ANKRD22 enhances breast cancer cell malignancy by activating the Wnt/β-catenin pathway via modulating NuSAP1 expression

Abstract

Breast cancer is one of the most prevalent malignancies in women worldwide. Although great progress has been achieved in the diagnosis and treatment of breast cancer, the prognosis of patients with breast cancer is still poor due to distal recurrence and metastasis after surgery. This study demonstrated that the expression level of ankyrin repeat domain 22 (ANKRD22) in human breast cancer tissues was significantly higher than that in normal breast tissues. ANKRD22 knockdown inhibited the proliferation, invasion, and epithelial-mesenchymal transition (EMT) of breast cancer cells. Further research indicated that ANKRD22 regulated the expression of nucleolar and spindle-associated protein 1 (NuSAP1) and then the activation of Wnt/β-catenin signaling pathway. Moreover, overexpression of NuSAP1 reversed the inhibitory effects of ANKRD22 knockdown on the proliferation, invasion, and EMT of breast cancer cells. In summary, this study demonstrated that ANKRD22 enhanced breast cancer cell malignancy by activating the Wnt/β-catenin pathway via modulating NuSAP1 expression, which might shed light on new therapeutic approaches for breast cancer.

Gene expression signatures of individual ductal carcinoma in situ lesions identify processes and biomarkers associated with progression towards invasive ductal carcinoma

“…Notably, down regulation of HOXC10 , HOXC11 or MNX1 has been reported to reduce cell proliferation in a variety of different cancers 49 – 52 , so could suggest a possible quiescent state prior to invasion. Similarly, knockdown of the ankyrin repeat domain 22 gene, ANKRD22 , inhibited the proliferation, invasion and epithelial-to-mesenchymal transition of breast cancer cells 53 , and a number of studies have reported high levels of expression being associated with poor outcome in non-small cell lung cancer 54 and prostate cancer 55 , an inverse correlation to what we observe here with a ductal in situ disease. The adenylate cyclase 5 gene, ADCY5 , is thought to be regulated by the expression of FOXP1 , a tumour suppressor.…”

Creating a ‘Timeline’ of ductal carcinoma in situ to identify processes and biomarkers for progression towards invasive ductal carcinoma

“…Notably, down regulation of HOXC10 , HOXC11 or MNX1 has been reported to reduce cell proliferation in a variety of different cancers 49-52 , so could suggest a possible quiescent state prior to invasion. Similarly, knockdown of the ankyrin repeat domain 22 gene, ANKRD22 , inhibited the proliferation, invasion and epithelial-to-mesenchymal transition of breast cancer cells 53 , and a number of studies have reported high levels of expression being associated with poor outcome in non-small cell lung cancer 54 and prostate cancer 55 , an inverse correlation to what we observe here with a ductal in situ disease. The adenylate cyclase 5 gene, ADCY5 , is thought to be regulated by the tumour suppressor gene FOXP1 , and knockdown of FOXP1 was followed by a significant upregulation of genes attributed to chemokine signalling pathways, including ADCY5 56 .…”

Genome-Wide Association Analysis and Genomic Prediction of Thyroglobulin Plasma Levels

“…According to the GTEx portal, this allele is also associated with an increase in Ankyrin repeat domain-containing protein 22 (ANKRD22) expression in the esophageal mucosa (although a significant association between this SNP and ANKRD22 expression was not observed in thyroid tissue). ANKRD22 can activate the Wnt/β-catenin signaling pathway [49] (thus, it can consequently lead to an increase in TG transcription (described earlier in the text) [26]). This SNP (rs11202702) is located within the intronic region of the renalase gene (RNLS).…”