Tri-methylation of H3K79 is decreased in TGF-β1-induced epithelial-to-mesenchymal transition in lung cancer
Abstract Background The epithelial-to-mesenchymal transition (EMT) enables epithelial cancer cells to acquire mesenchymal features and contributes to metastasis and resistance to treatment. This process involves epigenetic reprogramming for gene expression. We explored global histone modifications d...
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Gespeichert in:
| Autor*in: |
Emilie Evanno [verfasserIn] Julie Godet [verfasserIn] Nathalie Piccirilli [verfasserIn] Joëlle Guilhot [verfasserIn] Serge Milin [verfasserIn] Jean Marc Gombert [verfasserIn] Benoit Fouchaq [verfasserIn] Joëlle Roche [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2017 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
In: Clinical Epigenetics ; 9(2017), 1, Seite 14 volume:9 ; year:2017 ; number:1 ; pages:14 |
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Link aufrufen |
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| DOI / URN: |
10.1186/s13148-017-0380-0 |
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| Katalog-ID: |
DOAJ056923015 |
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| 520 | |a Abstract Background The epithelial-to-mesenchymal transition (EMT) enables epithelial cancer cells to acquire mesenchymal features and contributes to metastasis and resistance to treatment. This process involves epigenetic reprogramming for gene expression. We explored global histone modifications during TGF-β1-induced EMT in two non-small cell lung cancer (NSCLC) cell lines and tested different epigenetic treatment to modulate or partially reverse EMT. Results Loss of classical epithelial markers and gain of mesenchymal markers were verified in A549 and H358 cell lines during TGF-β1-induced EMT. In addition, we noticed increased expression of the axonal guidance protein semaphorin 3C (SEMA3C) and PD-L1 (programmed death-ligand 1) involved in the inhibition of the immune system, suggesting that both SEMA3C and PD-L1 could be the new markers of TGF-β1-induced EMT. H3K79me3 and H2BK120me1 were decreased in A549 and H358 cell lines after a 48-h TGF-β1 treatment, as well as H2BK120ac in A549 cells. However, decreased H3K79me3 was not associated with expression of the histone methyltransferase DOT1L. Furthermore, H3K79me3 was decreased in tumors compared in normal tissues and not associated with cell proliferation. Associations of histone deacetylase inhibitor (SAHA) with DOT1L inhibitors (EPZ5676 or SGC0946) or BET bromodomain inhibitor (PFI-1) were efficient to partially reverse TGF-β1 effects by decreasing expression of PD-L1, SEMA3C, and its receptor neuropilin-2 (NRP2) and by increasing epithelial markers such as E-cadherin. Conclusion Histone methylation was modified during EMT, and combination of epigenetic compounds with conventional or targeted chemotherapy might contribute to reduce metastasis and to enhance clinical responses. | ||
| 650 | 4 | |a Lung cancer | |
| 650 | 4 | |a NSCLC | |
| 650 | 4 | |a EMT | |
| 650 | 4 | |a H3K79me3 | |
| 650 | 4 | |a DOT1L | |
| 650 | 4 | |a PD-L1 | |
| 653 | 0 | |a Medicine | |
| 653 | 0 | |a R | |
| 653 | 0 | |a Genetics | |
| 700 | 0 | |a Julie Godet |e verfasserin |4 aut | |
| 700 | 0 | |a Nathalie Piccirilli |e verfasserin |4 aut | |
| 700 | 0 | |a Joëlle Guilhot |e verfasserin |4 aut | |
| 700 | 0 | |a Serge Milin |e verfasserin |4 aut | |
| 700 | 0 | |a Jean Marc Gombert |e verfasserin |4 aut | |
| 700 | 0 | |a Benoit Fouchaq |e verfasserin |4 aut | |
| 700 | 0 | |a Joëlle Roche |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i In |t Clinical Epigenetics |g 9(2017), 1, Seite 14 |
