Silence of TPPP3 suppresses cell proliferation, invasion and migration via inactivating NF-κB/COX2 signal pathway in breast cancer cell.

Abstract

Malignant phenotypes are leading causes of death in patients with breast cancer (BC). Previously, it has been proved that tubulin polymerization promoting protein 3 (TPPP3) participates in cell progressions in several human cancers. Little is known about the functions of TPPP3 in BC. Herein, we detected the expression of TPPP3 in 54 clinical BC tissues and two BC cell lines by immunohistochemistry and Western blot. CCK-8, wound healing, colony formation and Transwell assays were used to assess cell proliferation, clone formation, invasion and migration of MCF-7 and T47D cells after transfection with TPPP3 siRNA. Meanwhile, related-proteins expression was detected using Western blot. TPPP3 was found to be highly expressed in the tissues from the patients with BC. Poor outcomes were associated with the high expression of TPPP3 in all patients with BC. When MCF-7 and T47D cells receiving TPPP3 siRNA transfection, the capacities of proliferation, clone formation, invasion and migration were suppressed and the expression of MMP-2/-9 and NF-κB p65/COX2 was notably reduced. The dual-luciferase reporter assay indicated that the promoter regions of NF-κB p65 could combine to TPPP3. Overall, the present study demonstrated that TPPP3 played a significant role in BC, and its inhibition lead to the suppression of NF-κB/COX-2 signalling pathway along with the reduction of malignant phenotypes. SIGNIFICANCE OF THIS STUDY: Previously, it has been proved that tubulin polymerization promoting protein 3 (TPPP3) participates in cell progression in several human cancers. Little is known about the function of TPPP3 in BC. Our study was the first direct evidence to support the role of TPPP3 in tumorigenesis and metastasis of BC. Although the underlying mechanism has not been fully delineated, these findings suggested that TPPP3 was an important factor in the tumour progression and metastasis of BC cells and provided a molecular basis for potential therapeutic implications in the treatment of patients with BC.