Acrylamide inhibits cellular differentiation of human neuroblastoma and glioblastoma cells

• Published in: Food and chemical toxicology Vol. 82; pp. 27 - 35
• Main Authors: Chen, Jong-Hang, Chou, Chin-Cheng
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.08.2015
• Subjects: Acrylamide; Acrylamide - toxicity; acrylamides; butyric acid; Butyric Acid - pharmacology; caffeine; cell differentiation; Cell Differentiation - drug effects; Cell Line, Tumor - drug effects; cell proliferation; Cell Proliferation - drug effects; Cellular differentiation; dose response; Down-Regulation - drug effects; Extracellular Signal-Regulated MAP Kinases - metabolism; Glioblastoma; Glioblastoma - drug therapy; Glioblastoma - metabolism; Glioblastoma - pathology; Humans; Janus Kinases - metabolism; mitogen-activated protein kinase; Neurites - drug effects; Neuroblastoma; Neuroblastoma - drug therapy; Neuroblastoma - metabolism; Neuroblastoma - pathology; neurogenesis; non-specific protein-tyrosine kinase; phosphorylation; Phosphorylation - drug effects; retinoic acid; Signal Transduction - drug effects; STAT Transcription Factors - metabolism; toxicology; Tretinoin - pharmacology; Acrylamide; Neuroblastoma; Cellular differentiation; Glioblastoma
• ISSN: 0278-6915; 1873-6351
• DOI: 10.1016/j.fct.2015.04.030

•ACR attenuated RA-induced neurogenesis of SH-SY5Y and BA-induced astrogliogenesis of U-1240 MG.•ACR induced down regulation of MAPs expression and JAK-STAT signaling in cellular differentiation of SH-SY5Y and U-1240 MG.•ACR decreased the phosphorylation of ERK and JNK in glioblastoma cells. This study explores human neuroblastoma (SH-SY5Y) and human glioblastoma (U-1240 MG) cellular differentiation changes under exposure to acrylamide (ACR). Differentiation of SH-SY5Y and U-1240 MG cells were induced by retinoic acid (RA) and butyric acid (BA), respectively. Morphological observations and MTT assay showed that the induced cellular differentiation and cell proliferation were inhibited by ACR in a time- and dose-dependent manner. ACR co-treatment with RA attenuated SH-SY5Y expressions of neurofilament protein-L (NF-L), microtubule-associated protein 1b (MAP1b; 1.2 to 0.7, p < 0.001), MAP2c (2.2 to 0.8, p < 0.05), and Janus kinase1 (JAK1; 1.9 to 0.6, p < 0.001), while ACR co-treatment with BA attenuated U-1240 MG expressions of glial fibrillary acidic protein (GFAP), MAP1b (1.2 to 0.6, p < 0.001), MAP2c (1.5 to 0.7, p < 0.01), and JAK1 (2.1 to 0.5, p < 0.001), respectively. ACR also decreased the phosphorylation of extracellular-signal-regulated kinases (ERK) and c-Jun N-terminal kinases (JNK) in U-1240 MG cells, while caffeine reversed this suppression of ERK and JNK phosphorylation caused by ACR treatment. These results showed that RA-induced neurogenesis of SH-SY5Y and BA-induced astrogliogenesis of U-1240 MG cells were attenuated by ACR and were associated with down-regulation of MAPs expression and JAK-STAT signaling.