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BioMed Research International
Volume 2015, Article ID 404368, 10 pages
Research Article

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

1Departamento de Ciencias Naturales, Universidad Autónoma Metropolitana, Unidad Cuajimalpa, Avenida Vasco de Quiroga 4871, 05348 Colonia Santa Fe Cuajimalpa, DF, Mexico
2Facultad de Enfermería, Universidad Autónoma de San Luis Potosí, Avenida Niño Artillero 130, 78240 Zona Universitaria, SLP, Mexico
3Departamento de Biomedicina Molecular, Centro de Investigación y de Estudios Avanzados del IPN, Avenida Instituto Politécnico Nacional 2508, 14740 Colonia San Pedro Zacatenco, DF, Mexico

Received 8 December 2014; Accepted 2 March 2015

Academic Editor: M. Ruzzene

Copyright © 2015 Reyna Sara Quintero Barceinas et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Supplementary Material

FIGURE S1. Effect of MEK inhibitor PD98059 on ATRA-induced Akt activation. A549 cells were serum-starved for 18 h, treated or non-treated (NT) with 5 µM of ATRA for 15 minutes alone or in combination with 25 µM of PD98059 for 90 minutes. The phosphorylated form of Akt and total proteins were detected by western blot using specific antibodies. β-Actin was used as the loading control. The graph represents the densitometric analysis of Akt phosphorylation in three independent experiments (means ± SEM, *p< 0.05; **p< 0.001 compared with NT cells; analysis of variance and Newman-Keuls test).

  1. Supplementary Material