ANKRD17 (Ankyrin Repeat Domain 17)

P=N/A, N=125, Recruiting, Boston Children's Hospital | N=60 --> 125 | Trial completion date: Dec 2026 --> Dec 2030 | Trial primary completion date: Dec 2026 --> Dec 2030

Clinically, higher ANKRD17 expression correlated with aggressive HCC progression. These findings suggest that ANKRD17 enhances metastatic progression in HCC by activating pro-metastatic and pro-survival pathways.

Furthermore, employing these HKGs for normalization, we assessed TNF-α and VEGF expression in tissues and discerned significant disparities among groups. We posit that this constitutes the inaugural delineation of an ideal HKG for experiments utilizing the 4T1 model, particularly in vivo settings.

Our data implies that hypoxia augments circRNA biogenesis which might subsequently play a role in tumor progression.

MALAT1 major transcript levels thus estimated in TNBC cell lines were found to be statistically significantly reduced compared to levels in both MCF-10A cells and luminal breast cancer cell lines, while MALAT1 minority splice variants were found to be increased in almost all breast cancer cell lines. CCSER2-normalized qPCR results indicate MALAT1 downregulation in cell lines representing the more aggressive breast cancer subtype compared to both the normal breast epithelial cell line and the estrogen receptor-positive breast cancer cell lines.

We further show that circANKRD17 acts to accelerate glycolysis in BC cells by acting as a sponge for miR-143 and in turn overrides the repressive effect of miR-143, a well-documented glycolytic repressor, on hexokinase 2 in BC cells, thus resulting in enhanced glycolysis in BC cells. These data suggest the circANKRD17-miR-143 cascade as a novel mechanism in controlling glucose metabolic reprogramming in BC cells and suggest circANKRD17 as a promising therapeutic target to interrupt cancerous glycolysis.