title: Silencing of FABP3 inhibits proliferation and promotes apoptosis in embryonic carcinoma cells.
abstract: Fatty acid-binding protein 3 (FABP3) facilitates the movement of fatty acids in cardiac muscle. Previously, we reported that FABP3 is highly upregulated in the myocardium of ventricular septal defect patients and overexpression of FABP3 inhibited proliferation and promoted apoptosis in embryonic carcinoma cells (P19 cells). In this study, we aimed to investigate the effect of FABP3 gene silencing on P19 cell differentiation, proliferation and apoptosis. We used RNA interference and a lentiviral-based vector system to create a stable FABP3-silenced P19 cell line; knockdown of FABP3 was confirmed by quantitative real-time PCR. Expression analysis of specific differentiation marker genes using quantitative real-time PCR and observation of morphological changes using an inverted microscope revealed that knockdown of FABP3 did not significantly affect the differentiation of P19 cells into cardiomyocytes. CCK-8 proliferation assays and cell cycle analysis demonstrated that FABP3 gene silencing significantly inhibited P19 cell proliferation. Furthermore, Annexin V-FITC/propidium iodide staining and the caspase-3 activity assay revealed that FABP3 gene silencing significantly promoted serum starvation-induced apoptosis in P19 cells. In agreement with our previous research, these results demonstrate that FABP3 may play an important role during embryonic heart development, and that either overexpression or silencing of FABP3 will lead to an imbalance between proliferation and apoptosis, which may result in embryonic cardiac malformations.
authors.affiliation: State Key Laboratory of Reproductive Medicine, Department of MICU, Nanjing Maternity and Child Health Care Hospital Affiliated to Nanjing Medical University, Nanjing, 210029, China.
authors.forename: Yahui
authors.initials: Y
authors.lastname: Shen
authors.forename: Guixian
authors.initials: G
authors.lastname: Song
authors.forename: Yaoqiu
authors.initials: Y
authors.lastname: Liu
authors.forename: Lijuan
authors.initials: L
authors.lastname: Zhou
authors.forename: Hailang
authors.initials: H
authors.lastname: Liu
authors.forename: Xiangqing
authors.initials: X
authors.lastname: Kong
authors.forename: Yanhui
authors.initials: Y
authors.lastname: Sheng
authors.forename: Kejiang
authors.initials: K
authors.lastname: Cao
authors.forename: Lingmei
authors.initials: L
authors.lastname: Qian
mesh_terms: D000818:Animals; D017209:Apoptosis; D053148:Caspase 3 / Q000235:genetics / Q000378:metabolism; D002454:Cell Differentiation; D049109:Cell Proliferation; D048430:Cell Shape; D002470:Cell Survival / Q000187:drug effects; D016895:Culture Media, Serum-Free; D004622:Embryo, Mammalian / Q000378:metabolism; D054278:Embryonal Carcinoma Stem Cells / Q000378:metabolism / Q000473:pathology*; D000074026:Fatty Acid Binding Protein 3; D050556:Fatty Acid-Binding Proteins / Q000235:genetics / Q000378:metabolism*; D018507:Gene Expression Regulation, Developmental; D020868:Gene Silencing; D006321:Heart / Q000196:embryology; D051379:Mice; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology
chemical_list: D016895:Culture Media, Serum-Free; C493409:Fabp3 protein, mouse; D000074026:Fatty Acid Binding Protein 3; D050556:Fatty Acid-Binding Proteins; C505409:Casp3 protein, mouse; D053148:Caspase 3