Impact of Musashi-1 and Musashi-2 Double Knockdown on Notch Signaling and the Pathogenesis of Endometriosis

The stem cell marker and RNA-binding protein Musashi-1 is overexpressed in endometriosis. Musashi-1-siRNA knockdown in Ishikawa cells altered the expression of stem cell related genes, such as OCT-4. To investigate the role of both human Musashi homologues (MSI-1 and MSI-2) in the pathogenesis of en...
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Autor*in:	Theresa Strauß [verfasserIn] Burkhard Greve [verfasserIn] Michael Gabriel [verfasserIn] Nurjannah Achmad [verfasserIn] Dhanusha Schwan [verfasserIn] Nancy Adriana Espinoza-Sanchez [verfasserIn] Antonio Simone Laganà [verfasserIn] Ludwig Kiesel [verfasserIn] Matti Poutanen [verfasserIn] Martin Götte [verfasserIn] Sebastian Daniel Schäfer [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	Musashi Notch stem cells endometriosis apoptosis HES-1

Übergeordnetes Werk:	In: International Journal of Molecular Sciences - MDPI AG, 2003, 23(2022), 5, p 2851
Übergeordnetes Werk:	volume:23 ; year:2022 ; number:5, p 2851

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.3390/ijms23052851

Katalog-ID:	DOAJ004682068

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allfields	10.3390/ijms23052851 doi (DE-627)DOAJ004682068 (DE-599)DOAJ2edfc8e5255c4499ae57bbf7b61c2b47 DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Theresa Strauß verfasserin aut Impact of Musashi-1 and Musashi-2 Double Knockdown on Notch Signaling and the Pathogenesis of Endometriosis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The stem cell marker and RNA-binding protein Musashi-1 is overexpressed in endometriosis. Musashi-1-siRNA knockdown in Ishikawa cells altered the expression of stem cell related genes, such as OCT-4. To investigate the role of both human Musashi homologues (MSI-1 and MSI-2) in the pathogenesis of endometriosis, immortalized endometriotic 12-Z cells and primary endometriotic stroma cells were treated with Musashi-1- and Musashi-2-siRNA. Subsequently, the impact on cell proliferation, cell apoptosis, cell necrosis, spheroid formation, stem cell phenotype and the Notch signaling pathway was studied in vitro. Using the ENDOMET Turku Endometriosis database, the gene expression of stem cell markers and Notch signaling pathway constituents were analyzed according to localization of the endometriosis lesions. The database analysis demonstrated that expression of Musashi and Notch pathway-related genes are dysregulated in patients with endometriosis. Musashi-1/2-double-knockdown increased apoptosis and necrosis and reduced stem cell gene expression, cell proliferation, and the formation of spheroids. Musashi silencing increased the expression of the anti-proliferation mediator p21. Our findings suggest the therapeutic potential of targeting the Musashi–Notch axis. We conclude that the Musashi genes have an impact on Notch signaling and the pathogenesis of endometriosis through the downregulation of proliferation, stemness characteristics and the upregulation of apoptosis, necrosis and of the cell cycle regulator p21. Musashi Notch stem cells endometriosis apoptosis HES-1 Biology (General) Chemistry Burkhard Greve verfasserin aut Michael Gabriel verfasserin aut Nurjannah Achmad verfasserin aut Dhanusha Schwan verfasserin aut Nancy Adriana Espinoza-Sanchez verfasserin aut Antonio Simone Laganà verfasserin aut Ludwig Kiesel verfasserin aut Matti Poutanen verfasserin aut Martin Götte verfasserin aut Sebastian Daniel Schäfer verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 23(2022), 5, p 2851 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:23 year:2022 number:5, p 2851 https://doi.org/10.3390/ijms23052851 kostenfrei https://doaj.org/article/2edfc8e5255c4499ae57bbf7b61c2b47 kostenfrei https://www.mdpi.com/1422-0067/23/5/2851 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 23 2022 5, p 2851
spelling	10.3390/ijms23052851 doi (DE-627)DOAJ004682068 (DE-599)DOAJ2edfc8e5255c4499ae57bbf7b61c2b47 DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Theresa Strauß verfasserin aut Impact of Musashi-1 and Musashi-2 Double Knockdown on Notch Signaling and the Pathogenesis of Endometriosis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The stem cell marker and RNA-binding protein Musashi-1 is overexpressed in endometriosis. Musashi-1-siRNA knockdown in Ishikawa cells altered the expression of stem cell related genes, such as OCT-4. To investigate the role of both human Musashi homologues (MSI-1 and MSI-2) in the pathogenesis of endometriosis, immortalized endometriotic 12-Z cells and primary endometriotic stroma cells were treated with Musashi-1- and Musashi-2-siRNA. Subsequently, the impact on cell proliferation, cell apoptosis, cell necrosis, spheroid formation, stem