ANIB1 (Aneurysm intracranial berry 1)

Notably, GR signaling selectively activated pathways driven by Myc in the AIB1 isoform-expressing population, and the reduction of Myc reduced invasion. These findings identify the emergence of an AIB1 isoform-expressing subpopulation as a key mechanism driving progression in TNBC and suggest sensitivity to GR-targeted therapies.

Our findings provide new clues that perturbation of normal homeostatic levels of AIB1 is linked with endometrial cancer. These findings suggest that targeting AIB1-mediated regulation of aerobic glycolysis may offer a novel therapeutic approach for endometrial cancer with high AIB1 expression, opening new avenues for personalized diagnostics and treatment strategies in this disease.

DGUOK-AS1 is a good predictor of prognosis. Thus, the DGUOK-AS1/microRNA-145-5p/SIX1 axis strongly links DNL to tumor growth and metastasis and may become an avenue for liver cancer therapeutic intervention.

Here we review the normal and pathological functions of AIB1 in regard to its ERα-dependent and ERα-independent actions, as well as its genomic conservation and protein evolution. We also outline the efforts to target AIB1 in the treatment of breast cancer.

The expression level of AIB1 is correlated with the therapeutic effect of tamoxifen in breast cancer. Its high expression can cause tamoxifen resistance, while AR positive and High expression of AIB1 are more likely to cause tamoxifen resistance, and AIB1 can be used as an independent influencing factor for breast cancer tamoxifentreatment.

Knockdown of AIB1 expression in E6E7 immortalized human cervical cells significantly abolished cell proliferation. Taken together, these data support AIB1 as a novel target of HPV E6 and a biomarker of cervical cancer progression.

In conclusion, we provide a mechanistic interpretation to explain the differential role of PR isoforms in metastatic growth and highlight the therapeutic benefit of using antiprogestins in PRA-H tumors. The therapeutic effect of progestins in PRB-H tumors is suggested.

Collectively, these findings suggest that NCOA3 is critical in the initiation and development of thyroid cancer, and might be a possible marker for prognosis and therapy.

Cellular crosstalk was inhibited by the PPARγ agonist efatutazone but was enhanced by treatment with the GR agonist dexamethasone. In conclusion, expression of the AIB1Δ4-selective cistrome in a small subpopulation of cells triggers an "enabler" phenotype hallmarked by an invasive transcriptional program and collective malignant progression in a heterogeneous tumor population.