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10.1186/s13148-017-0380-0 doi (DE-627)DOAJ056923015 (DE-599)DOAJ27cceefc05bc4f75a54d88fbc4f19b04 DE-627 ger DE-627 rakwb eng QH426-470 Emilie Evanno verfasserin aut Tri-methylation of H3K79 is decreased in TGF-β1-induced epithelial-to-mesenchymal transition in lung cancer 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background The epithelial-to-mesenchymal transition (EMT) enables epithelial cancer cells to acquire mesenchymal features and contributes to metastasis and resistance to treatment. This process involves epigenetic reprogramming for gene expression. We explored global histone modifications during TGF-β1-induced EMT in two non-small cell lung cancer (NSCLC) cell lines and tested different epigenetic treatment to modulate or partially reverse EMT. Results Loss of classical epithelial markers and gain of mesenchymal markers were verified in A549 and H358 cell lines during TGF-β1-induced EMT. In addition, we noticed increased expression of the axonal guidance protein semaphorin 3C (SEMA3C) and PD-L1 (programmed death-ligand 1) involved in the inhibition of the immune system, suggesting that both SEMA3C and PD-L1 could be the new markers of TGF-β1-induced EMT. H3K79me3 and H2BK120me1 were decreased in A549 and H358 cell lines after a 48-h TGF-β1 treatment, as well as H2BK120ac in A549 cells. However, decreased H3K79me3 was not associated with expression of the histone methyltransferase DOT1L. Furthermore, H3K79me3 was decreased in tumors compared in normal tissues and not associated with cell proliferation. Associations of histone deacetylase inhibitor (SAHA) with DOT1L inhibitors (EPZ5676 or SGC0946) or BET bromodomain inhibitor (PFI-1) were efficient to partially reverse TGF-β1 effects by decreasing expression of PD-L1, SEMA3C, and its receptor neuropilin-2 (NRP2) and by increasing epithelial markers such as E-cadherin. Conclusion Histone methylation was modified during EMT, and combination of epigenetic compounds with conventional or targeted chemotherapy might contribute to reduce metastasis and to enhance clinical responses. Lung cancer NSCLC EMT H3K79me3 DOT1L PD-L1 Medicine R Genetics Julie Godet verfasserin aut Nathalie Piccirilli verfasserin aut Joëlle Guilhot verfasserin aut Serge Milin verfasserin aut Jean Marc Gombert verfasserin aut Benoit Fouchaq verfasserin aut Joëlle Roche verfasserin aut In Clinical Epigenetics 9(2017), 1, Seite 14 volume:9 year:2017 number:1 pages:14 https://doi.org/10.1186/s13148-017-0380-0 kostenfrei https://doaj.org/article/27cceefc05bc4f75a54d88fbc4f19b04 kostenfrei http://link.springer.com/article/10.1186/s13148-017-0380-0 kostenfrei https://doaj.org/toc/1868-7075 Journal toc kostenfrei https://doaj.org/toc/1868-7083 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 9 2017 1 14 |
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10.1186/s13148-017-0380-0 doi (DE-627)DOAJ056923015 (DE-599)DOAJ27cceefc05bc4f75a54d88fbc4f19b04 DE-627 ger DE-627 rakwb eng QH426-470 Emilie Evanno verfasserin aut Tri-methylation of H3K79 is decreased in TGF-β1-induced epithelial-to-mesenchymal transition in lung cancer 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background The epithelial-to-mesenchymal transition (EMT) enables epithelial cancer cells to acquire mesenchymal features and contributes to metastasis and resistance to treatment. This process involves epigenetic reprogramming for gene expression. We explored global histone modifications during TGF-β1-induced EMT in two non-small cell lung cancer (NSCLC) cell lines and tested different epigenetic treatment to modulate or partially reverse EMT. Results Loss of classical epithelial markers and gain of mesenchymal markers were verified in A549 and H358 cell lines during TGF-β1-induced EMT. In addition, we noticed increased expression of the axonal guidance protein semaphorin 3C (SEMA3C) and PD-L1 (programmed death-ligand 1) involved in the inhibition of the immune system, suggesting that both SEMA3C and PD-L1 could be the new markers of TGF-β1-induced EMT. H3K79me3 and H2BK120me1 were decreased in A549 and H358 cell lines after a 48-h TGF-β1 treatment, as well as H2BK120ac in A549 cells. However, decreased H3K79me3 was not associated with expression of the histone methyltransferase DOT1L. Furthermore, H3K79me3 was decreased in tumors compared in normal tissues and not associated with cell