scholarly journals PTPRA facilitates cancer growth and migration via the TNF‑α‑mediated PTPRA‑NF‑κB pathway in MCF‑7 breast cancer cells

2020 ◽  
Vol 20 (5) ◽  
pp. 1-1
Author(s):  
Canfeng Lin ◽  
Shubo Xin ◽  
Xiaoguang Huang ◽  
Feiran Zhang
2014 ◽  
Vol 344 (1) ◽  
pp. 129-137 ◽  
Author(s):  
Xue-Gang Luo ◽  
Chun-Ling Zhang ◽  
Wen-Wen Zhao ◽  
Zhi-Peng Liu ◽  
Lei Liu ◽  
...  

2020 ◽  
Vol 10 (4) ◽  
pp. 507-511
Author(s):  
Jie Zhao ◽  
Guoqin Jiang

Background: The present study focused on the effects of dual-targeting MiR-4282 and ABCC4 on drug resistance of breast cancer cells and the molecular mechanisms, expecting to provide a new approach for treating drug-resistant breast cancer. Material and methods: MiR-4282 overexpression and ABCC4 interference double gene lentiviral vectors were constructed. CCK-8, flow cytometry, Transwell assay and scratch assay were used to determine the overexpression of A and B Group, as well as the expression, proliferation, apoptosis, invasion and migration of C and D Group cells respectively. CCK-8 assay was applied to detect doxorubicin sensitivity. WB was used to detect the expressions of ABCC4, p53 and P-gp proteins in each group. Results: Overexpression of MiR4282 and downregulation of ABCC4 expression inhibited proliferation, invasion and migration of the cells, impeded normal cell cycle progression, and promoted apoptosis of the cells. The effect of dual-targeting MiR-4282 and ABCC4 on cell function is more pronounced. The results of CCK-8 assay showed that overexpression of MiR-4282 and downregulation of ABCC4 expression significantly promoted the sensitivity of MCF-7-ADR to doxorubicin, and dual-targeting MiR-4282 and ABCC4 were sensitive to the cell. The promotion effect is more obvious. WB analysis showed that overexpression of MiR-4282 and downregulation of ABCC4 expression significantly inhibited p53 protein in the cells, plus the inhibitory effects of dual-targeting MiR-4282 and ABCC4 were more obvious. MiR-4282 overexpression could prominently inhibit P-gp protein expression in the cells. Conclusion: Overexpression of MiR-4282 and downregulation of ABCC4 expression inhibit the proliferation, invasion and migration of MCF-7-ADR.


2009 ◽  
Vol 390 (7) ◽  
Author(s):  
Aurélie Cazet ◽  
Sophie Groux-Degroote ◽  
Béatrice Teylaert ◽  
Kyung-Min Kwon ◽  
Sylvain Lehoux ◽  
...  

Abstract The disialoganglioside GD3 is an oncofetal marker of a variety of human tumors including melanoma and neuroblastoma, playing a key role in tumor progression. GD3 and 9-O-acetyl-GD3 are overexpressed in approximately 50% of invasive ductal breast carcinoma, but no relationship has been established between disialoganglioside expression and breast cancer progression. In order to determine the effect of GD3 expression on breast cancer development, we analyzed the biosynthesis of gangliosides in several breast epithelial cell lines including MDA-MB-231, MCF-7, BT-20, T47-D, and MCF10A, by immunocytochemistry, flow cytometry, and real-time PCR. Our results show that, in comparison to tumors, cultured breast cancer cells express a limited pattern of gangliosides. Disialogangliosides were not detected in any cell line and GM3 was only observed at the cell surface of MDA-MB-231 cells. To evaluate the influence of GD3 in breast cancer cell behavior, we established and characterized MDA-MB-231 cells overexpressing GD3 synthase. We show that GD3 synthase expressing cells accumulate GD3, GD2, and GT3 at the cell surface. Moreover, GD3 synthase overexpression bypasses the need of serum for cell growth and increases cell migration. This suggests that GD3 synthase overexpression may contribute to increasing the malignant properties of breast cancer cells.


2021 ◽  
Author(s):  
Didem Turgut Cosan ◽  
Ahu SOYOCAK ◽  
İbrahim Uğur ÇALIŞ

Abstract Molecular receptor signaling mechanisms play an important role in many pathophysiological processes, including breast cancer. The spread of cancer from peripheral tissue to distant organs by metastasis is the cause of death of most breast cancer patients. For that reason, the most important step in the treatment of cancer is to prevent metastasis. Sphingosine-1-phosphate receptors and potassium channels play role of cancer cell migration, invasion and they may interact with each other in the progression of cancer. In this study, it was aimed to determine the effects of combined silencing of receptors and channels on the invasion and migration of MCF-7 and MDA-MB-231 breast cancer cells and their interactions on cells. We examined the expression levels of S1P1, S1P3, Kv1.3, and Kv10.1 in MCF-7 and MDA-MB-231 breast cancer cell lines by qRT-PCR. The effects of migration and invasion of breast cancer cells were determined through invasian and wound healing assays. It was observed that high invasion and lateral motility in cells decreased with the combined silencing of S1P1, S1P3, Kv1.3 and Kv10.1 in both cell types. It has been determined that silencing the receptors and channels together is more effective than silencing individually. Our data demonstrated the roles of S1P receptors and potassium channels were associated with invasion and migration signaling pathway. Therefore, these are might be possible therapeutic target for breast cancer metastasis.


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