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Background: Drug resistance prevents the effective treatment of cancers. DNA methylation has been found to participate in the development of cancer drug resistance.
Methods: We performed the wound-healing and invasion assays to test the effect of the paraoxonase gene PON3 on esophageal cancer (EC) cells. In addition, in vivo EC-derived tumor xenografts in nude mice were generated to test the effect of PON3 on the chemoresistance of EC cells.
Results: We found that PON3 is hypermethylated in drug-resistant EC cell line K150, which in-return down-regulates its expression. The following experiments by the forced changes of PON3 level in vitro and in vivo demonstrated that the PON3 expression negatively correlates with drug resistance in EC cells. Further wound-healing and invasion assays showed that PON3 suppresses the migration and invasion of EC cells.
Conclusion: Our data established that PON3 is associated with the EC drug resistance, which may serve as a biomarker for the potential therapeutic treatment of EC.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6198441 | PMC |
| http://dx.doi.org/10.1186/s12935-018-0657-1 | DOI Listing |
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