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[Study on gene expression pattern in 16HBE cells treated with NiS]
Xiaonong Bin1, Jiachun Lv, Min Tan
1Institute for Chemical Carcinogenesis, Guangzhou Medical College, Guangzhou, Guangdong 510182, P.R.China.
Background:
Recent researches have found that NiS can cause the malignant transforming activity and carcinogenicity on human bronchial epithelial cells (16HBE). Its molecular mechanism may be involved in mutation of genes and abnormal expression of transcription factors on 16HBE. And so, this study takes advantage of a model of 16HBE transformed by NiS and screens the differentially expressed genes between 16HBE cells and NiS treated 16HBE cells (NiS-16HBE) using cDNA microarray.
Methods:
The total RNA was extracted from 16HBE cells and NiS-16HBE cells. The cDNA probes were prepared by labeling with Cy3-dCTP and Cy5-dCTP respectively through reverse transcription. The mixed probes were then hybridized to the cDNA microarray chips containing 4000 human genes. The chips were scanned by ScanArray 4000 laser scanner. The acquired fluorescent signals were analyzed by GenPix Pro 3.0 software. Bioinformation function of those differentially expressed genes was analysed.
Results:
A total of 151 genes exhibited differential expression between 16HBE cells and NiS-16HBE cells. The expression of 70 genes ( 46.36%) was down-regulated and that of 81 genes (53.64%) was up-regulated.
Conclusions:
The regulation of genes including stress response genes, immune related genes, DNA synthesis and repair genes, metabolism genes, pro-oncogenes and tumor suppressor genes may be involved in transforming activity of NiS.
Insights
Nickel sulfide (NiS) exposure transforms human bronchial epithelial cells (16HBE), altering gene expression. This study identified 151 differentially expressed genes, revealing potential molecular mechanisms of NiS carcinogenicity.
Area of Science:
- Environmental Toxicology
- Molecular Biology
- Genomics
Context:
- Nickel sulfide (NiS) is recognized for its malignant transforming activity and carcinogenicity.
- Human bronchial epithelial cells (16HBE) are susceptible to NiS-induced cellular transformation.
- The molecular mechanisms underlying NiS carcinogenicity may involve gene mutations and altered transcription factor expression.
Purpose:
- To screen differentially expressed genes in 16HBE cells transformed by NiS.
- To identify genes and pathways affected by NiS exposure in bronchial epithelial cells.
Summary:
- A cDNA microarray analysis was performed on 16HBE cells and NiS-treated 16HBE cells (NiS-16HBE).
- Total RNA was extracted, converted to cDNA probes, and hybridized to a microarray containing 4000 human genes.
- Analysis revealed 151 differentially expressed genes, with 70 down-regulated and 81 up-regulated.
Impact:
- Identifies key genes and biological processes, including stress response, immune function, DNA repair, metabolism, and oncogenes/tumor suppressors, potentially involved in NiS-induced cell transformation.
- Provides a foundation for understanding the molecular basis of NiS carcinogenicity.
- Highlights potential targets for future research into prevention and treatment strategies.
