COPB2 is up‐regulated in breast cancer and plays a vital role in the metastasis via N‐cadherin and Vimentin
Autor: | Dependra Tamang, Yubaraj Thapa, Chen Zheng, Xiaohe Ye, Ruida Quan, Namrata Sindan, Ouchen Wang, Duping Huang, Erjie Xia, Adheesh Bhandari, Namita Sindan |
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Rok vydání: | 2019 |
Předmět: |
Adult
0301 basic medicine Epithelial-Mesenchymal Transition Breast Neoplasms Vimentin Coatomer Protein Metastasis 03 medical and health sciences breast cancer 0302 clinical medicine Breast cancer Downregulation and upregulation medicine Humans Cell Proliferation Oncogene biology Cadherin business.industry EMT COPB2 Original Articles Cell Biology Middle Aged Cadherins medicine.disease Gene Expression Regulation Neoplastic 030104 developmental biology Lymphatic Metastasis 030220 oncology & carcinogenesis Cohort MCF-7 Cells Cancer research biology.protein Molecular Medicine Female Original Article business |
Zdroj: | Journal of Cellular and Molecular Medicine |
ISSN: | 1582-4934 1582-1838 |
Popis: | Breast cancer (BC) is a common malignant tumour for the adult female and its relative incidence has increased continuously in recent years. The primary molecular mechanisms of breast tumourigenesis remain unclear. With the sequencing technology, we found that coatomer protein complex subunit beta 2 (COPB2) gene is overexpressed in breast cancer tissues. However, the biological function of COPB2 in BC has yet to be determined. This current research demonstrates, significant up‐regulation of COPB2 in tissues of breast cancer while comparing the adjacent normal tissue both invalidated cohort and TCGA cohort. Up‐regulated expression of COPB2 was correlated with lymph node metastasis (LNM) and oestrogen receptor (ER) in the TCGA cohort and a high level of COPB2 was associated with age and lymph node metastasis in the validated cohort. Besides, logistic analysis illustrated in BC patient COPB2 expression, tumour size, age, ER and disease stage were independent high‐risk factors of LNM. Loss of function experiments revealed that down‐regulation of COPB2 could inhibit capacities of proliferation and cell invasion in MDA‐MB‐231 and BT‐549 cell lines. Moreover, underexpression of COPB2 could decrease the EMT‐related protein N‐cadherin and vimentin which may lead to cell invasion. This current research provides new shreds of evidence that COPB2 overexpression shows significant character in the progression of breast cancer. To best of our knowledge, our findings indicated that COPB2 was vital oncogene which was associated with breast cancer. |
Databáze: | OpenAIRE |
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