膵がんの発生進展を制御するエピゲノム修飾酵素
エピゲノムとは，様々な細胞外環境に応答しつつ遺伝子の転写を調節している可逆的な発現制御状態の総称である．そのシステムはDNAメチル化修飾，ヒストン修飾，クロマチン構造変化などを担う数多くの酵素・分子群により複雑かつ巧妙に調節される．エピゲノム制御はゲノム変異のような塩基配列自体の変化を介さないことが前提だが，次世代シークエンス解析は「エピゲノムを調節する分子自体のゲノム変異」という一見逆説的な興味深い知見をもたらした．さらに“がん細胞特有なエピゲノム”が俯瞰できるようになって悪性形質との関連が解析され，膵がんにおけるエピゲノムの役割も着実に解明されつつある．本章ではヒストン脱メチル化酵素KDM...
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| Published in | 膵臓 Vol. 31; no. 1; pp. 69 - 75 |
|---|---|
| Main Authors | , , |
| Format | Journal Article |
| Language | Japanese |
| Published |
日本膵臓学会
25.02.2016
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0913-0071 1881-2805 |
| DOI | 10.2958/suizo.31.69 |
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| Abstract | エピゲノムとは，様々な細胞外環境に応答しつつ遺伝子の転写を調節している可逆的な発現制御状態の総称である．そのシステムはDNAメチル化修飾，ヒストン修飾，クロマチン構造変化などを担う数多くの酵素・分子群により複雑かつ巧妙に調節される．エピゲノム制御はゲノム変異のような塩基配列自体の変化を介さないことが前提だが，次世代シークエンス解析は「エピゲノムを調節する分子自体のゲノム変異」という一見逆説的な興味深い知見をもたらした．さらに“がん細胞特有なエピゲノム”が俯瞰できるようになって悪性形質との関連が解析され，膵がんにおけるエピゲノムの役割も着実に解明されつつある．本章ではヒストン脱メチル化酵素KDM6Bと膵がんの浸潤能・腫瘍形成能の関連に焦点をあてる．今後は膵がん特異的なエピゲノム制御メカニズムを明らかにすることで，診断・治療における新たな標的化戦略を提示することが可能になると考えられる． |
|---|---|
| AbstractList | エピゲノムとは，様々な細胞外環境に応答しつつ遺伝子の転写を調節している可逆的な発現制御状態の総称である．そのシステムはDNAメチル化修飾，ヒストン修飾，クロマチン構造変化などを担う数多くの酵素・分子群により複雑かつ巧妙に調節される．エピゲノム制御はゲノム変異のような塩基配列自体の変化を介さないことが前提だが，次世代シークエンス解析は「エピゲノムを調節する分子自体のゲノム変異」という一見逆説的な興味深い知見をもたらした．さらに“がん細胞特有なエピゲノム”が俯瞰できるようになって悪性形質との関連が解析され，膵がんにおけるエピゲノムの役割も着実に解明されつつある．本章ではヒストン脱メチル化酵素KDM6Bと膵がんの浸潤能・腫瘍形成能の関連に焦点をあてる．今後は膵がん特異的なエピゲノム制御メカニズムを明らかにすることで，診断・治療における新たな標的化戦略を提示することが可能になると考えられる． 「要旨」: エピゲノムとは, 様々な細胞外環境に応答しつつ遺伝子の転写を調節している可逆的な発現制御状態の総称である. そのシステムはDNAメチル化修飾, ヒストン修飾, クロマチン構造変化などを担う数多くの酵素・分子群により複雑かつ巧妙に調節される. エピゲノム制御はゲノム変異のような塩基配列自体の変化を介さないことが前提だが, 次世代シークエンス解析は「エピゲノムを調節する分子自体のゲノム変異」という一見逆説的な興味深い知見をもたらした. さらに"がん細胞特有なエピゲノム"が俯瞰できるようになって悪性形質との関連が解析され, 膵がんにおけるエピゲノムの役割も着実に解明されつつある. 本章ではヒストン脱メチル化酵素KDM6Bと膵がんの浸潤能・腫瘍形成能の関連に焦点をあてる. 今後は膵がん特異的なエピゲノム制御メカニズムを明らかにすることで, 診断・治療における新たな標的化戦略を提示することが可能になると考えられる. |
| Author | 立石, 敬介 山本, 恵介 小池, 和彦 |
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| DOI | 10.2958/suizo.31.69 |
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| References | 18) Noushmehr H, Weisenberger DJ, Diefes K, et al. Cancer Genome Atlas Research Network. Identification of a CpG island methylator phenotype that defines a distinct subgroup of glioma. Cancer Cell 2010; 17: 510-22. 12) Baylin SB, Jones PA. A decade of exploring the cancer epigenome - biological and translational implications. Nat Rev Cancer 2011; 11: 726-34. 27) Tateishi K, Ohta M, Kanai F, et al. Dysregulated expression of stem cell factor Bmi1 in precancerous lesions of the gastrointestinal tract. Clin Cancer Res 2006; 12: 6960-6. 29) Agger K, Cloos PA, Rudkjaer L, et al. The H3K27me3 demethylase JMJD3 contributes to the activation of the INK4A-ARF locus in response to oncogene- and stress-induced senescence. Genes Dev 2009; 23: 1171-6. 6) Ijichi H, Chytil A, Gorska AE, et al. Aggressive pancreatic ductal adenocarcinoma in mice caused by pancreas-specific blockade of transforming growth factor-beta signaling in cooperation with active Kras expression. Genes Dev 2006; 20: 3147-60. 21) von Figura G, Fukuda A, Roy N, et al. The chromatin regulator Brg1 suppresses formation of intraductal papillary mucinous neoplasm and pancreatic ductal adenocarcinoma. Nat Cell Biol 2014; 16: 255-67. 