Liver cell-specific transcriptional regulation of connexin32

Piechocki, Marie P.; Toti, Rosanne M.; Fernström, Martha J.; Burk, Robert D.; Ruch, Randall J.

doi:10.1016/s0167-4781(00)00036-1

Cited by 42 publications

(24 citation statements)

References 33 publications

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“…Many previous studies indicated that high doses of DDT and other nongenotoxic carcinogens inhibit Cx32, resulting in the loss of the function of gap junction intracellular communication (GJIC) and release of potentially initiated cells from growth constraints imposed by normal neighboring cells, resulting in clonal expansion and ultimately tumor formation and progression [66][67][68][69][70] . In the present study, mRNA expression of one of the transcriptional factors, HNF-1α, which regulates Cx32 expression 71,72 , was in good correlation with that of Cx32 61 . Differential alteration of HNF-1α is suggested to be one of the possible mechanisms by which DDT might inhibit or promote rat hepatocarcinogenesis.…”

Section: Possibility Of a Hormesis For Hepatocarcinogenicity Of Ddtsupporting

confidence: 64%

Hormesis in Carcinogenicity of Non-genotoxic Carcinogens

et al. 2006

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Abstract:Recently the idea of hormesis, a biphasic dose-response relationship in which a chemical exerts opposite effects dependent on the dose, has attracted interest in the field of carcinogenesis. With non-genotoxic agents there is considerable experimental evidence in support of hormesis and the present review highlights current knowledge of doseresponse effects. In particular, several in vivo studies have provided support for the idea that non-genotoxic carcinogens may inhibit hepatocarcinogenesis at low doses. Here, we survey the examples and discuss possible mechanisms of hormesis with cytochrome P450 inducers, such as phenobarbital, 1,1-bis(p-chlorophenyl)-2,2,2-trichloroethane (DDT), α-benzene hexachloride (α-BHC), and other non-genotoxins. Epigenetic processes differentially can be affected by agents that impinge on oxidative stress, DNA repair, cell proliferation, apoptosis, intracellular communication and cell signaling. Non-genotoxic carcinogens may target nuclear receptors, cause aberrant DNA methylation at the genomic level and induce post-translational modifications at the protein level, thereby impacting on the stability or activity of key regulatory proteins, including oncoproteins and tumor suppressor proteins. Via multiple epigenetic lesions, nongenotoxic carcinogens can elicit a variety of changes contributing to cellular carcinogenesis. (J Toxicol Pathol 2006; 19: 111-122)

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Section: Possibility Of a Hormesis For Hepatocarcinogenicity Of Ddtsupporting

confidence: 64%

Hormesis in Carcinogenicity of Non-genotoxic Carcinogens

et al. 2006

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“…The P1 promoter directs Cx32 gene expression in liver, salivary glands and pancreatic epithelial cells, while the downstream P2 promoter is responsible for Cx32 expression in cells of the spinal cord and brain (Neuhaus et al, 1995). Studies from the Ruch laboratory (Koffler et al, 2002;Piechocki et al, 2000) have shown that liver-specific expression of the Cx32 gene relies on the winged-helix transcription factor HNF-1, which is also present in the pancreas. However, adult pancreatic HNF-1 expression is primarily confined to cells of the endocrine compartment where Cx32 is not expressed (Edlund, 2002; Although the DNA binding and dimerization domains of Mist1 are required to achieve Cx32 gene transcription, the precise mechanism(s) by which Mist1 activates Cx32 gene expression is not known.…”

Section: Discussionmentioning

confidence: 99%

Exocrine specific expression of Connexin32 is dependent on the basic helix-loop-helix transcription factor Mist1

Rukstalis

Kowalik

Zhu

et al. 2003

Journal of Cell Science

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“…Cx32 is the main gap junction proteins expressed in hepatocytes and plays an important role in the regulation of signal transfer and growth control in the liver by constructing gap junction channels and gap junctional intercellular communication [40,41]. However, the specific functions and the regulation of the Cx genes in hepatocytes are still unclear.…”

Section: Article In Pressmentioning

confidence: 99%