proliferation. Associations of histone deacetylase inhibitor (SAHA) with DOT1L inhibitors (EPZ5676 or SGC0946) or BET bromodomain inhibitor (PFI-1) were efficient to partially reverse TGF-β1 effects by decreasing expression of PD-L1, SEMA3C, and its receptor neuropilin-2 (NRP2) and by increasing epithelial markers such as E-cadherin. Conclusion Histone methylation was modified during EMT, and combination of epigenetic compounds with conventional or targeted chemotherapy might contribute to reduce metastasis and to enhance clinical responses. Lung cancer NSCLC EMT H3K79me3 DOT1L PD-L1 Medicine R Genetics Julie Godet verfasserin aut Nathalie Piccirilli verfasserin aut Joëlle Guilhot verfasserin aut Serge Milin verfasserin aut Jean Marc Gombert verfasserin aut Benoit Fouchaq verfasserin aut Joëlle Roche verfasserin aut In Clinical Epigenetics 9(2017), 1, Seite 14 volume:9 year:2017 number:1 pages:14 https://doi.org/10.1186/s13148-017-0380-0 kostenfrei https://doaj.org/article/27cceefc05bc4f75a54d88fbc4f19b04 kostenfrei http://link.springer.com/article/10.1186/s13148-017-0380-0 kostenfrei https://doaj.org/toc/1868-7075 Journal toc kostenfrei https://doaj.org/toc/1868-7083 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 9 2017 1 14 |
| allfields_unstemmed |
10.1186/s13148-017-0380-0 doi (DE-627)DOAJ056923015 (DE-599)DOAJ27cceefc05bc4f75a54d88fbc4f19b04 DE-627 ger DE-627 rakwb eng QH426-470 Emilie Evanno verfasserin aut Tri-methylation of H3K79 is decreased in TGF-β1-induced epithelial-to-mesenchymal transition in lung cancer 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background The epithelial-to-mesenchymal transition (EMT) enables epithelial cancer cells to acquire mesenchymal features and contributes to metastasis and resistance to treatment. This process involves epigenetic reprogramming for gene expression. We explored global histone modifications during TGF-β1-induced EMT in two non-small cell lung cancer (NSCLC) cell lines and tested different epigenetic treatment to modulate or partially reverse EMT. Results Loss of classical epithelial markers and gain of mesenchymal markers were verified in A549 and H358 cell lines during TGF-β1-induced EMT. In addition, we noticed increased expression of the axonal guidance protein semaphorin 3C (SEMA3C) and PD-L1 (programmed death-ligand 1) involved in the inhibition of the immune system, suggesting that both SEMA3C and PD-L1 could be the new markers of TGF-β1-induced EMT. H3K79me3 and H2BK120me1 were decreased in A549 and H358 cell lines after a 48-h TGF-β1 treatment, as well as H2BK120ac in A549 cells. However, decreased H3K79me3 was not associated with expression of the histone methyltransferase DOT1L. Furthermore, H3K79me3 was decreased in tumors compared in normal tissues and not associated with cell proliferation. Associations of histone deacetylase inhibitor (SAHA) with DOT1L inhibitors (EPZ5676 or SGC0946) or BET bromodomain inhibitor (PFI-1) were efficient to partially reverse TGF-β1 effects by decreasing expression of PD-L1, SEMA3C, and its receptor neuropilin-2 (NRP2) and by increasing epithelial markers such as E-cadherin. Conclusion Histone methylation was modified during EMT, and combination of epigenetic compounds with conventional or targeted chemotherapy might contribute to reduce metastasis and to enhance clinical responses. Lung cancer NSCLC EMT H3K79me3 DOT1L PD-L1 Medicine R Genetics Julie Godet verfasserin aut Nathalie Piccirilli verfasserin aut Joëlle Guilhot verfasserin aut Serge Milin verfasserin aut Jean Marc Gombert verfasserin aut Benoit Fouchaq verfasserin aut Joëlle Roche verfasserin aut In Clinical Epigenetics 9(2017), 1, Seite 14 volume:9 year:2017 number:1 pages:14 https://doi.org/10.1186/s13148-017-0380-0 kostenfrei https://doaj.org/article/27cceefc05bc4f75a54d88fbc4f19b04 kostenfrei http://link.springer.com/article/10.1186/s13148-017-0380-0 kostenfrei https://doaj.org/toc/1868-7075 Journal toc kostenfrei https://doaj.org/toc/1868-7083 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 9 2017 1 14 |
| allfieldsGer |
