β-Catenin signaling induces CYP1A1 expression by disrupting adherens junctions in Caco-2 human colon carcinoma cells
The aryl hydrocarbon (Ah) receptor is one of the best known ligand-activated transcription factors. The present study has focused on the wound-healing process on Ah receptor function. Depletion of calcium from culture medium of Caco-2 human colon carcinoma cells by transfer to Minimal Essential Medi...
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| Veröffentlicht in: | Biochimica et biophysica acta Jg. 1830; H. 3; S. 2509 - 2516 |
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01.03.2013
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| Abstract | The aryl hydrocarbon (Ah) receptor is one of the best known ligand-activated transcription factors. The present study has focused on the wound-healing process on Ah receptor function.
Depletion of calcium from culture medium of Caco-2 human colon carcinoma cells by transfer to Minimal Essential Medium (Spinner Modification; S-MEM) destroyed adherens junctions and the cells were used as the model of wound-healing process.
Calcium depletion induced both nuclear translocation of the Ah receptor, and increased expression of CYP1A1 and Slug mRNAs in Caco-2 cells. However, expression of Slug mRNA was not significantly induced by treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin. Knockdown of the Ah receptor and treatment with Ah receptor antagonists decreased level of CYP1A1 mRNA. The fragment of E-cadherin released by γ-secretase was not involved in induction of CYP1A1 mRNA following S-MEM treatment. Knockdown of β-catenin increased levels of Ah receptor mRNA, which may be attributable to direct or indirect involvement of β-catenin in suppression of the Ah receptor gene.
Our results suggest that mRNA induction of some genes by destruction of adherens junctions depends on the Ah receptor. β-Catenin, one of the components of the adherens junction, was released from the E-cadherin complex, which resulted in its increased interaction with the Ah receptor, and was translocated into the nucleus, and consequently the target genes would be transcribed.
Our observations suggest that some aspects of the molecular mechanism of wound healing involve the Ah receptor.
► Depletion of calcium by transfer of cells to S-MEM destroyed adherens junctions. ► Nuclear translocation of the Ah receptor induced CYP1A1 and Slug mRNAs. ► β-Catenin was released from E-cadherin complexes by destruction of adherens junctions. ► Interaction between β-catenin and the Ah receptor increased after S-MEM treatment. ► Knockdown of β-catenin increased the level of Ah receptor mRNA. |
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| AbstractList | The aryl hydrocarbon (Ah) receptor is one of the best known ligand-activated transcription factors. The present study has focused on the wound-healing process on Ah receptor function.
Depletion of calcium from culture medium of Caco-2 human colon carcinoma cells by transfer to Minimal Essential Medium (Spinner Modification; S-MEM) destroyed adherens junctions and the cells were used as the model of wound-healing process.
Calcium depletion induced both nuclear translocation of the Ah receptor, and increased expression of CYP1A1 and Slug mRNAs in Caco-2 cells. However, expression of Slug mRNA was not significantly induced by treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin. Knockdown of the Ah receptor and treatment with Ah receptor antagonists decreased level of CYP1A1 mRNA. The fragment of E-cadherin released by γ-secretase was not involved in induction of CYP1A1 mRNA following S-MEM treatment. Knockdown of β-catenin increased levels of Ah receptor mRNA, which may be attributable to direct or indirect involvement of β-catenin in suppression of the Ah receptor gene.
Our results suggest that mRNA induction of some genes by destruction of adherens junctions depends on the Ah receptor. β-Catenin, one of the components of the adherens junction, was released from the E-cadherin complex, which resulted in its increased interaction with the Ah receptor, and was translocated into the nucleus, and consequently the target genes would be transcribed.
Our observations suggest that some aspects of the molecular mechanism of wound healing involve the Ah receptor.
