View in EDS PDF Full Text

Global Gene Expression Associated with Hepatocarcinogenesis in Adult Male Mice Induced by in Utero Arsenic Exposure.

Saved in:
Bibliographic Details
Title: Global Gene Expression Associated with Hepatocarcinogenesis in Adult Male Mice Induced by in Utero Arsenic Exposure.
Authors: Jie Liu1, Yaxiong Xie1, Ducharme, Danica M. K.2, Jun Shen1, Diwan, Bhalchandra A.3, Merrick, B. Alex2, Grissom, Sherry F.2, Tucker, Charles J.2, Paules, Richard S.2, Tennant, Raymond2, Waalkes, Michael P.1 waalkes@niehs.nih.gov
Source: Environmental Health Perspectives. Mar2006, Vol. 114 Issue 3, p404-411. 8p.
Subject Terms: *Arsenic, *Carcinogenesis, *Arsenic content of drinking water, Liver cancer, Gene expression, Laboratory mice, Genetic regulation, Oncogenes, Tumors
Abstract: Our previous work has shown that exposure to inorganic arsenic in utero produces hepatocellular carcinoma (HCC) in adult male mice. To explore further the molecular mechanisms of transplacental arsenic hepatocarcinogenesis, we conducted a second arsenic transplacental carcinogenesis study and used a genomewide microarray to profile arsenic-induced aberrant gene expression more extensively. Briefly, pregnant C3H mice were given drinking water containing 85 ppm arsenic as sodium arsenite or unaltered water from days 8 to 18 of gestation. The incidence of HCC in adult male offspring was increased 4-fold and tumor multiplicity 3-fold after transplacental arsenic exposure. Samples of normal liver and liver tumors were taken at autopsy for genomic analysis. Arsenic exposure in utero resulted in significant alterations (p < 0.001) in the expression of 2,010 genes in arsenic-exposed liver samples and in the expression of 2,540 genes in arsenic-induced HCC. Ingenuity Pathway Analysis revealed that significant alterations in gene expression occurred in a number of biological networks, and Myc plays a critical role in one of the primary networks. Realtime reverse transcriptase-polymerase chain reaction and Western blot analysis of selected genes/proteins showed > 90% concordance. Arsenic-altered gene expression included activation of oncogenes and HCC biomarkers, and increased expression of cell proliferation-related genes, stress proteins, and insulin-like growth factors and genes involved in cell-cell communications. Liver feminization was evidenced by increased expression of estrogen-linked genes and altered expression of genes that encode gender-related metabolic enzymes. These novel findings are in agreement with the biology and histology of arsenic-induced HCC, thereby indicating that multiple genetic events are associated with transplacental arsenic hepatocarcinogenesis. [ABSTRACT FROM AUTHOR]
Copyright of Environmental Health Perspectives is the property of National Institute of Environmental Health Sciences and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: GreenFILE
FullText Links:
  – Type: pdflink
Text:
  Availability: 0
Header DbId: 8gh
DbLabel: GreenFILE
An: 20232207
AccessLevel: 6
PubType: Academic Journal
PubTypeId: academicJournal
PreciseRelevancyScore: 0
IllustrationInfo
Items – Name: Title
  Label: Title
  Group: Ti
  Data: Global Gene Expression Associated with Hepatocarcinogenesis in Adult Male Mice Induced by in Utero Arsenic Exposure.
– Name: Author
  Label: Authors
  Group: Au
  Data: &lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Jie+Liu%22&quot;&gt;Jie Liu&lt;/searchLink&gt;&lt;relatesTo&gt;1&lt;/relatesTo&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Yaxiong+Xie%22&quot;&gt;Yaxiong Xie&lt;/searchLink&gt;&lt;relatesTo&gt;1&lt;/relatesTo&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Ducharme%2C+Danica+M%2E+K%2E%22&quot;&gt;Ducharme, Danica M. K.&lt;/searchLink&gt;&lt;relatesTo&gt;2&lt;/relatesTo&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Jun+Shen%22&quot;&gt;Jun Shen&lt;/searchLink&gt;&lt;relatesTo&gt;1&lt;/relatesTo&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Diwan%2C+Bhalchandra+A%2E%22&quot;&gt;Diwan, Bhalchandra A.&lt;/searchLink&gt;&lt;relatesTo&gt;3&lt;/relatesTo&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Merrick%2C+B%2E+Alex%22&quot;&gt;Merrick, B. Alex&lt;/searchLink&gt;&lt;relatesTo&gt;2&lt;/relatesTo&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Grissom%2C+Sherry+F%2E%22&quot;&gt;Grissom, Sherry F.&lt;/searchLink&gt;&lt;relatesTo&gt;2&lt;/relatesTo&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Tucker%2C+Charles+J%2E%22&quot;&gt;Tucker, Charles J.&lt;/searchLink&gt;&lt;relatesTo&gt;2&lt;/relatesTo&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Paules%2C+Richard+S%2E%22&quot;&gt;Paules, Richard S.&lt;/searchLink&gt;&lt;relatesTo&gt;2&lt;/relatesTo&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Tennant%2C+Raymond%22&quot;&gt;Tennant, Raymond&lt;/searchLink&gt;&lt;relatesTo&gt;2&lt;/relatesTo&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Waalkes%2C+Michael+P%2E%22&quot;&gt;Waalkes, Michael P.&lt;/searchLink&gt;&lt;relatesTo&gt;1&lt;/relatesTo&gt;&lt;i&gt; waalkes@niehs.nih.gov&lt;/i&gt;
– Name: TitleSource
  Label: Source
  Group: Src
  Data: &lt;searchLink fieldCode=&quot;JN&quot; term=&quot;%22Environmental+Health+Perspectives%22&quot;&gt;Environmental Health Perspectives&lt;/searchLink&gt;. Mar2006, Vol. 114 Issue 3, p404-411. 8p.
