BCL9 (BCL9 Transcription Coactivator)

Some variants appeared to segregate with specific types of lymphoid cancers; others were shared across different subtypes. Identifying factors predisposing to different types of lymphoid cancers will help understand the etiology of these neoplasms.

Our findings highlight the pivotal role of DARS-AS1 in enhancing GC progression through the activation of angiogenesis via the Wnt signaling pathway. By elucidating the mechanism underlying DARS-AS1-mediated tumorigenesis, we posit that DARS-AS1 could serve as a prognostic biomarker and a potential therapeutic target for GC intervention, warranting further exploration in clinical settings.

This in turn rejuvenates T cell immunity via enhanced macrophage-mediated antigen presentation. Our data extend our understanding of how tumor-derived Wnt/β-catenin signaling impedes the innate and adaptive immune responses in the tumor microenvironment and provide preliminary evidence that targeting BCL9 is a promising preclinical strategy to mitigate ICI resistance in HCC.

In oncology research, BCL9 affects tumour cell proliferation and metastasis by regulating the Wnt/β-catenin pathway, thus emerging as a promising target for anticancer therapy. In this paper, we conducted a comprehensive review of the discovery, structure, and mechanism of action of BCL9 within the Wnt/β-catenin signaling pathway, along with its potential applications in bone development, tissue regeneration, and cancer therapy, with the intention of furnishing novel perspectives and a theoretical foundation for future investigations.

Furthermore, these hybrid peptidomimetics demonstrate enhanced serum stability, which augments their potential as therapeutic agents for future applications. In addition, this study paves a new way to modulate a myriad of PPIs.

Importantly, Bcl9@TP demonstrated favorable systemic biocompatibility and safety. Our findings indicate that disrupting the β-catenin/BCL9 interaction with a peptide-based nanoprodrug represents a compelling strategy to suppress oncogenic signaling and enhance immunotherapy responses in CRC, providing a new angle to boost checkpoint sensitivity.

We found that LINC01232 competes with miR-516a-5p for binding, thereby reducing its expression and subsequently increasing BCL9 expression. In conclusion, our results indicate that LINC01232 facilitates the malignant development of TNBC through the miR-516a-5p/BCL9 pathway, providing fresh perspectives on the pathogenesis of TNBC and pinpointing potential therapeutic targets.

Our study demonstrates the oncogenic role of PYGO1 in GC and identifies PGG as a potential inhibitor, highlighting the PYGO1/ITGB1/CD47 axis as a promising therapeutic target for GC.

Furthermore, this compound's effectiveness and safety were confirmed in both MH/NRASG12D BCP-ALL mouse model and MB patient-derived xenograft (PDX) model, outperforming conventional therapies. These results support the therapeutic potential of dual-pathway inhibition in MEF2D fusion (+) BCP-ALL and suggest CUDC-907 as a promising candidate for precision treatment in fusion-driven leukemias with similar molecular dependencies.

This study unveils TRAF2-mediated nucleocytoplasmic transport as a druggable mechanism, advancing targeted therapies against Wnt-driven colorectal cancers.

Our findings underscore the intricate network interactions among transcription factors, signal transduction pathways in development, and cytokines modulated by BCL9 deficiency. Targeting BCL9 emerges as a promising strategy for melanoma therapy, bolstering NK cell maturation and cytotoxicity, and overcoming challenges in NK cell-based immunotherapies.

Elevated BCL9 and TPX2 are associated with poor prognosis in ccRCC. These proteins are potential prognostic markers and therapeutic targets.