SEMA6D inhibits the malignant progression of triple-negative breast cancer through AURKA
10.19405/j.cnki.issn1000-1492.2025.05.004
- Author:
Jingni Zhou
1
;
Rongrong Zhao
1
;
Wenwu Luo
1
;
Xian Wang
2
;
Qianying Guo
1
;
Zhengsheng Wu
3
Author Information
1. Dept of Pathology , The First Afiliated Hospital of Anhui Medical University , Hefei 230022
2. Dept of Pathology , The Second Afiliated Hospital of Anhui Medical University , Hefei 230601
3. Dept of Pathology , The First Afiliated Hospital of Anhui Medical University , Hefei 230022; Dept of Pathology , School of Basic Medical Sciences , Anhui Medical University , Hefei 230032
- Publication Type:Review
- Keywords:
triple_negative breast cancer;
semaphoring 6D;
AURKA;
migration;
invasion;
EMT
- From:
Acta Universitatis Medicinalis Anhui
2025;60(5):788-795
- CountryChina
- Language:Chinese
-
Abstract:
Objective :To explore the role of semaphoring 6d(SEMA6D) in the malignant progression of triple-negative breast cancer(TNBC).
Methods :Bioinformatics and Immunohistochemistry(IHC) were used to analyze the expression level of SEMA6D in TNBC and paracancer non-tumor tissues and its relationship with patients′ clinicopathological features. MDA-MB-231 cell line stably knocking down the expression of SEMA6D was constructed, and the effects of SEMA6D on migration and invasion of TNBC cells were investigated by Wound-healing assays and Transwell assays. cBioPortal and GEPIA2 databases were used to screen out the gene negatively associated with it, namely aurora kinase A(AURKA). Bioinformatics and IHC were used to analyze the expression level of AURKA in TNBC and paracancer non-tumor tissues and its relationship with patients' clinicopathological features. Western blot assay was used to analyze the expression of AURKA and the effect of epithelial-mesenchymal transition(EMT) makers Claudin-1, N-cadherin and Vimentin after knocking downSEMA6D.
Results: Bioinformatics analysis and IHC results showed that the expression of SEMA6D in TNBC tissues was significantly lower than that in paracancer non-tumor tissues(bothP<0.05). The expression of AURKA in TNBC tissues was significantly higher than that in paracancer non-tumor tissues(bothP<0.05), SEMA6D and AURKA were significantly negatively correlated in TNBC(P<0.01). Both low expression of SEMA6D and high expression of AURKA were positively correlated with tumor size, tumor histological grade, clinical stage and lymph node metastasis in TNBC patients(allP<0.05). The knockdown ofSEMA6Dsignificantly promoted the migration and invasion ability of TNBC cells(bothP<0.01). Western blot results showed that the knockdown ofSEMA6Dupregulated AURKA expression, promoted the expression of N-cadherin and Vimentin, and inhibited the expression of Claudin-1 in tumor cells.
Conclusion :Down-regulation of SEMA6D expression in TNBC may be involved in the malignant progression of TNBC through up-regulation of AURKA expression and promotion of EMT.
- Full text:2026020510150695240信号蛋白6D通过AURKA抑制三阴性乳腺癌的恶性进展_周静妮.pdf
