EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)

Our study demonstrated that the overexpression of EZH2 was significantly associated with advanced tumor stage and poor 5-year overall survival in a Chinese ETBSCC cohort. These findings highlight the applicability of EZH2 as a candidate therapeutic target for integrated therapies. Further exploration and validation through a stable cell line are needed.

Mechanistically, SPI1 transcriptionally suppresses ACSL4 expression through the EZH2/H3K27me3 pathway, leading to inhibition of intracellular lipid peroxidation. Thus, SPI1 knockdown synergizes with erastin to promote lipid peroxidation and ferroptosis, suggesting that targeting SPI1 may represent a promising therapeutic strategy for renal cell carcinoma.

TPP1, induced by H. pylori, promoted GC metastasis by enhancing ERS via interaction with GRP78. Targeting the TPP1/ERS axis may offer a novel therapeutic strategy for GC.

PINK1 acts as a tumor suppressor in colorectal cancer by inhibiting proliferation and migration, promoting apoptosis, and remodeling the epigenetic landscape through altering histone modifications and enhancing chromatin accessibility.

Inhibition of the RAD51B-EZH2 axis allows the re-expression of functional ERα, making TNBC targetable by endocrine therapy. Consistently, the combination of EZH2 inhibitor with tamoxifen effectively reduces TNBC progression, suggesting that the RAD51B-EZH2 axis is a potential therapeutic target for TNBC.

Methylation analysis identified six CpG sites significantly associated with survival. In conclusion, EZH2 is a key regulator of HCC progression and potential prognostic biomarker and therapeutic target.

Since Scribble tethers PHLPP1 and PTEN to antagonize Akt, repression of Scribble induces EMT. In summary, FBL safeguards epithelial integrity, by regulating the expression of Scribble, uncovering an FBL-EZH2 axis in EMT and metastasis.

In vivo experiments confirmed that ginsenoside CK suppressed tumor formation by downregulating EZH2, activating the dendritic cell-NK cell axis, and remodeling the tumor immune microenvironment. Ginsenoside CK inhibits EZH2, activating the dendritic cell-NK cell axis and remodeling the tumor immune microenvironment, thereby suppressing HCC cell activity and tumorigenicity.

Nonetheless, translational barriers such as delivery efficiency, scalability, pediatric safety, and regulatory challenges must be addressed before these strategies reach clinical practice. This review integrates insights into ATRT biology, conventional management, and emerging molecular-, immunological-, and nanotechnology-based approaches, emphasizing opportunities and challenges in advancing outcomes for children affected by this devastating tumor.

This research provides novel evidence for elucidating the immune escape mechanism of DLBCL. EZH2 and its associated signaling cascades hold the potential to serve as promising targets for the immunotherapy of DLBCL.

As EZH2 is highly expressed in numerous precancers, PPT@GSK126 has broad application prospects for reducing these tumor burdens. Schematic images presenting the mechanism of action regarding EZH2 in promoting MT of OLK into HNSCC via inhibiting MHC-I associated APM (left panel) and the proposed therapeutic strategy for preventing OLK carcinogenesis (right panel).

A cancer cell membrane (CCm)-camouflaged nanoplatform (CCm-HSA-Taz) was engineered to encapsulate the EZH2 inhibitor Tazemetostat (Taz), enabling tumor-targeted delivery...Nuclear medicine imaging revealed reduced tumor glucose metabolism and improved immune cell cytotoxicity. Utilizing components approved by the FDA suggests the potential for this strategy to be translated into clinical settings.