AI Article Synopsis
- The study investigates how amitrole may cause thyroid tumors in a specific cell line (Nthy-ori-3-1) using microarray analysis.
- Amitrole treatment did not significantly affect cell proliferation, but it significantly altered the expression of 90 genes, with 55 up-regulated and 35 down-regulated.
- Key genes identified, including bmp2, arnt2, and wnt5b, may contribute to tumor development through various signaling pathways.
Article Abstract
Objective: To explore the possible mechanism of amitrole causing thyroid tumor in Nthy-ori-3-1 cell by differential expression microarray analysis.
Methods: After the Nthy-ori-3-1cells were treated with 1 ~ 100 g / m L amitrole for 24 h, and the effect of amitrole on the proliferation of the cells was detected by MTT assay. Then cells were treated with 100 g / m L amitrole for 24 h, and the differential expression microarray was tested. The microarray results was analyzed by GO analysis and pathway analysis. The microarray results were verified by real-time quantitative PCR.
Results: MTT results showed that amitole had no significant effect on the proliferation of Nthy-ori-3-1 cells. Microarray results showed that 90( 55 up-regulated, 35 down regulated) genes were significantly changed. GO analysis showed that 43( 37 up-regulated, 6 down-regulated) of the 90 changed genes were related to biological processes, and 42( 37 up-regulated, 5down-regulated) were related to molecular function, and 44( 38 up-regulated, 6 downregulated) were related to cell components. Pathway results showed that 44 signalingpathways were influenced by the differentially expressed genes, and 10 of them were closely related to tumor. The qRT-PCR results were consistent with microarray results. wnt5 b, arnt2 and bmp2 genes were significantly related with multiple tumor-associated pathways.
Conclusion: Amitrole may cause thyroid tumor by multiple signaling pathways, and bmp2, arnt2 and wnt5 b may beits major target genes.
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