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Cancer is a well\u2010established DNA mutation\u2010linked disease; however, epigenetic events are perhaps more important and harmful than genetic alterations. Unfortunately, we do not have reliable screening methods to assess\/validate the epigenetic (promoter) effects of a physical or a chemical agent. We propose a mechanism of action whereby mercury acts as a possible promoter carcinogen. In the present contribution, we resume our previous studies on mercury tested at concentrations comparable with its occurrence as environmental pollutant. It is shown that Hg(II) elicits a prooxidative state in keratinocytes linked to inhibition of gap junction\u2010mediated intercellular communication and proinflammatory cytokine production. These combined effects may on one hand isolate cells from tissue\u2010specific homeostasis promoting their proliferation and on the other hand tamper the immune system defense\/surveillance checkmating the whole organism. Since Hg(II) is not a mutagenic\/genotoxic compound directly affecting gene expression, in a broader sense, mercury might be an example of an epigenetic tumor promoter or, further expanding this concept, a \u201cmetagenetic\u201d effector.<\/jats:p>","DOI":"10.1155\/2017\/7028583","type":"journal-article","created":{"date-parts":[[2017,12,21]],"date-time":"2017-12-21T23:32:55Z","timestamp":1513899175000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":71,"title":["Possible Mechanisms of Mercury Toxicity and Cancer Promotion: Involvement of Gap Junction Intercellular Communications and Inflammatory 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