AXIN2 (Axin 2)

The possible mechanism of NIN on UC could be explained starting from the inflammation-cancer transformation. Furthermore, comprehensive research is expected between inflammation and cancer development.

In 3D culture, YAP loss reduces β-catenin nuclear localization and spheroid viability in a stiffness-dependent manner. These findings identify a mechanically gated YAP-β-catenin axis that integrates multiple microenvironmental cues to shape transcriptional programs in metastatic breast cancer.

Moreover, overexpression of both RNF43 and HUNK was associated with prolonged OS compared to the overexpression or unaltered expression of HUNK alone. Conclusion Collectively, these results suggest RNF43 and AXIN2 as favorable prognostic factors and HUNK as a poor prognostic factor and therapeutic target for patients with GC.

This study expands the mutational spectrum of AXIN2-associated isolated tooth agenesis and provides in vitro functional evidence supporting the pathogenicity of the identified variants. These findings offer important insights for genetic diagnosis and counseling in affected families.

Collectively, this study establishes AP2M1 as a key regulator of stemness in HCC, operating through the Wnt signaling pathway. Our findings validate AP2M1 as a promising biomarker and potential therapeutic target for HCC.

Our work uncovers a novel function of AFAP1-AS1 in regulating RNA alternative splicing through the modulation of splicing factors phase separation. This mechanism highlights an unrecognized pathway by which AFAP1-AS1 promotes drug resistance in lung adenocarcinoma, suggesting that AFAP1-AS1 and its regulated splicing events may serve as potential biomarkers or therapeutic targets for the treatment of lung adenocarcinoma.

These findings highlighted the regenerative dynamics of neuromast cells in Mexican tetra. This work lays the foundation for future therapeutic strategies targeting human sensory deficits, particularly those involving inner ear hair cell degeneration.

Importantly, we found that the demethylation drug decitabine (DCA) could reverse gefitinib resistance in PC9TET2 KD cells and mouse models. These results indicate that the methylation of AXIN2 induced by TET2 repression is a novel resistance mechanism of EGFR TKIs in EGFR-mutant NSCLC. Demethylation drugs have the potential to overcome EGFR TKI resistance induced by loss-of-function TET2 mutations.

Pharmacological inhibition of BMI1 using PTC-209 significantly attenuated cell proliferation, migration, and cell cycle progression in both SH-SY5Y neuroblastoma cells and primary enteric neural crest cells (ENCCs), whereas BMI1 overexpression produced the opposite effects...Molecular level probing revealed that BMI1 binds to the promoter region of Axin2, an inhibitor of the Wnt signaling pathway, and inhibited Axin2 transcription by increasing H2AK119ub and decreasing H3K4me3 in the Axin2 promoter, thereby hindering Wnt signaling. This study revealed that the BMI1/Axin2/Wnt axis may play an important role in the pathogenesis of HSCR.

The increase in the Bax protein, a key player in apoptosis induction, along with the decrease in the anti-apoptotic protein Bcl-2, suggests the activation of cell death mechanisms. Notably, its targeted impact on the CD44+/CD24- population suggests that niclosamide could enhance the sensitivity of CSCs to treatment, thereby preventing tumor recurrence.

The NOTCH pathway converges with the WNT pathway. Differential expression of the immunohistochemical markers of these pathways helps in the semiquantitation of various epithelial components, guides adjuvant treatment, and patient prognostication.

Notably, Y-99 exerted a significant antiproliferation effect in Wnt-addicted tumor cell lines, accompanied by reduced LRP6 phosphorylation and downregulation of Wnt-related gene expression, including AXIN2 and CCND1. Taken together, these findings highlight that Y-99, which was identified through in silico screening and validated in vitro, is a promising PORCN inhibitor, which has the potential for further research and development.