Inhibition of Either Phosphatidylinositol 3-kinase/Akt or the Mitogen/Extracellular-regulated Kinase, MEK/ERK, Signaling Pathways Suppress Growth of Breast Cancer Cell Lines, but MEK/ERK Signaling is Critical for Cell Survival

2005 ◽  
Vol 93 (2) ◽  
pp. 177-188 ◽  
Author(s):  
Maureen O. Ripple ◽  
Sahana Kalmadi ◽  
Alan Eastman
2009 ◽  
Vol 10 (3) ◽  
pp. R31 ◽  
Author(s):  
Laura M Heiser ◽  
Nicholas J Wang ◽  
Carolyn L Talcott ◽  
Keith R Laderoute ◽  
Merrill Knapp ◽  
...  

2021 ◽  
Vol 16 ◽  
Author(s):  
Esha Sarkar ◽  
Aparna Misra ◽  
Abbas Ali Mahdi ◽  
Anchal Trivedi ◽  
Afreen Khan

: Chemoresistance is one of the biggest hurdles while treating cancer clinically. Due to its heterogeneous nature, complications of the chemoresistance mechanisms of breast cancer are cannot be completely elucidated. Existing mechanisms of main-line drug treatment can slow down the process of malignancy with part and parcel called drug resistance. The combinatorial effect of several chemotherapeutic drugs, targeting different pathways at the same time can work efficiently, yet the toxicity and drug-drug interaction remain intact. To overcome this hurdle, a number of strategies are getting invented, such as novel agents, drug carriers and combination treatment, etc. target mediated drug delivery system; nano-medicine and the use of phytocompounds can transfer the drug particularly to the cancerous cells with minimal side effects to the neighboring healthy cells. The cell cycle checkpoint proteins and genes are induced to the deranged cells can inhibit the resistance mechanism towards the drug. Modification of cell signaling pathways can also help to treat breast cancer chemoresistance mechanism in the long run. This article reviews the execution and onset of chemoresistance in various cancers and would further discuss potential therapeutic approaches to deal with the resistance mechanism. In this review, we’ll try to summarize the possible mechanisms and signaling pathways causing chemoresistance in breast cancer cell lines and discuss the alternative therapy to overcome under pre-clinical and clinical infrastructure.


2020 ◽  
Vol 26 (3) ◽  
pp. 497-508
Author(s):  
Kutlwano Xulu ◽  
Raquel Duarte ◽  
Tanya Augustine

AbstractThromboembolic disorders are the second leading cause of death in breast cancer. Antiplatelet therapy combined with cancer therapy is a potential treatment strategy against cancer-associated thromboembolic disorders; however, the efficacy of such dual treatment has not been established. This study reports novel findings on the response of hormone-dependent breast cancer cell lines (MCF7/T47D) following 24 h treatment with Anastrozole, combined with Aspirin and Clopidogrel cocktail; and Atopaxar. Neutral red and lactate dehydrogenase assays were conducted to assess viability and cytotoxicity respectively. Flow cytometric Annexin-V/PI assay was used to assess the mode of cell death. Morphological alterations were studied using scanning electron microscopy. Statistical analysis was conducted using Statistica V13. Definitive outcomes were established with flow cytometric detection of phosphatidylserine exposure and propidium iodide staining, complemented with ultrastructural analysis. Results showed that a few cells were undergoing death mainly through secondary necrosis. Morphological features suggesting induced cell motility (pseudopodia/ruffled membranes) were observed in both cell lines; notably, T47D cells presented pronounced features than MCF7 cells. Overall, these findings suggest that such combined treatment may differentially promote cell survival, inducing a more aggressive breast cancer phenotype.


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