Overexpression of NuSAP1 is predictive of an unfavourable prognosis and promotes proliferation and invasion of triple-negative breast cancer cells via the Wnt/β-catenin/EMT signalling axis.

We analysed the effect of expression of nucleolar spindle-associated protein 1 (NuSAP1) on the prognosis of breast cancer (BC) and investigated its potential mechanism of tumourigenicity in triple-negative breast cancer (TNBC) cell lines. We downloaded the RNA-seq breast cancer (BC) data from The Cancer Genome Atlas (TCGA) and screened for the NuSAP1 gene using R software. The clinical data for patients with BC were screened and analysed using R software. A survival curve was drawn using the Kaplan-Meier Plotter. Cell proliferation and invasion were verified by the Cell Counting Kit-8 and Transwell assays. Expression of NuSAP1, the Wnt/β-catenin pathway, and epithelial-mesenchymal-transition-related proteins in TNBC was detected using real-time quantitative polymerase chain reaction (qRT-PCR) and western blotting (WB). Expression of NuSAP1 was upregulated in BC. The change in NuSAP1 expression levels was associated with multiple clinicopathological factors, and the higher the expression of NuSAP1 was, the shorter the survival time. In MDA-MB-231 and BT549 cells, knockdown of NuSAP1 expression resulted in a significant decrease in cell proliferation and invasion; a decrease in expression of cyclin D1, vimentin, Slug, Twist, wnt3a, and pβ-catenin; and an increase in expression of e-cadherin. The results of the sh-NuSAP1 + ov-NuSPA1 group were the opposite of the results of the sh-NuSAP1 group. NuSAP1 is a carcinogen that facilitates progression of TNBC through the Wnt/β-catenin and epithelial-mesenchymal transition pathways.

Sun L ，Shi C ，Liu S ，Zhang E ，Yan L ，Ji C ，Zhao Y ... -  《-》

CircRNA_069718 promotes cell proliferation and invasion in triple-negative breast cancer by activating Wnt/β-catenin pathway.

Zhang J ，Xu HD ，Xing XJ ，Liang ZT ，Xia ZH ，Zhao Y ... -  《-》

LINC01614 activated by SP1 promoted malignant behavior of triple-negative breast cancer cells via the WNT/b-Catenin signaling pathway.

Chen T ，Shi K ，Sun S 《Revista de Investigacion Clinica-Clinical and Translational Investigation》

Nucleolar and spindle associated protein 1 promotes metastasis of cervical carcinoma cells by activating Wnt/β-catenin signaling.

Li H ，Zhang W ，Yan M ，Qiu J ，Chen J ，Sun X ，Chen X ，Song L ，Zhang Y ... -  《JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH》

Upregulation of collagen type X alpha 1 promotes the progress of triple-negative breast cancer via Wnt/β-catenin signaling.

Triple-negative breast cancer (TNBC) is a malignant tumor with high degree of malignancy and lack of effective target treatment. The research aims to explore the role and mechanism of X collagen alpha-1 chain protein (COL10A1 gene) in TNBC. UALCAN and Kaplan-Meier were used to detect the expression of COL10A1 and its role in the prognosis of breast cancer patients. The cells with stably expressing high levels of COL10A1 were obtained by recombinant lentivirus infection. The expression of COL10A1 in cells was temporarily downregulated by siRNA interference fragments. Real-time quantitative polymerase chain reaction and western blot analysis were utilized to detect the changes of COL10A1 mRNA and protein expression. The biological functions of the cells were evaluated by colony formation, cell counting kit-8, cell invasion and wound healing experiments. In addition, the effect of COL10A1 on angiogenesis was investigated by tube formation assay. Xenograft tumor model was used to confirm the effect of COL10A1 on tumorigenicity in vivo and multiplex fluorescent immunohistochemistry to detect multiple proteins simultaneously. The possible molecular mechanism of the function of COL10A1 was speculated through the detection of proteins in functionally related pathways. COL10A1 is highly expressed and is significantly associated with worse overall survival (OS) and recurrence-free survival (RFS) in TNBC. Overexpression of COL10A1 increased the clone formation rate and cell migration capacity of TNBC cells. In the COL10A1 overexpression group, the clone formation rates of MD-MB-231 and BT-549 cells (21.5 ± 0.62, 27.83 ± 3.72)% were significantly higher than those in the control group(15.23 ± 2.79, 19.4 ± 1.47)%, and the relative migration ratio (47.40 ± 3.09, 41.26 ± 4.33)% were higher than those in the control group (34.48 ± 2.03, 21.80 ± 1.03)%. When the expression of COL10A1 was downregulated, the ability of clone formation and wound-healing migration capacity in TNBC cells was weakened. Upregulated COL10A1 in TNBC cells generated more junctions and longer total segments between vascular endothelial cells, and promoted angiogenesis of the cells, and thus enhanced the tumorigenesis. In TNBC, it was found that COL10A1 might affect epithelial-mesenchymal transition (EMT) of the cells through Wnt/β-catenin signaling pathway by the detection of the related pathway proteins. COL10A1 is highly expressed in TNBC, and its high expression leads to poor OS and RFS. COL10A1 may enhance TNBC cell proliferation, migration and tumor-related angiogenesis, and promote tumorigenesis in vivo via Wnt/β-catenin signaling.

Peng J ，Liu X ，Mao Y ，Lv M ，Ma T ，Liu J ，Zhou Q ，Han Y ，Li X ，Wang H ... -  《-》