TFAP2A (Transcription Factor AP-2 Alpha)

In summary, our mechanistic investigations revealed TFAP2C as a novel oncogenic driver in OC and a key regulator of ferroptosis via its epigenetic modulation of the KEAP1-NRF2 axis. These findings highlight TFAP2C as a potential therapeutic target for ferroptosis-inducing therapies in OC patients with high TFAP2C expression.

The presence of DAO in peroxisomes, autophagosomes, lysosomes, and exosomes indicated diverse intracellular localization within CPECs. This distribution may enable efficient metabolism of blood-derived D-serine in CPECs.

Additionally, IGF2BP2 was found to bind to the m6A site in LDHA mRNA, thereby enhancing its stability. Overall, TFAP2A facilitated aerobic glycolysis and PC progression via IGF2BP2-mediated stabilization of LDHA mRNA, providing novel insights for PC therapy.

Notably, CDK inhibitors markedly inhibit ESCC cell proliferation. This research delineates the potential cellular origins of ESCC and their key regulons, thereby pioneering a single-cell-derived therapeutic strategy that exposes vulnerabilities in tumor-initiating cells.

Further analysis revealed that TFAP2C directly binds to the VEGFA promoter to activate its transcription, thereby facilitating VEGFA/VEGFR2-dependent angiogenesis. Together, these findings not only broaden the understanding of propofol's pharmacological profile, but also identify TFAP2C as a novel transcriptional regulator of VEGFA, offering new perspectives for therapeutic targeting of VEGFA-mediated angiogenesis.

Therefore, TFAP2A transcriptionally activated CST2, contributing to the malignant progression of NSCLC. These findings underscored the potential clinical significance of targeting the TFAP2A/CST2 axis as a novel therapeutic strategy for the treatment of NSCLC.

In summary, TFAP2A dysregulation resulted in CES3 overexpression and the following NSCLC tumorigenesis. Targeting the TFAP2A/CES3 axis may represent a promising therapeutic strategy for NSCLC in the future.

Our findings demonstrate that DEAF1 attenuates ADR-induced apoptosis and pyroptosis in MM by enhancing DNA damage repair and suppressing GSDME cleavage via the FER/GSDME axis. This study provides a novel therapeutic target for the treatment of MM.

ACC and DLBC shared a consensus expression program, whereas STAD diverged; chromatin analysis showed AP-2 motifs near microbe-responsive genes in ACC and DLBC but not STAD, supporting cohort-specific regulation. Collectively, AP-2 family members emerge as plausible mediators of tumor microbiota-host interplay, warranting further mechanistic and translational research.

Both HER2 and ESR1 are determinant of KN026 efficacy in advanced HER2-positive breast cancer, implying the potential of KN026 combined with endocrine therapy in HER2- and ER-positive breast cancer.

Overall, this study elucidates that super enhancer-driven IGF2BP3 targets CACNA1A via m6A modification, in turn which inhibits ferroptosis in ovarian cancer. It highlights that targeting the IGF2BP3-CACNA1A regulatory axis could be an effective strategy impeding ovarian cancer progression.

These changes were accompanied by a significant increase in cell migration speed under front-targeted inhibition, while rear-targeted inhibition had no significant effect on speed and neither treatment altered persistence. Together, these findings suggest that endocytic polarity regulates adhesion dynamics and cell migration under confinement, offering a mechanistic insight into processes relevant to cancer cell invasion.