Identification of Seven Hub Genes as the Novel Biomarkers in Triple-negative Breast Cancer and Breast Cancer Metastasis

2020 ◽  
Author(s):  
Huanxian Wu ◽  
Huining Lian ◽  
Qianqing Chen ◽  
Jinlamao Yang ◽  
Baofang Ou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Protein Interactions ◽  
Cancer Metastasis ◽  
Triple Negative ◽  
Malignant Tumors ◽  
Underlying Disease ◽  
Breast Cancer Metastasis ◽  
Hub Genes ◽  
Cancer Subtypes

Abstract Background: Breast cancer is one of the most common malignant tumors with the highest morbidity and mortality among women. Compared with the other breast cancer subtypes, Triple-negative breast cancer (TNBC) has a higher probability of recurrence and is prone to distant metastasis. To reveal the underlying disease mechanisms and identify more effective biomarkers for TNBC and breast cancer metastasis. Methods: Gene Ontology and KEGG pathway analysis were used for investigating the role of overlapping differentially expressed genes (DEGs). Hub genes among these DEGs were determined by the protein-protein interactions network analysis and CytoHubba. Oncomine databases were used for verifying the clinical relevance of hub genes. Furthermore, the differences in the expression of these genes in cancer and normal tissues were validated in the cellular, animal and human tissue.Results: Seven hub genes, including TTK, KIF11, SPAG5, RRM2, BUB1, CDCA8 and CDC25C, were identified that might be associated with TNBC and breast cancer metastasis. Meanwhile, these genes have been verified highly expressed in tumor cells and tumor tissues, and patients with higher expression of these genes have a poorer prognosis. Conclusions: Seven hub genes were potential biomarkers for the diagnosis and therapy of TNBC and breast cancer metastasis.

scholarly journals CPSF4 promotes triple negative breast cancer metastasis by upregulating MDM4

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Kaping Lee ◽  
Qiufan Zheng ◽  
Qianyi Lu ◽  
Fei Xu ◽  
Ge Qin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Cancer Metastasis ◽  
Triple Negative ◽  
Breast Cancer Metastasis

scholarly journals DCAF13 promotes triple-negative breast cancer metastasis by mediating DTX3 mRNA degradation

Cell Cycle ◽  
2020 ◽  
Vol 19 (24) ◽  
pp. 3622-3631
Author(s):  
Jiazhe Liu ◽  
Hongchang Li ◽  
Anwei Mao ◽  
Jingfeng Lu ◽  
Weiyan Liu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Cancer Metastasis ◽  
Triple Negative ◽  
Mrna Degradation ◽  
Breast Cancer Metastasis

scholarly journals MicroRNA-200b targets protein kinase Cα and suppresses triple-negative breast cancer metastasis

2014 ◽  
Vol 35 (10) ◽  
pp. 2254-2263 ◽  
Author(s):  
Brock Humphries ◽  
Zhishan Wang ◽  
Aaron L. Oom ◽  
Theresa Fisher ◽  
Dongfeng Tan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Protein Kinase ◽  
Triple Negative Breast Cancer ◽  
Cancer Metastasis ◽  
Triple Negative ◽  
Breast Cancer Metastasis ◽  
Protein Kinase Cα

scholarly journals Sanguisorba officinalis L. Suppresses Triple-Negative Breast Cancer Metastasis by Inhibiting Late-Phase Autophagy via Hif-1α/Caveolin-1 Signaling

2020 ◽  
Vol 11 ◽  
Author(s):  
Neng Wang ◽  
Gulizeba Muhetaer ◽  
Xiaotong Zhang ◽  
Bowen Yang ◽  
Caiwei Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Molecular Mechanisms ◽  
Cancer Metastasis ◽  
Triple Negative ◽  
Late Phase ◽  
Breast Cancer Metastasis ◽  
Chinese Herbs ◽  
Caveolin 1 ◽  
Sanguisorba Officinalis

Sanguisorba officinalis L. (SA) is a common herb for cancer treatment in the clinic, particularly during the consolidation phase to prevent occurrence or metastasis. Nevertheless, there are limited studies reporting the molecular mechanisms about its anti-metastatic function. It is well demonstrated that autophagy is one of the critical mechanisms accounting for metastasis and anti-cancer pharmacological actions of Chinese herbs. On the threshold, the regulatory effects and molecular mechanisms of SA in suppressing autophagy-related breast cancer metastasis were investigated in this study. In vitro findings demonstrated that SA potently suppressed the proliferation, colony formations well as metastasis process in triple-negative breast cancer. Network and biological analyses predicted that SA mainly targeted caveolin-1 (Cav-1) to induce anti-metastatic effects, and one of the core mechanisms was via regulation of autophagy. Further experiments—including western blotting, transmission electron microscopy, GFP-mRFP-LC3 immunofluorescence, and lysosomal-activity detection—validated SA as a potent late-stage autophagic inhibitor by increasing microtubule-associated light chain 3-II (LC3-II) conversion, decreasing acidic vesicular-organelle formation, and inducing lysosomal dysfunction even under conditions of either starvation or hypoxia. Furthermore, the anti-autophagic and anti-metastatic activity of SA was Cav-1-dependent. Specifically, Cav-1 knockdown significantly facilitated SA-mediated inhibition of autophagy and metastasis. Furthermore, hypoxia inducible factor-1α (Hif-1α) overexpression attenuated the SA-induced inhibitory activities on Cav-1, autophagy, and metastasis, indicating that SA may have inhibited autophagy-related metastasis via Hif-1α/Cav-1 signaling. In both mouse breast cancer xenograft and zebrafish xenotransplantation models, SA inhibited breast cancer growth and inhibited late-phase autophagy in vivo, which was accompanied by suppression of Hif-1α/Cav-1 signaling and the epithelial-mesenchymal transition. Overall, our findings not only indicate that SA acts as a novel late-phase autophagic inhibitor with anti-metastatic activities in triple-negative breast cancer, but also highlight Cav-1 as a regulator in controlling late-phase autophagic activity.

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