Baohuoside I Suppresses Invasion of Cervical and Breast Cancer Cells through the Downregulation of CXCR4 Chemokine Receptor Expression

Biochemistry ◽  
2014 ◽  
Vol 53 (48) ◽  
pp. 7562-7569 ◽  
Author(s):  
Buyun Kim ◽  
Byoungduck Park
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Chemokine Receptor ◽  
Breast Cancer Cells ◽  
Receptor Expression ◽  
Chemokine Receptor Expression

scholarly journals Effect of fetal bovine serum on erythropoietin receptor expression and viability of breast cancer cells

2020 ◽  
Vol 27 (2) ◽  
pp. 653-658
Author(s):  
Guan-Young Teo ◽  
Abdullah Rasedee ◽  
Nagi. A. AL-Haj ◽  
Chaw Yee Beh ◽  
Chee Wun How ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Bovine Serum ◽  
Breast Cancer Cells ◽  
Fetal Bovine Serum ◽  
Erythropoietin Receptor ◽  
Receptor Expression ◽  
Fetal Bovine

scholarly journals Involvement of the ERK/HIF-1α/EMT Pathway in XCL1-Induced Migration of MDA-MB-231 and SK-BR-3 Breast Cancer Cells

2020 ◽  
Vol 22 (1) ◽  
pp. 89
Author(s):  
Ha Thi Thu Do ◽  
Jungsook Cho
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Chemokine Receptor ◽  
Intracellular Signaling ◽  
Breast Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Mitogen Activated Protein Kinase ◽  
Mesenchymal Transition

Chemokine–receptor interactions play multiple roles in cancer progression. It was reported that the overexpression of X-C motif chemokine receptor 1 (XCR1), a specific receptor for chemokine X-C motif chemokine ligand 1 (XCL1), stimulates the migration of MDA-MB-231 triple-negative breast cancer cells. However, the exact mechanisms of this process remain to be elucidated. Our study found that XCL1 treatment markedly enhanced MDA-MB-231 cell migration. Additionally, XCL1 treatment enhanced epithelial–mesenchymal transition (EMT) of MDA-MB-231 cells via E-cadherin downregulation and upregulation of N-cadherin and vimentin as well as increases in β-catenin nucleus translocation. Furthermore, XCL1 enhanced the expression of hypoxia-inducible factor-1α (HIF-1α) and phosphorylation of extracellular signal-regulated kinase (ERK) 1/2. Notably, the effects of XCL1 on cell migration and intracellular signaling were negated by knockdown of XCR1 using siRNA, confirming XCR1-mediated actions. Treating MDA-MB-231 cells with U0126, a specific mitogen-activated protein kinase kinase (MEK) 1/2 inhibitor, blocked XCL1-induced HIF-1α accumulation and cell migration. The effect of XCL1 on cell migration was also evaluated in ER-/HER2+ SK-BR-3 cells. XCL1 also promoted cell migration, EMT induction, HIF-1α accumulation, and ERK phosphorylation in SK-BR-3 cells. While XCL1 did not exhibit any significant impact on the matrix metalloproteinase (MMP)-2 and -9 expressions in MDA-MB-231 cells, it increased the expression of these enzymes in SK-BR-3 cells. Collectively, our results demonstrate that activation of the ERK/HIF-1α/EMT pathway is involved in the XCL1-induced migration of both MDA-MB-231 and SK-BR-3 breast cancer cells. Based on our findings, the XCL1–XCR1 interaction and its associated signaling molecules may serve as specific targets for the prevention of breast cancer cell migration and metastasis.

Detection and downregulation of type I IGF receptor expression by antibody-conjugated quantum dots in breast cancer cells

2008 ◽  
Vol 114 (2) ◽  
pp. 277-285 ◽  
Author(s):  
Hua Zhang ◽  
Deepali Sachdev ◽  
Chun Wang ◽  
Allison Hubel ◽  
Martine Gaillard-Kelly ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Quantum Dots ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Receptor Expression ◽  
Type I ◽  
Type I Igf Receptor ◽  
Igf Receptor

Chronobiological features of melatonin receptors (MT1) expression in breast cancer cells.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e12581-e12581
Author(s):  
Alexandre Tavartkiladze ◽  
Ani Gvajaia ◽  
Pati Revazishvili
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Venous Blood ◽  
Receptor Expression ◽  
Melatonin Receptors ◽  
Breast Cancer Patients ◽  
Melatonin Receptor ◽  
Circadian Expression ◽  
Immunocytochemical Method

e12581 Background: According to WHO data, Breast Cancer is the most prevalent malignancy in women. The biological role of Melatonin in the etiology and pathogenesis of the tumour disease has already been approved by a number of research studies. The purpose of our investigation was the assessment of features of Melatonin receptor circadian expression in circulating tumour cells of breast cancer (CTCs). Methods: We observed 34 patients (aged 36-68) with breast cancer (various immunophenotypes). CTCs were separated from patients’ venous blood every third day, in 02:00-04:00 pm and in 02:00-04:00 am intervals. The cells were taken from each patient 4 times. On CTCs, MT1 – receptor expression was assessed using immunocytochemical method. Results: Results of the study revealed that Melatonin receptor expression in breast cancer patients is characterised by the noticable circadian rhythmics. MT1–receptor expression peak by CTCs was detected at 02:00-04:00 am i.e. at night. The less aggressive tumor the higher is the extent of the receptor expression (density). Respectively, in hormone dependent and Her2/neu (negative) tumors the highest expression of the MT1–receptor occurs in hormone dependent and Her2/neu(positive) tumors–medium expression and in triple negative breast Cancer (TNBC) cells–the lowest expression, while in some TNBC–circulating tumor cells MT1 receptor expression has not been detected at all. Conclusions: Hence, based on our the results, we can conclude that Melatonin as the expression of main biochemical marker receptors of bio-rhythms in breast cancer cells, has highly expressed chronobiological nature and directly correlates with histological types of tumor, that provides conditions for the development of new chronotherapeutic strategies in breast cancer treatment.

Urokinase-like Plasminogen Activator Receptor Expression on Disseminated Breast Cancer Cells

2001 ◽  
Vol 10 (1) ◽  
pp. 141-145 ◽  
Author(s):  
Florian Tögel ◽  
Chonda Datta ◽  
Anita Badbaran ◽  
Nicolaus Kröger ◽  
Helmut Renges ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Plasminogen Activator ◽  
Breast Cancer Cells ◽  
Receptor Expression ◽  
Plasminogen Activator Receptor
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