10.1186/s13148-017-0380-0 doi (DE-627)DOAJ056923015 (DE-599)DOAJ27cceefc05bc4f75a54d88fbc4f19b04 DE-627 ger DE-627 rakwb eng QH426-470 Emilie Evanno verfasserin aut Tri-methylation of H3K79 is decreased in TGF-β1-induced epithelial-to-mesenchymal transition in lung cancer 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background The epithelial-to-mesenchymal transition (EMT) enables epithelial cancer cells to acquire mesenchymal features and contributes to metastasis and resistance to treatment. This process involves epigenetic reprogramming for gene expression. We explored global histone modifications during TGF-β1-induced EMT in two non-small cell lung cancer (NSCLC) cell lines and tested different epigenetic treatment to modulate or partially reverse EMT. Results Loss of classical epithelial markers and gain of mesenchymal markers were verified in A549 and H358 cell lines during TGF-β1-induced EMT. In addition, we noticed increased expression of the axonal guidance protein semaphorin 3C (SEMA3C) and PD-L1 (programmed death-ligand 1) involved in the inhibition of the immune system, suggesting that both SEMA3C and PD-L1 could be the new markers of TGF-β1-induced EMT. H3K79me3 and H2BK120me1 were decreased in A549 and H358 cell lines after a 48-h TGF-β1 treatment, as well as H2BK120ac in A549 cells. However, decreased H3K79me3 was not associated with expression of the histone methyltransferase DOT1L. Furthermore, H3K79me3 was decreased in tumors compared in normal tissues and not associated with cell proliferation. Associations of histone deacetylase inhibitor (SAHA) with DOT1L inhibitors (EPZ5676 or SGC0946) or BET bromodomain inhibitor (PFI-1) were efficient to partially reverse TGF-β1 effects by decreasing expression of PD-L1, SEMA3C, and its receptor neuropilin-2 (NRP2) and by increasing epithelial markers such as E-cadherin. Conclusion Histone methylation was modified during EMT, and combination of epigenetic compounds with conventional or targeted chemotherapy might contribute to reduce metastasis and to enhance clinical responses. Lung cancer NSCLC EMT H3K79me3 DOT1L PD-L1 Medicine R Genetics Julie Godet verfasserin aut Nathalie Piccirilli verfasserin aut Joëlle Guilhot verfasserin aut Serge Milin verfasserin aut Jean Marc Gombert verfasserin aut Benoit Fouchaq verfasserin aut Joëlle Roche verfasserin aut In Clinical Epigenetics 9(2017), 1, Seite 14 volume:9 year:2017 number:1 pages:14 https://doi.org/10.1186/s13148-017-0380-0 kostenfrei https://doaj.org/article/27cceefc05bc4f75a54d88fbc4f19b04 kostenfrei http://link.springer.com/article/10.1186/s13148-017-0380-0 kostenfrei https://doaj.org/toc/1868-7075 Journal toc kostenfrei https://doaj.org/toc/1868-7083 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 9 2017 1 14 |
| allfieldsSound |
10.1186/s13148-017-0380-0 doi (DE-627)DOAJ056923015 (DE-599)DOAJ27cceefc05bc4f75a54d88fbc4f19b04 DE-627 ger DE-627 rakwb eng QH426-470 Emilie Evanno verfasserin aut Tri-methylation of H3K79 is decreased in TGF-β1-induced epithelial-to-mesenchymal transition in lung cancer 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background The epithelial-to-mesenchymal transition (EMT) enables epithelial cancer cells to acquire mesenchymal features and contributes to metastasis and resistance to treatment. This process involves epigenetic reprogramming for gene expression. We explored global histone modifications during TGF-β1-induced EMT in two non-small cell lung cancer (NSCLC) cell lines and tested different epigenetic treatment to modulate or partially reverse EMT. Results Loss of classical epithelial markers and gain of mesenchymal markers were verified in A549 and H358 cell lines during TGF-β1-induced EMT. In addition, we noticed increased expression of the axonal guidance protein semaphorin 3C (SEMA3C) and PD-L1 (programmed death-ligand 1) involved in the inhibition of the immune system, suggesting that both SEMA3C and PD-L1 could be the new markers of TGF-β1-induced EMT. H3K79me3 and H2BK120me1 were decreased in A549 and H358 cell