YY1 (YY1 Transcription Factor)

These results reveal a previously unknown ∆40p53/miR-4671-5p/SGSH axis that, when dysregulated, induces intra-S-phase cell cycle arrest and may contribute to cancer outcomes. Our findings highlight the distinct regulatory role of ∆40p53, independent of FLp53, in maintaining cellular and metabolic homeostasis via miRNA-mediated mechanisms.

The upregulated LGALS1 is then secreted via SUSD2 assistance, ultimately suppressing CD8+ T cell function and inducing apoptosis. Our findings define a stromal-immune axis in pancreatic cancer, linking miR-181b-5p from CAFs to the establishment of an immune-suppressive niche via the STING pathway in tumor cells, thereby revealing this cascade as a targetable mechanism to counteract immune evasion.

These findings demonstrate that UBE2D4 promotes glioma progression through YY1-mediated transcriptional activation, acceleration of cell cycle progression, and inhibition of p53-dependent tumor suppression. UBE2D4 may serve as a potential prognostic biomarker and therapeutic target for glioma.

PDIA6, driven by KRASG12D, alleviates ICD and promotes immune evasion, functioning as a predictive biomarker to screen ICB-sensitive patients and a therapeutic target to improve ICB efficacy in PDAC with KRAS mutations.

This ZF/DNA binding was abrogated by H2S; however, when DNA was bound to YY1-ZF2-ZF3, it was unreactive to H2S modification suggesting a protective effect of the DNA macromolecule. In addition, H2S disrupted the secondary structure of all three YY1 constructs as measured by circular dichroism.

In conclusion, this study reveals that FBXL8 suppresses PC progression by stabilizing IκBα through non-degradative ubiquitination, and its downregulation via the NF-κB-YY1 axis promotes oncogenic progression. The FBXL8-IκBα-NF-κB pathway represents a promising novel therapeutic target for PC.

This review explores the mechanistic basis of the TGF-β-YY1 cross-talk regulation in the immune evasion of PDAC. It also discusses emerging therapeutic opportunities in targeting the TGF-β-YY1 axis to overcome immune escape and improve treatment outcomes in PDAC.

Moreover, knocking down APMAP reduced NSCLC proliferation in vivo, mainly through reduced tumor volume, reduced KI-67 and GPX4 expressions, and decreased p-pI3K, p-AKT, and p-mTOR protein levels. APMAP regulated by YY1 transcription enhanced NSCLC proliferation, invasion, and repressed cell ferroptosis via activating PI3K/AKT/mTOR.

Our research suggested the OXCT1/Wnt signaling axis pathway as a critical regulator of CRLM. And these findings offered valuable insights, and potential therapeutic targets for CRLM.

Emerging evidence further identifies YY1 as a clock-controlled gene and architectural regulator of circadian transcription, bridging together enhancer-promoter communication, chromatin state, and the temporal dimension of gene expression. In this context, its deregulation links circadian misalignment with oncogenic signaling, underscoring its key role as a diagnostic and prognostic biomarker, as well as a therapeutic target, thus highlighting its relevance in precision oncology.

These results suggest that YY1 plays an important role in progression of H. pylori-induced gastric cancer by activating EMT.