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.

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...

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Publicado en:BioMed Research International Vol. 2015; pp. 1 - 11
Autores principales: Quintero Barceinas, Reyna Sara, García-Regalado, Alejandro, Aréchaga-Ocampo, Elena, Villegas-Sepúlveda, Nicolás, González-De la Rosa, Claudia Haydée
Formato: pictorial research tables/charts Journal Article
Publicado: Wiley-Blackwell 10/18/2015
Acceso en línea:Ver este registro en EBSCOhost
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      dt: 10/18/2015
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      pub: Wiley-Blackwell
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        10.1155/2015/404368
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        atl: 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.
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        au:
          Quintero Barceinas, Reyna Sara
          García-Regalado, Alejandro
          Aréchaga-Ocampo, Elena
          Villegas-Sepúlveda, Nicolás
          González-De la Rosa, Claudia Haydée
        affil: Departamento de Ciencias Naturales, Universidad Autónoma Metropolitana, Unidad Cuajimalpa, Avenida Vasco de Quiroga 4871, 05348 Colonia Santa Fe Cuajimalpa, DF, Mexico
      sug:
        subj:
          Cell Movement Drug Effects
          Cell Proliferation Drug Effects
          Cell Viability Drug Effects
          Lung Neoplasms Drug Therapy
          Signal Transduction Drug Effects
          Gene Expression Drug Effects
          Tretinoin Pharmacodynamics
          Human
          Apoptosis
          Receptors, Cytoplasmic and Nuclear Drug Effects
      ab: 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 RARα and PI3K, promoting growth, survival, and migration in lung cancer cells. Until now, thismechanism was unknown in lung cancer cells.Theinhibition 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.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
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      ougenre: Article
    language: English
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