► Depletion of calcium by transfer of cells to S-MEM destroyed adherens junctions. ► Nuclear translocation of the Ah receptor induced CYP1A1 and Slug mRNAs. ► β-Catenin was released from E-cadherin complexes by destruction of adherens junctions. ► Interaction between β-catenin and the Ah receptor increased after S-MEM treatment. ► Knockdown of β-catenin increased the level of Ah receptor mRNA. The aryl hydrocarbon (Ah) receptor is one of the best known ligand-activated transcription factors. The present study has focused on the wound-healing process on Ah receptor function. Depletion of calcium from culture medium of Caco-2 human colon carcinoma cells by transfer to Minimal Essential Medium (Spinner Modification; S-MEM) destroyed adherens junctions and the cells were used as the model of wound-healing process. Calcium depletion induced both nuclear translocation of the Ah receptor, and increased expression of CYP1A1 and Slug mRNAs in Caco-2 cells. However, expression of Slug mRNA was not significantly induced by treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin. Knockdown of the Ah receptor and treatment with Ah receptor antagonists decreased level of CYP1A1 mRNA. The fragment of E-cadherin released by gamma-secretase was not involved in induction of CYP1A1 mRNA following S-MEM treatment. Knockdown of beta-catenin increased levels of Ah receptor mRNA, which may be attributable to direct or indirect involvement of beta-catenin in suppression of the Ah receptor gene. Our results suggest that mRNA induction of some genes by destruction of adherens junctions depends on the Ah receptor. beta-Catenin, one of the components of the adherens junction, was released from the E-cadherin complex, which resulted in its increased interaction with the Ah receptor, and was translocated into the nucleus, and consequently the target genes would be transcribed. Our observations suggest that some aspects of the molecular mechanism of wound healing involve the Ah receptor. The aryl hydrocarbon (Ah) receptor is one of the best known ligand-activated transcription factors. The present study has focused on the wound-healing process on Ah receptor function.BACKGROUNDThe aryl hydrocarbon (Ah) receptor is one of the best known ligand-activated transcription factors. The present study has focused on the wound-healing process on Ah receptor function.Depletion of calcium from culture medium of Caco-2 human colon carcinoma cells by transfer to Minimal Essential Medium (Spinner Modification; S-MEM) destroyed adherens junctions and the cells were used as the model of wound-healing process.METHODSDepletion of calcium from culture medium of Caco-2 human colon carcinoma cells by transfer to Minimal Essential Medium (Spinner Modification; S-MEM) destroyed adherens junctions and the cells were used as the model of wound-healing process.Calcium depletion induced both nuclear translocation of the Ah receptor, and increased expression of CYP1A1 and Slug mRNAs in Caco-2 cells. However, expression of Slug mRNA was not significantly induced by treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin. Knockdown of the Ah receptor and treatment with Ah receptor antagonists decreased level of CYP1A1 mRNA. The fragment of E-cadherin released by gamma-secretase was not involved in induction of CYP1A1 mRNA following S-MEM treatment. Knockdown of beta-catenin increased levels of Ah receptor mRNA, which may be attributable to direct or indirect involvement of beta-catenin in suppression of the Ah receptor gene.RESULTSCalcium depletion induced both nuclear translocation of the Ah receptor, and increased expression of CYP1A1 and Slug mRNAs in Caco-2 cells. However, expression of Slug mRNA was not significantly induced by treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin. Knockdown of the Ah receptor and treatment with Ah receptor antagonists decreased level of CYP1A1 mRNA. The fragment of E-cadherin released by gamma-secretase was not involved in induction of CYP1A1 mRNA following S-MEM treatment. Knockdown of beta-catenin increased levels of Ah receptor mRNA, which may be attributable to direct or indirect involvement of beta-catenin in suppression of the Ah receptor gene.Our results suggest that mRNA induction of some genes by destruction of adherens junctions depends on the Ah receptor. beta-Catenin, one of the components of the adherens junction, was released from the E-cadherin complex, which resulted in its increased interaction with the Ah receptor, and was translocated into the nucleus, and consequently the target genes would be transcribed.CONCLUSIONSOur results suggest that mRNA induction of some genes by destruction of adherens junctions depends on the Ah receptor. beta-Catenin, one of the components of the adherens junction, was released from the E-cadherin complex, which resulted in its increased interaction with the Ah receptor, and was translocated into the nucleus, and consequently the target genes would be transcribed.Our observations suggest that some aspects of the molecular mechanism of wound healing involve the Ah receptor.GENERAL SIGNIFICANCEOur observations suggest that some aspects of the molecular mechanism of wound healing involve the Ah receptor. BACKGROUND: The aryl hydrocarbon (Ah) receptor is one of the best known ligand-activated transcription factors. The present study has focused on the wound-healing process on Ah receptor function. METHODS: Depletion of calcium from culture medium of Caco-2 human colon carcinoma cells by transfer to Minimal Essential Medium (Spinner Modification; S-MEM) destroyed adherens junctions and the cells were used as the model of wound-healing process. RESULTS: Calcium depletion induced both nuclear translocation of the Ah receptor, and increased expression of CYP1A1 and Slug mRNAs in Caco-2 cells. However, expression of Slug mRNA was not significantly induced by treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin. Knockdown of the Ah receptor and treatment with Ah receptor antagonists decreased