cell phenotype and the Notch signaling pathway was studied in vitro. Using the ENDOMET Turku Endometriosis database, the gene expression of stem cell markers and Notch signaling pathway constituents were analyzed according to localization of the endometriosis lesions. The database analysis demonstrated that expression of Musashi and Notch pathway-related genes are dysregulated in patients with endometriosis. Musashi-1/2-double-knockdown increased apoptosis and necrosis and reduced stem cell gene expression, cell proliferation, and the formation of spheroids. Musashi silencing increased the expression of the anti-proliferation mediator p21. Our findings suggest the therapeutic potential of targeting the Musashi–Notch axis. We conclude that the Musashi genes have an impact on Notch signaling and the pathogenesis of endometriosis through the downregulation of proliferation, stemness characteristics and the upregulation of apoptosis, necrosis and of the cell cycle regulator p21. Musashi Notch stem cells endometriosis apoptosis HES-1 Biology (General) Chemistry Burkhard Greve verfasserin aut Michael Gabriel verfasserin aut Nurjannah Achmad verfasserin aut Dhanusha Schwan verfasserin aut Nancy Adriana Espinoza-Sanchez verfasserin aut Antonio Simone Laganà verfasserin aut Ludwig Kiesel verfasserin aut Matti Poutanen verfasserin aut Martin Götte verfasserin aut Sebastian Daniel Schäfer verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 23(2022), 5, p 2851 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:23 year:2022 number:5, p 2851 https://doi.org/10.3390/ijms23052851 kostenfrei https://doaj.org/article/2edfc8e5255c4499ae57bbf7b61c2b47 kostenfrei https://www.mdpi.com/1422-0067/23/5/2851 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 23 2022 5, p 2851
allfields_unstemmed	10.3390/ijms23052851 doi (DE-627)DOAJ004682068 (DE-599)DOAJ2edfc8e5255c4499ae57bbf7b61c2b47 DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Theresa Strauß verfasserin aut Impact of Musashi-1 and Musashi-2 Double Knockdown on Notch Signaling and the Pathogenesis of Endometriosis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The stem cell marker and RNA-binding protein Musashi-1 is overexpressed in endometriosis. Musashi-1-siRNA knockdown in Ishikawa cells altered the expression of stem cell related genes, such as OCT-4. To investigate the role of both human Musashi homologues (MSI-1 and MSI-2) in the pathogenesis of endometriosis, immortalized endometriotic 12-Z cells and primary endometriotic stroma cells were treated with Musashi-1- and Musashi-2-siRNA. Subsequently, the impact on cell proliferation, cell apoptosis, cell necrosis, spheroid formation, stem cell phenotype and the Notch signaling pathway was studied in vitro. Using the ENDOMET Turku Endometriosis database, the gene expression of stem cell markers and Notch signaling pathway constituents were analyzed according to localization of the endometriosis lesions. The database analysis demonstrated that expression of Musashi and Notch pathway-related genes are dysregulated in patients with endometriosis. Musashi-1/2-double-knockdown increased apoptosis and necrosis and reduced stem cell gene expression, cell proliferation, and the formation of spheroids. Musashi silencing increased the expression of the anti-proliferation mediator p21. Our findings suggest the therapeutic potential of targeting the Musashi–Notch axis. We conclude that the Musashi genes have an impact on Notch signaling and the pathogenesis of endometriosis through the downregulation of proliferation, stemness characteristics and the upregulation of apoptosis, necrosis and of the cell cycle regulator p21. Musashi Notch stem cells endometriosis apoptosis HES-1 Biology (General) Chemistry Burkhard Greve verfasserin aut Michael Gabriel verfasserin aut Nurjannah Achmad verfasserin aut Dhanusha Schwan verfasserin aut Nancy Adriana Espinoza-Sanchez verfasserin aut Antonio Simone Laganà verfasserin aut Ludwig Kiesel verfasserin aut Matti Poutanen verfasserin aut Martin Götte verfasserin aut Sebastian Daniel Schäfer verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 23(2022), 5, p 2851 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:23 year:2022 number:5, p 2851 https://doi.org/10.3390/ijms23052851 kostenfrei https://doaj.org/article/2edfc8e5255c4499ae57bbf7b61c2b47 kostenfrei https://www.mdpi.com/1422-0067/23/5/2851 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 23 2022 5, p 2851
