Abstract 4975: All-trans retinoic acid induces proliferation, survival and migration in A549 lung cancer cells by activating the ERK signaling pathway through a transcription independent mechanism

2015 ◽  
Author(s):  
Reyna S. Quintero Barceinas ◽  
Alejandro García-Regalado ◽  
Elena Aréchaga-Ocampo ◽  
Claudia H. González-De la Rosa
Keyword(s):  
Lung Cancer ◽  
Retinoic Acid ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Erk Signaling ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Independent Mechanism ◽  
And Migration ◽  
A549 Lung

scholarly journals All-Trans Retinoic Acid Induces Proliferation, Survival, and Migration in A549 Lung Cancer Cells by Activating the ERK Signaling Pathway through a Transcription-Independent Mechanism

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Reyna Sara Quintero Barceinas ◽  
Alejandro García-Regalado ◽  
Elena Aréchaga-Ocampo ◽  
Nicolás Villegas-Sepúlveda ◽  
Claudia Haydée González-De la Rosa
Keyword(s):  
Lung Cancer ◽  
Retinoic Acid ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Lung Cancer Cells ◽  
Erk Signaling ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Independent Mechanism ◽  
And Migration

All-trans retinoic acid (ATRA) has been used as an antineoplastic because of its ability to promote proliferation, inhibition, and differentiation, primarily in leukemia; however, in other types of cancer, such as lung cancer, treatment with ATRA is restricted because not all the patients experience the same results. The ERK signaling pathway is dysregulated in cancer cells, including lung cancer, and this dysregulation promotes proliferation and cell invasion. In this study, we demonstrate that treatment with ATRA can activate the ERK signaling pathway by a transcription-independent mechanism through a signaling cascade that involves RARαand PI3K, promoting growth, survival, and migration in lung cancer cells. Until now, this mechanism was unknown in lung cancer cells. The inhibition of the ERK signaling pathway restores the beneficial effects of ATRA, reduces proliferation, increases apoptosis, and blocks the cell migration process in lung cancer cells. In conclusion, our results suggest that the combination of ATRA with ERK inhibitor in clinical trials for lung cancer is warranted.

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