level of CYP1A1 mRNA. The fragment of E-cadherin released by γ-secretase was not involved in induction of CYP1A1 mRNA following S-MEM treatment. Knockdown of β-catenin increased levels of Ah receptor mRNA, which may be attributable to direct or indirect involvement of β-catenin in suppression of the Ah receptor gene. CONCLUSIONS: Our results suggest that mRNA induction of some genes by destruction of adherens junctions depends on the Ah receptor. β-Catenin, one of the components of the adherens junction, was released from the E-cadherin complex, which resulted in its increased interaction with the Ah receptor, and was translocated into the nucleus, and consequently the target genes would be transcribed. GENERAL SIGNIFICANCE: Our observations suggest that some aspects of the molecular mechanism of wound healing involve the Ah receptor. The aryl hydrocarbon (Ah) receptor is one of the best known ligand-activated transcription factors. The present study has focused on the wound-healing process on Ah receptor function.Depletion of calcium from culture medium of Caco-2 human colon carcinoma cells by transfer to Minimal Essential Medium (Spinner Modification; S-MEM) destroyed adherens junctions and the cells were used as the model of wound-healing process.Calcium depletion induced both nuclear translocation of the Ah receptor, and increased expression of CYP1A1 and Slug mRNAs in Caco-2 cells. However, expression of Slug mRNA was not significantly induced by treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin. Knockdown of the Ah receptor and treatment with Ah receptor antagonists decreased level of CYP1A1 mRNA. The fragment of E-cadherin released by γ-secretase was not involved in induction of CYP1A1 mRNA following S-MEM treatment. Knockdown of β-catenin increased levels of Ah receptor mRNA, which may be attributable to direct or indirect involvement of β-catenin in suppression of the Ah receptor gene.Our results suggest that mRNA induction of some genes by destruction of adherens junctions depends on the Ah receptor. β-Catenin, one of the components of the adherens junction, was released from the E-cadherin complex, which resulted in its increased interaction with the Ah receptor, and was translocated into the nucleus, and consequently the target genes would be transcribed.Our observations suggest that some aspects of the molecular mechanism of wound healing involve the Ah receptor. |
| Author | Takumi, Ryo Kikuchi, Hideaki Kasai, Shuya Kamimura, Toru Ishigaki, Takanori |
| Author_xml | – sequence: 1 givenname: Shuya surname: Kasai fullname: Kasai, Shuya organization: Science of Biosources, United Graduate School of Agricultural Science, Iwate University, Morioka 020-8551, Japan – sequence: 2 givenname: Takanori surname: Ishigaki fullname: Ishigaki, Takanori organization: Department of Biochemistry and Molecular Biology, Faculty of Agriculture and Life Science, Hirosaki University, Hirosaki 036-8561, Japan – sequence: 3 givenname: Ryo surname: Takumi fullname: Takumi, Ryo organization: Department of Biochemistry and Molecular Biology, Faculty of Agriculture and Life Science, Hirosaki University, Hirosaki 036-8561, Japan – sequence: 4 givenname: Toru surname: Kamimura fullname: Kamimura, Toru organization: Department of Biochemistry and Molecular Biology, Faculty of Agriculture and Life Science, Hirosaki University, Hirosaki 036-8561, Japan – sequence: 5 givenname: Hideaki surname: Kikuchi fullname: Kikuchi, Hideaki email: hkikuchi@cc.hirosaki-u.ac.jp organization: Science of Biosources, United Graduate School of Agricultural Science, Iwate University, Morioka 020-8551, Japan |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23174221$$D View this record in MEDLINE/PubMed |
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| Keywords | HSP90 CTF2 PAS TCDD ARNT XRE Lef EMT E-cadherin Cytochrome P-450 1A1 bHLH Aryl hydrocarbon receptor MAF E-cadherin carboxy terminal fragment 2 CYP1A1 β-Catenin XAP-2 S-MEM FoxM1 GAPDH DAPT |
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| Snippet | The aryl hydrocarbon (Ah) receptor is one of the best known ligand-activated transcription factors. The present study has focused on the wound-healing process... BACKGROUND: The aryl hydrocarbon (Ah) receptor is one of the best known ligand-activated transcription factors. The present study has focused on the... |
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| SubjectTerms | adherens junctions Adherens Junctions - drug effects Adherens Junctions - metabolism Adherens Junctions - pathology Amyloid Precursor Protein Secretases - genetics Amyloid Precursor Protein Secretases - metabolism antagonists Aryl hydrocarbon receptor beta Catenin - genetics beta Catenin - metabolism Caco-2 Cells cadherins Cadherins - genetics Cadherins - metabolism calcium Calcium - deficiency Cell Nucleus - drug effects Cell Nucleus - metabolism colorectal neoplasms Culture Media Cytochrome P-450 1A1 Cytochrome P-450 CYP1A1 - genetics Cytochrome P-450 CYP1A1 - metabolism E-cadherin E-cadherin carboxy terminal fragment 2 Gene Expression Regulation - drug effects genes human cell lines Humans messenger RNA Models, Biological neoplasm cells Peptide Fragments - genetics Peptide Fragments - metabolism Polychlorinated Dibenzodioxins - pharmacology Protein Transport Receptors, Aryl Hydrocarbon - antagonists & inhibitors Receptors, Aryl Hydrocarbon - genetics Receptors, Aryl Hydrocarbon - metabolism RNA, Messenger - genetics RNA, Messenger - metabolism RNA, Small Interfering - genetics S-MEM Signal Transduction - drug effects Signal Transduction - genetics Snail Family Transcription Factors tetrachlorodibenzo-p-dioxin tissue repair transcription factors Transcription Factors - genetics Transcription Factors - metabolism Wound Healing - drug effects Wound Healing - genetics β-Catenin |
| Title | β-Catenin signaling induces CYP1A1 expression by disrupting adherens junctions in Caco-2 human colon carcinoma cells |
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