Suppression of the proliferation and invasion of breast cancer cells by ST7L occurs through inhibition of activation of Wnt/GSK‐3β/β‐catenin signalling

Abstract Emerging evidence has indicated that suppression of tumorigenicity 7‐like ( ST 7L) is a tumour suppressor in multiple types of cancers. However, the functional involvement of ST 7L has not been studied in breast cancer. In the present study, we aimed to investigate the potential biological function of ST 7L in breast cancer. Herein, we found that ST 7L expression was frequently downregulated in breast cancer cell lines. Functional assays revealed that ST 7L overexpression significantly inhibited the proliferation and invasion of breast cancer cells, while ST 7L silencing showed opposite effect. Notably, ST 7L was found to decrease glycogen synthase kinase ( GSK )‐3β phosphorylation and downregulate active β‐catenin protein expression, thereby leading to repression of β‐catenin transcriptional activity. Activation of Wnt/β‐catenin signalling by treatment of GSK ‐3β inhibitor significantly abrogated ST 7L‐mediated antitumour effect. Additionally, ST 7L overexpression blunted the tumorigenicity of breast cancer cells in vivo in xenograft mice. Taken together, our results demonstrate that ST 7L exerts antitumor function in breast cancer associated with the suppression of Wnt/β‐catenin signalling, suggesting ST 7L as a potential therapeutic target for breast cancer.