25) Waddell N, Pajic M, Patch AM. Whole genomes redefine the mutational landscape of pancreatic cancer. Nature 2015; 518: 495-501. 7) Yachida S, Jones S, Bozic I, et al. Distant metastasis occurs late during the genetic evolution of pancreatic cancer. Nature 2010; 467: 1114-7. 8) De Carvalho DD, Sharma S, You JS, et al. DNA methylation screening identifies driver epigenetic events of cancer cell survival. Cancer Cell 2012; 21: 655-67. 14) Johnson BE, Mazor T, Hong C, et al. Mutational analysis reveals the origin and therapy-driven evolution of recurrent glioma. Science 2014; 343: 189-93. 19) Caldas C, Hahn SA, da Costa LT, et al. Frequent somatic mutations and homozygous deletions of the p16 (MTS1) gene in pancreatic adenocarcinoma. Nat Genet 1994; 8: 27-32. 26) Martinez-Garcia E, Licht JD. Deregulation of H3K27 methylation in cancer. Nat Genet 2010; 42: 100-1. 10) Chi P, Allis CD, Wng GG. Covalent histone modifications -miswritten, misinterpreted and mis-erased in human cancers. Nat Rev Cancer 2010; 10: 457-69. 28) Lin LJ, Asaoka Y, Tada M, et al. Integrated analysis of copy number alterations and loss of heterozygosity in human pancreatic cancer using a high-resolution, single nucleotide polymorphism array. Oncology 2008; 75: 102-12. 1) Hruban RH, Goggins M, Parsons J, Kern SE. Progression model for pancreatic cancer. Clin Cancer Res 2000; 6: 2969-72. 3) Hingorani SR, Wang L, Multani AS, et al. Trp53R172H and KrasG12D cooperate to promote chromosomal instability and widely metastatic pancreatic ductal adenocarcinoma in mice. Cancer Cell 2005; 7: 469-83. 13) Gerlinger M, Rowan AJ, Horswell S, et al. Intratumor heterogeneity and branched evolution revealed by multiregion sequencing. N Engl J Med 2012; 366: 883-92. 31) Yamamoto K, Tateishi K, Kudo Y, et al. Loss of histone demethylase KDM6B enhances aggressiveness of pancreatic cancer through downregulation of C/EBPα. Carcinogenesis 2014; 35: 2404-14. 22) Tzatsos A, Paskaleva P, Ferrari F, et al. KDM2B promotes pancreatic cancer via Polycomb-dependent and -independent transcriptional programs. J Clin Invest 2013; 123: 727-39. 30) Barradas M, Anderton E, Acosta JC, et al. Histone demethylase JMJD3 contributes to epigenetic control of INK4a/ARF by oncogenic RAS. Genes Dev 2009; 23: 1177-82. 16) You JS, Jones PA. Cancer genetics and epigenetics: two sides of the same coin? Cancer Cell 2012; 22: 9-20. 4) Aguirre AJ, Bardeesy N, Sinha M, et al. Activated Kras and Ink4a/Arf deficiency cooperate to produce metastatic pancreatic ductal adenocarcinoma. Genes Dev 2003; 17: 3112-26. 17) Toyota M, Ahuja N, Ohe-Toyota M, et al. CpG island methylator phenotype in colorectal cancer. Proc Natl Acad Sci U S A 1999; 96: 8681-6. 11) Baylin SB, Höppener JW, de Bustros A, et al. DNA methylation patterns of the calcitonin gene in human lung cancers and lymphomas. DNA methylation patterns of the calcitonin gene in human lung cancers and lymphomas. Cancer Res 1986; 46: 2917-22. 5) Bardeesy N, Aguirre AJ, Chu GC, et al. Both p16 (Ink4a) and the p19 (Arf)-p53 pathway constrain progression of pancreatic adenocarcinoma in the mouse. Proc Natl Acad Sci U S A 2006; 103: 5947-52. 23) Mallen-St Clair J, Soydaner-Azeloglu R, Lee KE, et al. EZH2 couples pancreatic regeneration to neoplastic progression. Genes Dev 2012; 26: 439-44. 9) Mack SC, Witt H, Piro RM, et al. Epigenomic alterations define lethal CIMP-positive ependymomas of infancy. Nature 2014; 506: 445-50. 