Effects of CSK Homologous Kinase Overexpression on HER2/Neu-Mediated Signal Transduction Pathways in Breast Cancer Cells

2003 ◽  
Author(s):  
Radoslaw Zagozdzon ◽  
Hava Avraham
Keyword(s):  
Breast Cancer ◽  
Signal Transduction ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Signal Transduction Pathways

Oestrogen directly stimulates growth factor signal transduction pathways in human breast cancer cells

1991 ◽  
Vol 40 (1-3) ◽  
pp. 215-221 ◽  
Author(s):  
Bart van der Burg ◽  
Rolf P. de Groot ◽  
Linda Isbrücker ◽  
Wiebe Kruijer ◽  
Siegfried W. de Laat
Keyword(s):  
Breast Cancer ◽  
Signal Transduction ◽  
Growth Factor ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Signal Transduction Pathways ◽  
Human Breast Cancer Cells ◽  
Human Breast

scholarly journals Oleic acid induces migration through a FFAR1/4, EGFR and AKT-dependent pathway in breast cancer cells

2019 ◽  
Vol 8 (3) ◽  
pp. 252-265 ◽  
Author(s):  
Cleofas Marcial-Medina ◽  
Alejandra Ordoñez-Moreno ◽  
Christian Gonzalez-Reyes ◽  
Pedro Cortes-Reynosa ◽  
Eduardo Perez Salazar
Keyword(s):  
Breast Cancer ◽  
Signal Transduction ◽  
Oleic Acid ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Binding Activity ◽  
Migration And Invasion ◽  
Signal Transduction Pathways ◽  
Dna Binding Activity ◽  
Dependent Pathway

Free fatty acids (FFAs) are an energy source, and induce activation of signal transduction pathways that mediate several biological processes. In breast cancer cells, oleic acid (OA) induces proliferation, matrix metalloproteinase-9 (MMP-9) secretion, migration and invasion. However, the signal transduction pathways that mediate migration and invasion induced by OA in breast cancer cells have not been studied in detail. We demonstrate here that FFAR1 and FFAR4 mediate migration induced by OA in MDA-MB-231 and MCF-7 breast cancer cells. Moreover, OA induces migration, invasion, AKT1 and AKT2 activation, 12-LOX secretion and an increase of NFκB-DNA binding activity in breast cancer cells. Cell migration requires FFAR1, FFAR4, EGFR, AKT and PI3K activity, whereas invasion is mediated though a PI3K/Akt-dependent pathway. Furthermore, OA promotes relocalization of paxillin to focal contacts and it requires PI3K and EGFR activity, whereas NFκB-DNA binding activity requires PI3K and AKT activity.

scholarly journals Nitroxides Tempol and Tempo Induce Divergent Signal Transduction Pathways in MDA-MB 231 Breast Cancer Cells

1998 ◽  
Vol 273 (28) ◽  
pp. 17871-17878 ◽  
Author(s):  
Simeng Suy ◽  
James B. Mitchell ◽  
Desiree Ehleiter ◽  
Adriana Haimovitz-Friedman ◽  
Usha Kasid
Keyword(s):  
Breast Cancer ◽  
Signal Transduction ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Signal Transduction Pathways

scholarly journals Identification of signal transduction pathways involved in constitutive NF-κB activation in breast cancer cells

Oncogene ◽  
2002 ◽  
Vol 21 (13) ◽  
pp. 2066-2078 ◽  
Author(s):  
Poornima Bhat-Nakshatri ◽  
Christopher J Sweeney ◽  
Harikrishna Nakshatri
Keyword(s):  
Breast Cancer ◽  
Signal Transduction ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Signal Transduction Pathways

scholarly journals GSK-3β Can Regulate the Sensitivity of MIA-PaCa-2 Pancreatic and MCF-7 Breast Cancer Cells to Chemotherapeutic Drugs, Targeted Therapeutics and Nutraceuticals

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 816
Author(s):  
Stephen L. Abrams ◽  
Shaw M. Akula ◽  
Akshaya K. Meher ◽  
Linda S. Steelman ◽  
Agnieszka Gizak ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Signal Transduction ◽  
Cancer Cells ◽  
Mitochondrial Respiration ◽  
Breast Cancer Cells ◽  
Chemotherapeutic Drugs ◽  
Pancreatic Cancers ◽  
Signal Transduction Inhibitors ◽  
Gsk 3Β ◽  
Mcf 7

Glycogen synthase kinase-3 (GSK-3) is a regulator of signaling pathways. KRas is frequently mutated in pancreatic cancers. The growth of certain pancreatic cancers is KRas-dependent and can be suppressed by GSK-3 inhibitors, documenting a link between KRas and GSK-3. To further elucidate the roles of GSK-3β in drug-resistance, we transfected KRas-dependent MIA-PaCa-2 pancreatic cells with wild-type (WT) and kinase-dead (KD) forms of GSK-3β. Transfection of MIA-PaCa-2 cells with WT-GSK-3β increased their resistance to various chemotherapeutic drugs and certain small molecule inhibitors. Transfection of cells with KD-GSK-3β often increased therapeutic sensitivity. An exception was observed with cells transfected with WT-GSK-3β and sensitivity to the BCL2/BCLXL ABT737 inhibitor. WT-GSK-3β reduced glycolytic capacity of the cells but did not affect the basal glycolysis and mitochondrial respiration. KD-GSK-3β decreased both basal glycolysis and glycolytic capacity and reduced mitochondrial respiration in MIA-PaCa-2 cells. As a comparison, the effects of GSK-3 on MCF-7 breast cancer cells, which have mutant PIK3CA, were examined. KD-GSK-3β increased the resistance of MCF-7 cells to chemotherapeutic drugs and certain signal transduction inhibitors. Thus, altering the levels of GSK-3β can have dramatic effects on sensitivity to drugs and signal transduction inhibitors which may be influenced by the background of the tumor.

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