Dataset Information

Silica-exposed BEAS-2B epithelial cells

ABSTRACT: We used mass spectrometry to profile changes in metabolites, proteins, and phosphorylation in silica-exposed BEAS-2B epithelial cells.

ORGANISM(S): Homo Sapiens

SUBMITTER: Jin Chen

PROVIDER: PXD035608 | iProX | Thu Jul 28 00:00:00 GMT+01:00 2022

REPOSITORIES: iProX

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Publications

Profiling of metabolites, proteins, and protein phosphorylation in silica-exposed BEAS-2B epithelial cells.

Chen Jin J Wang Hanshi H Gao Hongzhi H Zeng Yiming Y

PloS one 20230411 4

Silicosis is an uncurable occupational disease induced by crystalline silica. Increased prevalence of silicosis has resulted in the increased need for development of treatment options. Although macrophages respond first to silica, epithelial cells are also involved in silicosis. However, changes in protein and metabolite levels have not been reported simultaneously. We used mass spectrometry to profile changes in metabolites, proteins, and phosphorylation in silica-exposed BEAS-2B epithelial cel ...[more]

PMID: 37040356

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Project description:This study chronically exposed human lung epithelial BEAS-2B cells to low-dose arsenic trioxide in vitro to elucidate cancer promoting gene signaling networks (GSNs) associated with As-transformed (B-As) cells. Following a six month exposure, exposed cells were assessed for enhanced cell proliferation, colony formation, invasion ability and in vivo tumor formation compared to control cell lines. Collected mRNA was subjected to whole genome expression microarray profiling followed by in silico Ingenuity Pathway Analysis (IPA) to identify lung carcinogenesis modes of action. B-As cells displayed significant increases in proliferation, colony formation and invasion ability compared to BEAS-2B cells. B-As injections into nude mice resulted in development of primary and secondary metastatic tumors. As exposure resulted in widespread up-regulation of genes associated with mitochondrial metabolism and increased ROS protection suggesting mitochondrial dysfunction. Carcinogenic initiation via ROS and epigenetic mechanisms was further supported by altered DNA repair, histone, and ROS-sensitive signaling. NF-ÎºB, MAPK and NCOR1 signaling disrupted PPARÎ±/Î´-mediated lipid homeostasis. A âpro-cancerâ GSN identified increased survival, proliferation, inflammation, metabolism, anti-apoptosis and mobility signaling. IPA-ranked signaling networks identified altered p21, EF1Î±, Akt, MAPK, and NF-ÎºB signaling networks promoting genetic disorder, altered cell cycle, cancer and changes in nucleic acid and energy metabolism. In conclusion, transformed B-As cells with their whole genome GSN profile provide an in vitro As model for future lung cancer signaling research and data for chronic As exposure risk assessment. Whole genome expression profiling was conducted on arsenic (III) oxide-exposed human immortalized lung epithelial cells (BEAS-2B) following 6 month in vitro chronic exposure. As2O3 exposed cells (B-As) gene expression were compared to unexposed, passage control (B-Control) cell gene expression. Three B-As and four B-Control biological replicate cDNA samples were analyzed.

Dataset Information

Silica-exposed BEAS-2B epithelial cells

Publications

Profiling of metabolites, proteins, and protein phosphorylation in silica-exposed BEAS-2B epithelial cells.

Similar Datasets

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