Cellular retinol binding protein 1 transfection reduces proliferation and AKT-related gene expression in H460 non-small lung cancer cells

In recent years, new treatments with novel action mechanisms have been explored for advanced non-small cell lung cancer (NSCLC). Retinoids promote cancer cell differentiation and death and their trafficking and action is mediated from specific cytoplasmic and nuclear receptors, respectively. The purpose of this study was to investigate the effect of Cellular retinol binding protein-1 (CRBP-1) transfection in H460 human NSCLC cell line, normally not expressing CRBP-1. H460 cells were transfected by using a vector pTargeT Mammalian expression system carrying the whole sequence of CRBP-1 gene. For proliferation and apoptosis studies, cells were treated with different concentrations of all-trans Retinoic Acid (atRA) and retinol. AKT-related gene expression was analyzed by using western blot and Signosis array and results analysed by one-way analysis of variance (ANOVA) or by t-student test. CRBP-1+ showed reduced proliferation and viability in basal condition and after atRA treatment when compared to empty-transfected H460 cells. Reduced proliferation in CRBP-1+ H460 cells associated to the down-regulation of pAKT/pERK/pEGFR-related genes. In particular, gene array documented the down-regulation of AKT and Stat-3-related genes, including M-Tor, Akt1, Akt2, Akt3, Foxo1, p27, Jun. Restoration of CRBP-1 expression in H460 cells reduced proliferation and viability in both basal condition and after atRA treatment, likely by down-regulating AKT-related gene level. Further studies are needed to better clarify how those CRBP-1-related intracellular pathways contribute to counteract NSCLC progression in order to suggest a potential tool to improve efficacy of retinoid anti lung cancer adjuvant therapy.

Cellular Retinol Binding Protein I transfection in H460 non-small lung carcinoma cells reduces proliferation and AKT-related gene expression

Background: In recent years, new treatments with novel action mechanisms have been explored for advancer lung cancer. Retinoids were shown to promote cancer cell differentiation and death of and their action is mediated from specific cytoplasmic and nuclear receptors. The purpose of this study was to investigate the effect of Cellular retinol binding Protein I (CRBPI) transfection in H460 human non-small cell lung cancer cell line normally not expressing that receptor.Methods: H460 cells were transfected by using a vector pTargeT Mammalian expression system carrying the whole sequence of CRBPI gene. For proliferation and apoptosis studies, cells were treated with different concentrations of all-trans retinoic acid ( at RA) and retinol. AKT-related gene expression was analyzed by using western blot and Signosis array. Results were analysed using d by one-way analysis of variance (ANOVA) followed from a Bonferroni post hoc test or with t-student test.Results: CRBPI + showed a reduced proliferation and viability in basal condition and after at RA treatment when compared to empty-transfected H460 cells. Reduced proliferation in CRBPI + H460 cells associated to the down-regulation of pAKT/pERK/pEGFR genes. In particular, gene array documented in CRBPI + H460 cells the down-regulation of AKT and Stat-3-related genes, including M-Tor, Akt1, Akt2, Akt3, Foxo1, Foxo3, p21, p27, pTen, Jun.Conclusion: Restoration of CRBPI expression in H460 cells reduced proliferation and viability in both basal condition and after at RA treatment, likely by down-regulating AKT-related gene level. Further studies are needed to better clarify how those CRBPI-related intracellular pathways contribute to counteract non-small cell lung carcinoma progression in order to suggest a potential tool to improve efficacy of retioid anti lung cancer adjuvant therapy.

Cellular Retinol Binding Protein I transfection in H460 non-small lung carcinoma cells reduces proliferation and AKT-related gene expression

Background In recent years, new treatments with novel action mechanisms have been explored for advancer lung cancer. Retinoids were shown to promote cancer cell differentiation and death of and their action is mediated from specific cytoplasmic and nuclear receptors.Objective The purpose of this study was to investigate the effect of Cellular retinol binding Protein I (CRBPI) transfection in H460 human non-small cell lung cancer cell line normally not expressing that receptor.Methods H460 cells were transfected by using a vector pTargeT Mammalian expression system carrying the whole sequence of CRBPI gene. For proliferation and apoptosis studies, cells were treated with different concentrations of all-trans retinoic acid ( at RA) and retinol. AKT-related gene expression was analyzed by using western blot and Signosis array. Results were analysed using d by one-way analysis of variance (ANOVA) followed from a Bonferroni post hoc test or with t-student test.Results CRBPI + showed a reduced proliferation and viability in basal condition and after at RA treatment when compared to empty-transfected H460 cells. Reduced proliferation in CRBPI + H460 cells associated to the down-regulation of pAKT/pERK/pEGFR genes. In particular, gene array documented in CRBPI + H460 cells the down-regulation of AKT and Stat-3-related genes, including M-Tor, Akt1, Akt2, Akt3, Foxo1, Foxo3, p21, p27, pTen, Jun.Conclusion Restoration of CRBPI expression in H460 cells reduced proliferation and viability in both basal condition and after at RA treatment, likely by down-regulating AKT-related gene level. Further studies are needed to better clarify how those CRBPI-related intracellular pathways contribute to counteract non-small cell lung carcinoma progression in order to suggest a potential tool to improve efficacy of retioid anti lung cancer adjuvant therapy.