lines after a 48-h TGF-β1 treatment, as well as H2BK120ac in A549 cells. However, decreased H3K79me3 was not associated with expression of the histone methyltransferase DOT1L. Furthermore, H3K79me3 was decreased in tumors compared in normal tissues and not associated with cell proliferation. Associations of histone deacetylase inhibitor (SAHA) with DOT1L inhibitors (EPZ5676 or SGC0946) or BET bromodomain inhibitor (PFI-1) were efficient to partially reverse TGF-β1 effects by decreasing expression of PD-L1, SEMA3C, and its receptor neuropilin-2 (NRP2) and by increasing epithelial markers such as E-cadherin. Conclusion Histone methylation was modified during EMT, and combination of epigenetic compounds with conventional or targeted chemotherapy might contribute to reduce metastasis and to enhance clinical responses. Lung cancer NSCLC EMT H3K79me3 DOT1L PD-L1 Medicine R Genetics Julie Godet verfasserin aut Nathalie Piccirilli verfasserin aut Joëlle Guilhot verfasserin aut Serge Milin verfasserin aut Jean Marc Gombert verfasserin aut Benoit Fouchaq verfasserin aut Joëlle Roche verfasserin aut In Clinical Epigenetics 9(2017), 1, Seite 14 volume:9 year:2017 number:1 pages:14 https://doi.org/10.1186/s13148-017-0380-0 kostenfrei https://doaj.org/article/27cceefc05bc4f75a54d88fbc4f19b04 kostenfrei http://link.springer.com/article/10.1186/s13148-017-0380-0 kostenfrei https://doaj.org/toc/1868-7075 Journal toc kostenfrei https://doaj.org/toc/1868-7083 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 9 2017 1 14 |
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This process involves epigenetic reprogramming for gene expression. We explored global histone modifications during TGF-β1-induced EMT in two non-small cell lung cancer (NSCLC) cell lines and tested different epigenetic treatment to modulate or partially reverse EMT. Results Loss of classical epithelial markers and gain of mesenchymal markers were verified in A549 and H358 cell lines during TGF-β1-induced EMT. In addition, we noticed increased expression of the axonal guidance protein semaphorin 3C (SEMA3C) and PD-L1 (programmed death-ligand 1) involved in the inhibition of the immune system, suggesting that both SEMA3C and PD-L1 could be the new markers of TGF-β1-induced EMT. H3K79me3 and H2BK120me1 were decreased in A549 and H358 cell lines after a 48-h TGF-β1 treatment, as well as H2BK120ac in A549 cells. However, decreased H3K79me3 was not associated with expression of the histone methyltransferase DOT1L. Furthermore, H3K79me3 was decreased in tumors compared in normal tissues and not associated with cell proliferation. Associations of histone deacetylase inhibitor (SAHA) with DOT1L inhibitors (EPZ5676 or SGC0946) or BET bromodomain inhibitor (PFI-1) were efficient to partially reverse TGF-β1 effects by decreasing expression of PD-L1, SEMA3C, and its receptor neuropilin-2 (NRP2) and by increasing epithelial markers such as E-cadherin. Conclusion Histone methylation was modified during EMT, and combination of epigenetic compounds with conventional or targeted chemotherapy might contribute to reduce metastasis and to enhance clinical responses.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Lung cancer</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">NSCLC</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">EMT</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">H3K79me3</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">DOT1L</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">PD-L1</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Medicine</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">R</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Genetics</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Julie Godet</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Nathalie Piccirilli</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Joëlle Guilhot</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Serge Milin</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Jean Marc