Abstract:
Objective To study aberrant DNAmethylation potentially resultingin the changes of the anti -7, 8, -dihydrodiol-9, 10-epoxide benzoapyrene(anti-BPDE)and nickel sulfide(NiS)transformed Human bronchial epithelia(16 HBE)as a possible epigenetic mechanism forcarcinogenesis.
Methods The product DNAisolated from five kinds of 16 HBEwas analyzed foraberrant methylation using PCRbased technique-methylation sensitive restriction fingerprinting technique(MSRF).Several DNAfragments differentially methylated in the transformed cells found by MSRFwere ligated to pMD18 TVectorand transformed into bacteria.The plasmid DNAwere sequenced and compared with data in GenBank by BLASTN.
Results DNA hypermethylation was indentified in the NiStransformed 16 HBE, and it was found that one of the DNAfragments homologized(99%)with ANKRD11 which encoded the susceptibility protein of nanopbaryngeal carcinoma and anotherhomologized(99%)with bomeo box A3.
Conclusion Anti-BPDEinduced 16 HBEdid not showaberrant genome Cp Gmethylation, which suggestes that aberrant methylation of genes may nothappen foranti-BPDE-induced cells transformation and carcinogenesis.DNA hypermethylation is known to resultin gene silencing, and it appears that hypermethylation of gene may represent a possible epigenetic mechanism forNiSinduced cells transformation and carcinogenesis.
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