– Name: Subject
  Label: Subject Terms
  Group: Su
  Data: *&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Arsenic%22&quot;&gt;Arsenic&lt;/searchLink&gt;&lt;br /&gt;*&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Carcinogenesis%22&quot;&gt;Carcinogenesis&lt;/searchLink&gt;&lt;br /&gt;*&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Arsenic+content+of+drinking+water%22&quot;&gt;Arsenic content of drinking water&lt;/searchLink&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Liver+cancer%22&quot;&gt;Liver cancer&lt;/searchLink&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Gene+expression%22&quot;&gt;Gene expression&lt;/searchLink&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Laboratory+mice%22&quot;&gt;Laboratory mice&lt;/searchLink&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Genetic+regulation%22&quot;&gt;Genetic regulation&lt;/searchLink&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Oncogenes%22&quot;&gt;Oncogenes&lt;/searchLink&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Tumors%22&quot;&gt;Tumors&lt;/searchLink&gt;
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Our previous work has shown that exposure to inorganic arsenic in utero produces hepatocellular carcinoma (HCC) in adult male mice. To explore further the molecular mechanisms of transplacental arsenic hepatocarcinogenesis, we conducted a second arsenic transplacental carcinogenesis study and used a genomewide microarray to profile arsenic-induced aberrant gene expression more extensively. Briefly, pregnant C3H mice were given drinking water containing 85 ppm arsenic as sodium arsenite or unaltered water from days 8 to 18 of gestation. The incidence of HCC in adult male offspring was increased 4-fold and tumor multiplicity 3-fold after transplacental arsenic exposure. Samples of normal liver and liver tumors were taken at autopsy for genomic analysis. Arsenic exposure in utero resulted in significant alterations (p &lt; 0.001) in the expression of 2,010 genes in arsenic-exposed liver samples and in the expression of 2,540 genes in arsenic-induced HCC. Ingenuity Pathway Analysis revealed that significant alterations in gene expression occurred in a number of biological networks, and Myc plays a critical role in one of the primary networks. Realtime reverse transcriptase-polymerase chain reaction and Western blot analysis of selected genes/proteins showed &gt; 90% concordance. Arsenic-altered gene expression included activation of oncogenes and HCC biomarkers, and increased expression of cell proliferation-related genes, stress proteins, and insulin-like growth factors and genes involved in cell-cell communications. Liver feminization was evidenced by increased expression of estrogen-linked genes and altered expression of genes that encode gender-related metabolic enzymes. These novel findings are in agreement with the biology and histology of arsenic-induced HCC, thereby indicating that multiple genetic events are associated with transplacental arsenic hepatocarcinogenesis. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: &lt;i&gt;Copyright of Environmental Health Perspectives is the property of National Institute of Environmental Health Sciences and its content may not be copied or emailed to multiple sites without the copyright holder&#39;s express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.&lt;/i&gt; (Copyright applies to all Abstracts.)
PLink https://search.ebscohost.com/login.aspx?direct=true&site=eds-live&db=8gh&AN=20232207
RecordInfo BibRecord:
  BibEntity:
    Identifiers:
      – Type: doi
        Value: 10.1289/ehp.8534
    Languages:
      – Code: eng
        Text: English
    PhysicalDescription:
      Pagination:
        PageCount: 8
        StartPage: 404
    Subjects:
      – SubjectFull: Arsenic
        Type: general
      – SubjectFull: Carcinogenesis
        Type: general
      – SubjectFull: Arsenic content of drinking water
        Type: general
      – SubjectFull: Liver cancer
        Type: general
      – SubjectFull: Gene expression
        Type: general
      – SubjectFull: Laboratory mice
        Type: general
      – SubjectFull: Genetic regulation
        Type: general
      – SubjectFull: Oncogenes
        Type: general
      – SubjectFull: Tumors
        Type: general
    Titles:
      – TitleFull: Global Gene Expression Associated with Hepatocarcinogenesis in Adult Male Mice Induced by in Utero Arsenic Exposure.
        Type: main
  BibRelationships:
    HasContributorRelationships:
      – PersonEntity:
          Name:
            NameFull: Jie Liu
      – PersonEntity:
          Name:
            NameFull: Yaxiong Xie
      – PersonEntity:
          Name:
            NameFull: Ducharme, Danica M. K.
      – PersonEntity:
          Name:
            NameFull: Jun Shen
      – PersonEntity:
          Name:
            NameFull: Diwan, Bhalchandra A.
      – PersonEntity:
          Name:
            NameFull: Merrick, B. Alex
      – PersonEntity:
          Name:
            NameFull: Grissom, Sherry F.
      – PersonEntity:
          Name:
            NameFull: Tucker, Charles J.
      – PersonEntity:
          Name:
            NameFull: Paules, Richard S.
      – PersonEntity:
          Name:
            NameFull: Tennant, Raymond
      – PersonEntity:
          Name:
            NameFull: Waalkes, Michael P.
    IsPartOfRelationships:
      – BibEntity:
          Dates:
            – D: 01
              M: 03
              Text: Mar2006
              Type: published
              Y: 2006
          Identifiers:
            – Type: issn-print
              Value: 00916765
          Numbering:
            – Type: volume
              Value: 114
            – Type: issue
              Value: 3
          Titles:
            – TitleFull: Environmental Health Perspectives
              Type: main
ResultId 1