ANKRD22 (Ankyrin Repeat Domain 22)

Gene expression profiles were obtained from GEO datasets (GSE63514, GSE6791), and RNA sequencing and clinical data were obtained from The Cancer Genome Atlas...ANKRD22 downregulation is associated with poor prognosis in SCC of the cervix. While these findings suggest prognostic relevance, further experimental studies are necessary to validate ANKRD22's clinical utility.

Blocking ANKRD22-mediated M2 polarization inhibited the migration and tube formation capacity of HUVEC cells. Our findings showed that ANKRD22 mediates the malignant progression of LUAD by inducing M2 polarization of tumor-associated macrophages, thereby promoting angiogenesis.

In vivo, silencing of ANKRD22 diminished the tumor size and weight, the expression of Ki-67 and ANKRD22, but increased apoptosis of NPC. ANKRD22 was transcriptionally modulated by MAZ, which promoted proliferation and invasion, but suppressed apoptosis of NPC.

ANKRD22 exhibited strong binding affinity (ΔG = -7.0 kcal/mol in molecular docking and ∆Gbind = -38.66 ± 6.09 kcal/mol in MDs). Taken together, ANKRD22 could be a promising theragnostic target that might be inhibited by fostamatinib, thereby suppressing PC growth.

CXCL2, ANKRD22, SPP1, and C1QB showed strong prognostic characteristics in CESC and significant predictive capabilities for patient outcomes. The study also emphasized the critical role of T cells in CESC progression.

P=N/A, N=200, Not yet recruiting, Chinese University of Hong Kong

P=N/A, N=192, Active, not recruiting, Chinese University of Hong Kong

Single-cell RNA sequencing, spatial transcriptomic studies, and subcutaneous xenograft experiments in mice revealed that Ankrd22 silencing altered the subtype distribution of macrophages, attenuated their proinflammatory activity, and enhanced their protumor activity. Additionally, we identified a small-molecule ANKRD22 upregulator that could aid in the development of novel therapeutics targeting TAM remodeling.

This study revealed the important significance of SM in PC and identified SM-associated molecular subtypes and prognostic model, which provided novel perspectives on the stratification, prognostic prediction, and precision treatment of PC patients.

Besides that, circ_0006225 silencing also repressed cisplatin resistance and tumor growth in lung cancer in vivo. In conclusion, knockdown of circ_0006225 restrained the growth and reduced cisplatin resistance in lung cancer by the miR-1236-3p/ANKRD22 axis, suggesting a better effective therapeutic target for overcoming cisplatin resistance in lung cancer patients.

The identified METTL14-ANKRD22-SLC25A1 axis emerges as a promising therapeutic target for NPC, and also these molecules may serve as novel diagnostic biomarkers.

The AOM/DSS-induced CRC carcinogenesis mouse model in mice indicated that DDX5 deletion due to chr17q loss promoted CRC development, consistent with the findings from the patient samples. Collectively, this study provides an informative resource for understanding the driving events of different stages of CRC and identifying the potential therapeutic targets.