15) Gundem G, Van Loo P, Kremeyer B, et al. The evolutionary history of lethal metastatic prostate cancer. Nature 2015; 520: 353-7. 2) Hingorani SR, Petricoin EF, Maitra A, et al. Preinvasive and invasive ductal pancreatic cancer and its early detection in the mouse. Cancer Cell 2003; 4: 437-50. 20) Fukushima N, Sato N, Ueki T, et al. Aberrant methylation of preproenkephalin and p16 genes in pancreatic intraepithelial neoplasia and pancreatic ductal adenocarcinoma. Am J Pathol 2002; 160: 1573-81. 24) Biankin AV, Waddell N, Kassahn KS, et al. Pancreatic cancer genomes reveal aberrations in axon guidance pathway genes. Nature 2012; 491: 399-405. |
| References_xml | – reference: 18) Noushmehr H, Weisenberger DJ, Diefes K, et al. Cancer Genome Atlas Research Network. Identification of a CpG island methylator phenotype that defines a distinct subgroup of glioma. Cancer Cell 2010; 17: 510-22. – reference: 7) Yachida S, Jones S, Bozic I, et al. Distant metastasis occurs late during the genetic evolution of pancreatic cancer. Nature 2010; 467: 1114-7. – reference: 29) Agger K, Cloos PA, Rudkjaer L, et al. The H3K27me3 demethylase JMJD3 contributes to the activation of the INK4A-ARF locus in response to oncogene- and stress-induced senescence. Genes Dev 2009; 23: 1171-6. – reference: 2) Hingorani SR, Petricoin EF, Maitra A, et al. Preinvasive and invasive ductal pancreatic cancer and its early detection in the mouse. Cancer Cell 2003; 4: 437-50. – reference: 24) Biankin AV, Waddell N, Kassahn KS, et al. Pancreatic cancer genomes reveal aberrations in axon guidance pathway genes. Nature 2012; 491: 399-405. – reference: 25) Waddell N, Pajic M, Patch AM. Whole genomes redefine the mutational landscape of pancreatic cancer. Nature 2015; 518: 495-501. – reference: 1) Hruban RH, Goggins M, Parsons J, Kern SE. Progression model for pancreatic cancer. Clin Cancer Res 2000; 6: 2969-72. – reference: 5) Bardeesy N, Aguirre AJ, Chu GC, et al. Both p16 (Ink4a) and the p19 (Arf)-p53 pathway constrain progression of pancreatic adenocarcinoma in the mouse. Proc Natl Acad Sci U S A 2006; 103: 5947-52. – reference: 28) Lin LJ, Asaoka Y, Tada M, et al. Integrated analysis of copy number alterations and loss of heterozygosity in human pancreatic cancer using a high-resolution, single nucleotide polymorphism array. Oncology 2008; 75: 102-12. – reference: 19) Caldas C, Hahn SA, da Costa LT, et al. Frequent somatic mutations and homozygous deletions of the p16 (MTS1) gene in pancreatic adenocarcinoma. Nat Genet 1994; 8: 27-32. – reference: 26) Martinez-Garcia E, Licht JD. Deregulation of H3K27 methylation in cancer. Nat Genet 2010; 42: 100-1. – reference: 10) Chi P, Allis CD, Wng GG. Covalent histone modifications -miswritten, misinterpreted and mis-erased in human cancers. Nat Rev Cancer 2010; 10: 457-69. – reference: 15) Gundem G, Van Loo P, Kremeyer B, et al. The evolutionary history of lethal metastatic prostate cancer. Nature 2015; 520: 353-7. – reference: 16) You JS, Jones PA. Cancer genetics and epigenetics: two sides of the same coin? Cancer Cell 2012; 22: 9-20. – reference: 21) von Figura G, Fukuda A, Roy N, et al. The chromatin regulator Brg1 suppresses formation of intraductal papillary mucinous neoplasm and pancreatic ductal adenocarcinoma. Nat Cell Biol 2014; 16: 255-67. – reference: 27) Tateishi K, Ohta M, Kanai F, et al. Dysregulated