Gombert</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Benoit Fouchaq</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Joëlle Roche</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Clinical Epigenetics</subfield><subfield code="g">9(2017), 1, Seite 14</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:9</subfield><subfield code="g">year:2017</subfield><subfield code="g">number:1</subfield><subfield code="g">pages:14</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1186/s13148-017-0380-0</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/27cceefc05bc4f75a54d88fbc4f19b04</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://link.springer.com/article/10.1186/s13148-017-0380-0</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/1868-7075</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/1868-7083</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_DOAJ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">9</subfield><subfield code="j">2017</subfield><subfield code="e">1</subfield><subfield code="h">14</subfield></datafield></record></collection>
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QH426-470 Tri-methylation of H3K79 is decreased in TGF-β1-induced epithelial-to-mesenchymal transition in lung cancer Lung cancer NSCLC EMT H3K79me3 DOT1L PD-L1 |
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misc QH426-470 misc Lung cancer misc NSCLC misc EMT misc H3K79me3 misc DOT1L misc PD-L1 misc Medicine misc R misc Genetics |
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misc QH426-470 misc Lung cancer misc NSCLC misc EMT misc H3K79me3 misc DOT1L misc PD-L1 misc Medicine misc R misc Genetics |
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Tri-methylation of H3K79 is decreased in TGF-β1-induced epithelial-to-mesenchymal transition in lung cancer |
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Tri-methylation of H3K79 is decreased in TGF-β1-induced epithelial-to-mesenchymal transition in lung cancer |
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tri-methylation of h3k79 is decreased in tgf-β1-induced epithelial-to-mesenchymal transition in lung cancer |
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QH426-470 |
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Tri-methylation of H3K79 is decreased in TGF-β1-induced epithelial-to-mesenchymal transition in lung cancer |
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Abstract Background The epithelial-to-mesenchymal transition (EMT) enables epithelial cancer cells to acquire mesenchymal features and contributes to metastasis and resistance to treatment. This process involves epigenetic reprogramming for gene expression. We explored global histone modifications during TGF-β1-induced EMT in two non-small cell lung cancer (NSCLC) cell lines and tested different epigenetic treatment to modulate or partially reverse EMT. Results Loss of classical epithelial markers and gain of mesenchymal markers were verified in A549 and H358 cell lines during TGF-β1-induced EMT. In addition, we noticed increased expression of the axonal guidance protein semaphorin 3C (SEMA3C) and PD-L1 (programmed death-ligand 1) involved in the inhibition of the immune system, suggesting that both SEMA3C and PD-L1 could be the new markers of TGF-β1-induced EMT. H3K79me3 and H2BK120me1 were decreased in A549 and H358 cell lines after a 48-h TGF-β1 treatment, as well as H2BK120ac in A549 cells. However, decreased H3K79me3 was not associated with expression of the histone methyltransferase DOT1L. Furthermore, H3K79me3 was decreased in tumors compared in normal tissues and not associated with cell proliferation. Associations of histone deacetylase inhibitor (SAHA) with DOT1L inhibitors (EPZ5676 or SGC0946) or BET bromodomain inhibitor (PFI-1) were efficient to partially reverse TGF-β1 effects by decreasing expression of PD-L1, SEMA3C, and its receptor neuropilin-2 (NRP2) and by increasing epithelial markers such as E-cadherin. Conclusion Histone methylation was modified during EMT, and combination of epigenetic compounds with conventional or targeted chemotherapy might contribute to reduce metastasis and to enhance clinical responses. |
