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 studyPreviously, 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.

Tubulin polymerization promoting protein family member 3 (TPPP3) overexpression inhibits cell proliferation and invasion in nasopharyngeal carcinoma

“…The mRNA expression levels of TPPP3 from the Oncomine database were significantly elevated in colorectal carcinoma and invasive ductal breast carcinoma ( Figure 1(a-b) ), which is consistent with previous published results [ 9 , 11 ]. However, this study analyzed NPC datasets GSE12452, GSE53819 and GSE61218, and found the mRNA expression levels of TPPP3 in NPC tissues were significantly lower than those in normal nasopharyngeal tissues ( Figure 1(c-e) ).…”

RSRC2 Expression Inhibits Malignant Progression of Triple-Negative Breast Cancer by Transcriptionally Regulating SCIN Expression

“…Further, the in vitro experiment demonstrated that RSRC2 could inhibit the MDA-MB-231 cells and MDA-MB-453 cells clonogenic ability, adhesion, migration and invasion ability. The transcriptome array data analysis identified differentially expressed genes in the MDA-MB-231 shRSRC2 cells and control cells and identified SCIN, IL6, CXCL8, CXCL1, PTGS2, IL1B, NOS3, ICAM1, moesin and DCAF6, which were reported to be involved in cell proliferation, migration and cell adhesion [ 15 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 ]. The intersection set analysis of the bioinformatics database and transcriptome array data identified six common genes, FSTL1, GDF15, IQSEC2, KDM3A, LTC4S and TCTEX1D4, in which most of them were involved in tumor cell proliferation and growth [ 29 , 30 , 31 , 32 , 33 , 34 ].…”

TPPP3 promote epithelial-mesenchymal transition via Snail1 in glioblastoma

“…by different ways. But in breast cancer 27 and non-small cell lung cancer 9 , there was a carcinogenic effect. Our research found that TPPP3 was an oncogene in glioma cells, which promoted the malignant biological behavior of glioblastoma cells.…”