expression of stem cell factor Bmi1 in precancerous lesions of the gastrointestinal tract. Clin Cancer Res 2006; 12: 6960-6. – reference: 14) Johnson BE, Mazor T, Hong C, et al. Mutational analysis reveals the origin and therapy-driven evolution of recurrent glioma. Science 2014; 343: 189-93. – reference: 11) Baylin SB, Höppener JW, de Bustros A, et al. DNA methylation patterns of the calcitonin gene in human lung cancers and lymphomas. DNA methylation patterns of the calcitonin gene in human lung cancers and lymphomas. Cancer Res 1986; 46: 2917-22. – reference: 4) Aguirre AJ, Bardeesy N, Sinha M, et al. Activated Kras and Ink4a/Arf deficiency cooperate to produce metastatic pancreatic ductal adenocarcinoma. Genes Dev 2003; 17: 3112-26. – reference: 22) Tzatsos A, Paskaleva P, Ferrari F, et al. KDM2B promotes pancreatic cancer via Polycomb-dependent and -independent transcriptional programs. J Clin Invest 2013; 123: 727-39. – reference: 3) Hingorani SR, Wang L, Multani AS, et al. Trp53R172H and KrasG12D cooperate to promote chromosomal instability and widely metastatic pancreatic ductal adenocarcinoma in mice. Cancer Cell 2005; 7: 469-83. – reference: 20) Fukushima N, Sato N, Ueki T, et al. Aberrant methylation of preproenkephalin and p16 genes in pancreatic intraepithelial neoplasia and pancreatic ductal adenocarcinoma. Am J Pathol 2002; 160: 1573-81. – reference: 17) Toyota M, Ahuja N, Ohe-Toyota M, et al. CpG island methylator phenotype in colorectal cancer. Proc Natl Acad Sci U S A 1999; 96: 8681-6. – reference: 12) Baylin SB, Jones PA. A decade of exploring the cancer epigenome - biological and translational implications. Nat Rev Cancer 2011; 11: 726-34. – reference: 13) Gerlinger M, Rowan AJ, Horswell S, et al. Intratumor heterogeneity and branched evolution revealed by multiregion sequencing. N Engl J Med 2012; 366: 883-92. – reference: 30) Barradas M, Anderton E, Acosta JC, et al. Histone demethylase JMJD3 contributes to epigenetic control of INK4a/ARF by oncogenic RAS. Genes Dev 2009; 23: 1177-82. – reference: 8) De Carvalho DD, Sharma S, You JS, et al. DNA methylation screening identifies driver epigenetic events of cancer cell survival. Cancer Cell 2012; 21: 655-67. – reference: 9) Mack SC, Witt H, Piro RM, et al. Epigenomic alterations define lethal CIMP-positive ependymomas of infancy. Nature 2014; 506: 445-50. – reference: 6) Ijichi H, Chytil A, Gorska AE, et al. Aggressive pancreatic ductal adenocarcinoma in mice caused by pancreas-specific blockade of transforming growth factor-beta signaling in cooperation with active Kras expression. Genes Dev 2006; 20: 3147-60. – reference: 31) Yamamoto K, Tateishi K, Kudo Y, et al. Loss of histone demethylase KDM6B enhances aggressiveness of pancreatic cancer through downregulation of C/EBPα. Carcinogenesis 2014; 35: 2404-14. – reference: 23) Mallen-St Clair J, Soydaner-Azeloglu R, Lee KE, et al. EZH2 couples pancreatic regeneration to neoplastic progression. Genes Dev 2012; 26: 439-44. |
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| Snippet | ... 「要旨」: エピゲノムとは, 様々な細胞外環境に応答しつつ遺伝子の転写を調節している可逆的な発現制御状態の総称である. そのシステムはDNAメチル化修飾, ヒストン修飾, クロマチン構造変化などを担う数多くの酵素・分子群により複雑かつ巧妙に調節される.... |
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| SubjectTerms | KDM6B エピゲノム ヒストン メチル化 膵がん |
| Title | 膵がんの発生進展を制御するエピゲノム修飾酵素 |
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