The Role of MEKK3 Signaling Pathway in the Resistance of Breast Cancer Cells to TNF-Alpha-Mediated Apoptosis

2006 ◽  
Author(s):  
Ling Yu ◽  
Qjaojia Huang ◽  
Bing Su
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Breast Cancer Cells ◽  
Tnf Alpha

scholarly journals APRIL and BAFF increase breast cancer cell stemness

2017 ◽  
Author(s):  
Vasiliki Pelekanou ◽  
George Notas ◽  
Paraskevi Athanasouli ◽  
Konstantinos Alexakis ◽  
Fotini Kiagiadaki ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Breast Cancer Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Pluripotency Genes

AbstractRecent advances in cancer immunology revealed immune-related properties of cancer cells as novel promising therapeutic targets. The two TNF superfamily members, APRIL and BAFF even though were primarily studied in lymphocyte maturation, they have also been associated with tumor growth and aggressiveness in a number of solid tumors, including breast cancer. In the present work we studied the effect of APRIL and BAFF on epithelial to mesenchymal transition and migration of breast cancer cells, and their action on the sub-population of cancer stem cells identified by autofluorescence and ALDH activity. Their action on an number of pluripotency genes was examined and breast cancer stem cell ability to form mammospheres was also utilized. The receptor and the signaling pathway involved as well as the role of steroid hormones in their action were also investigated. Our findings show that both APRIL and BAFF increase epithelial to mesenchymal transition and migratory capacity of breast cancer cells, as well as cancer stem cell numbers, by inducing pluripotency genes such as KLF4 and NANOG. These effects are mediated by their common receptor BCMA and the JNK signaling pathway. Interestingly, androgens enhance APRIL transcription and subsequently its pluripotency effect. In conclusion, our data support the significant role of APRIL and BAFF in breast cancer disease progression and provide evidence for a new possible mechanism of therapy resistance, that could be particularly relevant in aromatase inhibitors-treated patients, were local androgen is increased.

scholarly journals Linc00514 promotes breast cancer metastasis and M2 polarization of tumor-associated macrophages via Jagged1-mediated notch signaling pathway

2020 ◽  
Vol 39 (1) ◽  
Author(s):  
Sifeng Tao ◽  
Qiang Chen ◽  
Chen Lin ◽  
Haiying Dong
Keyword(s):  
Breast Cancer ◽  
Notch Signaling ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Breast Cancer Cells ◽  
Cancer Metastasis ◽  
Notch Signaling Pathway ◽  
M2 Macrophage ◽  
M2 Polarization

Abstract Background Tumor-associated macrophages (TAMs) and tumor cells are important components of the tumor microenvironment. M2 polarization of TAMs, which is a major actor in breast cancer malignancy and metastasis, can be induced by breast cancer cells. However, the potential mechanisms of the interaction between breast cancer cells and TAMs remain unclear. Methods The candidate breast cancer-associated long non-coding RNAs (lncRNAs) were analyzed using the GEO database. Functional assays, including MTT assay, Transwell assay, and EdU labeling detection, were performed to investigate the oncogenic role of linc00514 in breast cancer progression. The co-culture and ELISA assays were used to assess the role of linc00514 in macrophage recruitment and M2 polarization. RNA immunoprecipitation, RNA pull-down, and luciferase reporter assays were applied to determine the mechanism of linc00514 in breast cancer metastasis. Mouse xenograft models, mouse pulmonary metastatic models, and mouse primary tumor models were used to assess the role of linc00514 in M2 macrophage polarization and breast cancer tumorigenicity. Results Linc00514 was highly expressed in clinical breast cancer tissues and breast cancer cell lines. Overexpression of linc00514 promoted the proliferation and invasion of breast cancer cells and increased xenograft tumor volumes and pulmonary metastatic nodules. Overexpression of linc00514 also increased the percentage of macrophages expressing M2 markers CD206 and CD163. Mechanistically, linc00514 promoted Jagged1 expression in a transcriptional manner by increasing the phosphorylation of a transcription factor STAT3. Subsequently, Jagged1-mediated Notch signaling pathway promoted IL-4 and IL-6 secretions in breast cancer cells and ultimately inducing M2 polarization of macrophages. Conclusion Linc00514 plays an important role in regulating breast cancer tumorigenicity and M2 macrophage polarization via Jagged1-mediated Notch signaling pathway.

The Mechanism of Adaptation of Breast Cancer Cells to Hypoxia: Role of AMPK/mTOR Signaling Pathway

2016 ◽  
Vol 160 (4) ◽  
pp. 555-559 ◽  
Author(s):  
D. V. Sorokin ◽  
A. M. Scherbakov ◽  
I. A. Yakushina ◽  
S. E. Semina ◽  
M. V. Gudkova ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Breast Cancer Cells ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway

The role of simvastatin in inhibiting migration and proliferation of breast cancer cells through Rho/ROCK signaling pathway

2016 ◽  
Vol 5 (1) ◽  
pp. 10
Author(s):  
Erwin Danil Yulian ◽  
Muchlis Ramli ◽  
Rianto Setiabudy ◽  
Nurjati Chairani Siregar ◽  
Arleni Bustami ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Breast Cancer Cells

Mechanism of estrogen-induced apoptosis in breast cancer cells: Role of the NF-κB signaling pathway

2007 ◽  
Vol 72 (3) ◽  
pp. 320-327 ◽  
Author(s):  
Yu. S. Lobanova ◽  
A. M. Scherbakov ◽  
V. A. Shatskaya ◽  
M. A. Krasil’nikov
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Breast Cancer Cells ◽  
Induced Apoptosis
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