Role of the TPX2/NCOA5 axis in regulating proliferation, migration, invasion and angiogenesis of breast cancer cells

Abstract

Breast cancer is a common malignant tumor in women. Increasing evidence has demonstrated that nuclear receptor coactivator 5 (NCOA5) and targeting protein for xenopus kinesin-like protein 2 (TPX2) serve vital roles in the progression of breast cancer. However, to the best of our knowledge, the molecular mechanisms underlying the involvement of TPX2/NCOA5 in the development of breast cancer are not fully understood at present. In the present study, the expression levels of NCOA5 and TPX2 were compared between paired non-tumor and tumor tissues of patients with breast cancer using the TNMplot tool. Expression differences of NCOA5 and TPX2 in human breast epithelial cell lines (MCF10A and MCF12A) and human breast cancer cell lines (MCF7 and T47D) were assessed via reverse transcription-quantitative PCR and western blotting. Additionally, proliferation, migration and invasion of breast cancer cells were determined via Cell Counting Kit-8, would healing and transwell assays. In vitro angiogenesis was determined using a tube formation assay. Furthermore, TPX2 was identified as a high-confidence NCOA5 interactor based on BioPlex network data sets. A co-immunoprecipitation assay was adopted to confirm the interaction between TPX2 and NCOA5. The present study revealed that TPX2 and NCOA5 were highly expressed in breast cancer cells. TPX2 interacted with NCOA5 and there was a positive association between TPX2 and NCOA5 expression. NOCA5 knockdown repressed the proliferation, migration, invasion and in vitro angiogenesis of breast cancer cells. In addition, TPX2 knockdown suppressed the proliferation, migration and invasion of breast cancer cells, and inhibited in vitro angiogenesis, and all of these effects were reversed following NCOA5 overexpression. In conclusion, NCOA5 was a downstream target of TPX2 in enhancing proliferation, migration, invasion and angiogenesis of breast cancer cells.