High BTBD7 expression positive is correlated with SLUG-predicted poor prognosis in hormone receptor-negative breast cancer

Hormone receptor-negative breast cancer (HRNBC), which includes triple-negative breast cancer (TNBC) and human epidermal growth factor receptor 2 (HER-2) overexpressing breast cancer, is prone to metastasis and has a poor prognosis. BTB/POZ domain-containing protein 7 (Btbd7) is thought to regulate SLUG and the epithelial-mesenchymal transition (EMT) process. However, the role of Btbd7 in HRNBC is unclear.

The study data indicated that BTBD7 was inversely associated with SLUG expression. Higher BTBD7 was associated with poor clinicopathologic features and prognosis in HRNBC patients. BTBD7 silencing inhibited EMT through regulation of SLUG expression. BTBD7 might act as a potential molecular target for gene therapy in HRNBC patients.

Expression of BTBD7 and SLUG in HRNBC tumor tissue and normal adjacent tissue (NAT) as well as breast cancer cells were characterized by immunohistochemistry and immunofluorescence. MDA-MA-231 cells was transfected with BTBD7 siRNA and detected by qRT-PCR and western blot. Expression levels of Slug and EMT related proteins were detected western blot analysis. cell invasion assays were used to analyse cell invasion ability of MDA-MA-231. GO and KEGG analyses was used to analysis the gene function.

The total positive rate of BTBD7 expression in HRNBC tumor tissue was 66.7%, which was higher than that in NAT (52.1%) and benign breast lesion tissues (20%). Co-expression of SLUG and BTBD7 proteins could be found in HRNBC tissue and MDA-MA-231 cells. BTBD7 silencing significantly up-regulated the epithelial marker E-cadherin, down-regulated the mesenchymal markers α-SMA and SLUG and suppressed the invasion abilities of MDA-MA-231 cells. GO and KEGG analyses based on 322 DEGs showed that BTBD7 may be associated with generic transcription in breast cancer. Conclusions: The study data indicated that BTBD7 was inversely associated with SLUG expression. Higher BTBD7 was associated with poor clinicopathologic features and prognosis in HRNBC patients. BTBD7 silencing inhibited EMT through regulation of SLUG expression. BTBD7 might act as a potential molecular target for gene therapy in HRNBC patients.