| abstractGer |
Abstract Background The epithelial-to-mesenchymal transition (EMT) enables epithelial cancer cells to acquire mesenchymal features and contributes to metastasis and resistance to treatment. This process involves epigenetic reprogramming for gene expression. We explored global histone modifications during TGF-β1-induced EMT in two non-small cell lung cancer (NSCLC) cell lines and tested different epigenetic treatment to modulate or partially reverse EMT. Results Loss of classical epithelial markers and gain of mesenchymal markers were verified in A549 and H358 cell lines during TGF-β1-induced EMT. In addition, we noticed increased expression of the axonal guidance protein semaphorin 3C (SEMA3C) and PD-L1 (programmed death-ligand 1) involved in the inhibition of the immune system, suggesting that both SEMA3C and PD-L1 could be the new markers of TGF-β1-induced EMT. H3K79me3 and H2BK120me1 were decreased in A549 and H358 cell lines after a 48-h TGF-β1 treatment, as well as H2BK120ac in A549 cells. However, decreased H3K79me3 was not associated with expression of the histone methyltransferase DOT1L. Furthermore, H3K79me3 was decreased in tumors compared in normal tissues and not associated with cell proliferation. Associations of histone deacetylase inhibitor (SAHA) with DOT1L inhibitors (EPZ5676 or SGC0946) or BET bromodomain inhibitor (PFI-1) were efficient to partially reverse TGF-β1 effects by decreasing expression of PD-L1, SEMA3C, and its receptor neuropilin-2 (NRP2) and by increasing epithelial markers such as E-cadherin. Conclusion Histone methylation was modified during EMT, and combination of epigenetic compounds with conventional or targeted chemotherapy might contribute to reduce metastasis and to enhance clinical responses. |
| abstract_unstemmed |
Abstract Background The epithelial-to-mesenchymal transition (EMT) enables epithelial cancer cells to acquire mesenchymal features and contributes to metastasis and resistance to treatment. This process involves epigenetic reprogramming for gene expression. We explored global histone modifications during TGF-β1-induced EMT in two non-small cell lung cancer (NSCLC) cell lines and tested different epigenetic treatment to modulate or partially reverse EMT. Results Loss of classical epithelial markers and gain of mesenchymal markers were verified in A549 and H358 cell lines during TGF-β1-induced EMT. In addition, we noticed increased expression of the axonal guidance protein semaphorin 3C (SEMA3C) and PD-L1 (programmed death-ligand 1) involved in the inhibition of the immune system, suggesting that both SEMA3C and PD-L1 could be the new markers of TGF-β1-induced EMT. H3K79me3 and H2BK120me1 were decreased in A549 and H358 cell lines after a 48-h TGF-β1 treatment, as well as H2BK120ac in A549 cells. However, decreased H3K79me3 was not associated with expression of the histone methyltransferase DOT1L. Furthermore, H3K79me3 was decreased in tumors compared in normal tissues and not associated with cell proliferation. Associations of histone deacetylase inhibitor (SAHA) with DOT1L inhibitors (EPZ5676 or SGC0946) or BET bromodomain inhibitor (PFI-1) were efficient to partially reverse TGF-β1 effects by decreasing expression of PD-L1, SEMA3C, and its receptor neuropilin-2 (NRP2) and by increasing epithelial markers such as E-cadherin. Conclusion Histone methylation was modified during EMT, and combination of epigenetic compounds with conventional or targeted chemotherapy might contribute to reduce metastasis and to enhance clinical responses. |
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Tri-methylation of H3K79 is decreased in TGF-β1-induced epithelial-to-mesenchymal transition in lung cancer |
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Julie Godet Nathalie Piccirilli Joëlle Guilhot Serge Milin Jean Marc Gombert Benoit Fouchaq Joëlle Roche |
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