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BEAS-2B Arsenic/Nickel treatmen iTRAQ proteomic analysis

ABSTRACT: Lung cancer accounts for approximately 2.2 million new cases worldwide, making it the second most prevalent cancer. Annually, it results in 1.8 million fatalities, rendering it the cancer with the highest mortality rate. A significant proportion of lung cancer patients have a history of environmental and occupational exposures. Both the International Agency for Research on Cancer (IARC) and the U.S. Environmental Protection Agency (EPA) identify arsenic and nickel as significant environmental carcinogens. However, the specific mechanisms by which these substances induce lung cancer remain unclear. Therefore, we conducted acute exposure experiments on human bronchial epithelial cells using varying concentrations of arsenic and nickel compounds, followed by proteomic analysis to identify the altered proteins. This study aims to elucidate the potential carcinogenic mechanisms associated with arsenic and nickel compounds.

ORGANISM(S): Homo Sapiens

SUBMITTER: Haishan Huang

PROVIDER: PXD067927 | iProX | Mon Sep 01 00:00:00 GMT+01:00 2025

REPOSITORIES: iProX

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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.

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BEAS-2B Arsenic/Nickel treatmen iTRAQ proteomic analysis

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