reflecting the status of blood lymphocytes, monocytes, and neutrophils. A pan-cancer study suggested it could serve as a new clinical prognostic marker and therapeutic target across various cancer types. This model may aid in the diagnosis of CS and AS. The findings offer new insights into the pathogenesis of these diseases.

Intriguingly, disrupting CREB5 super-enhancers with ABBV-075 significantly reduces its expression and inhibits H3.3K27M DIPG tumor growth. Combined treatment with ABBV-075 and a BRG1 inhibitor presents a promising therapeutic strategy for clinical translation in H3.3K27M DIPG treatment.

In summary, our findings suggest that ERS activation promotes EMT in liver cancer cells via SE-mediated upregulation of the CREB5/TNC pathway. This result provides a new direction for uncovering how ERS regulates EMT and a foundation for preventing the progression of EMT in HCC.

The findings of this study support a mechanism between JIA and an increased risk of breast cancer.