allfieldsGer	10.3390/ijms23052851 doi (DE-627)DOAJ004682068 (DE-599)DOAJ2edfc8e5255c4499ae57bbf7b61c2b47 DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Theresa Strauß verfasserin aut Impact of Musashi-1 and Musashi-2 Double Knockdown on Notch Signaling and the Pathogenesis of Endometriosis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The stem cell marker and RNA-binding protein Musashi-1 is overexpressed in endometriosis. Musashi-1-siRNA knockdown in Ishikawa cells altered the expression of stem cell related genes, such as OCT-4. To investigate the role of both human Musashi homologues (MSI-1 and MSI-2) in the pathogenesis of endometriosis, immortalized endometriotic 12-Z cells and primary endometriotic stroma cells were treated with Musashi-1- and Musashi-2-siRNA. Subsequently, the impact on cell proliferation, cell apoptosis, cell necrosis, spheroid formation, stem cell phenotype and the Notch signaling pathway was studied in vitro. Using the ENDOMET Turku Endometriosis database, the gene expression of stem cell markers and Notch signaling pathway constituents were analyzed according to localization of the endometriosis lesions. The database analysis demonstrated that expression of Musashi and Notch pathway-related genes are dysregulated in patients with endometriosis. Musashi-1/2-double-knockdown increased apoptosis and necrosis and reduced stem cell gene expression, cell proliferation, and the formation of spheroids. Musashi silencing increased the expression of the anti-proliferation mediator p21. Our findings suggest the therapeutic potential of targeting the Musashi–Notch axis. We conclude that the Musashi genes have an impact on Notch signaling and the pathogenesis of endometriosis through the downregulation of proliferation, stemness characteristics and the upregulation of apoptosis, necrosis and of the cell cycle regulator p21. Musashi Notch stem cells endometriosis apoptosis HES-1 Biology (General) Chemistry Burkhard Greve verfasserin aut Michael Gabriel verfasserin aut Nurjannah Achmad verfasserin aut Dhanusha Schwan verfasserin aut Nancy Adriana Espinoza-Sanchez verfasserin aut Antonio Simone Laganà verfasserin aut Ludwig Kiesel verfasserin aut Matti Poutanen verfasserin aut Martin Götte verfasserin aut Sebastian Daniel Schäfer verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 23(2022), 5, p 2851 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:23 year:2022 number:5, p 2851 https://doi.org/10.3390/ijms23052851 kostenfrei https://doaj.org/article/2edfc8e5255c4499ae57bbf7b61c2b47 kostenfrei https://www.mdpi.com/1422-0067/23/5/2851 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 23 2022 5, p 2851
allfieldsSound	10.3390/ijms23052851 doi (DE-627)DOAJ004682068 (DE-599)DOAJ2edfc8e5255c4499ae57bbf7b61c2b47 DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Theresa Strauß verfasserin aut Impact of Musashi-1 and Musashi-2 Double Knockdown on Notch Signaling and the Pathogenesis of Endometriosis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The stem cell marker and RNA-binding protein Musashi-1 is overexpressed in endometriosis. Musashi-1-siRNA knockdown in Ishikawa cells altered the expression of stem cell related genes, such as OCT-4. To investigate the role of both human Musashi homologues (MSI-1 and MSI-2) in the pathogenesis of endometriosis, immortalized endometriotic 12-Z cells and primary endometriotic stroma cells were treated with Musashi-1- and Musashi-2-siRNA. Subsequently, the impact on cell proliferation, cell apoptosis, cell necrosis, spheroid formation, stem cell phenotype and the Notch signaling pathway was studied in vitro. Using the ENDOMET Turku Endometriosis database, the gene expression of stem cell markers and Notch signaling pathway constituents were analyzed according to localization of the endometriosis lesions. The database analysis demonstrated that expression of Musashi and Notch pathway-related genes are dysregulated in patients with endometriosis. Musashi-1/2-double-knockdown increased apoptosis and necrosis and reduced stem cell gene expression, cell proliferation, and the formation of spheroids. Musashi silencing increased the expression of the anti-proliferation mediator p21. Our findings suggest the therapeutic potential of targeting the Musashi–Notch axis. We conclude that the Musashi genes have an impact on Notch signaling and the pathogenesis of endometriosis through the downregulation of proliferation, stemness characteristics and the upregulation of apoptosis, necrosis and of the cell cycle regulator p21. Musashi Notch stem cells endometriosis apoptosis HES-1 Biology (General) Chemistry Burkhard Greve verfasserin aut Michael Gabriel verfasserin aut Nurjannah Achmad verfasserin aut Dhanusha Schwan verfasserin aut Nancy Adriana Espinoza-Sanchez verfasserin aut Antonio Simone Laganà verfasserin aut Ludwig Kiesel verfasserin aut Matti Poutanen verfasserin aut Martin Götte verfasserin aut Sebastian Daniel Schäfer verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 23(2022), 5, p 2851 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:23 year:2022 number:5, p 2851 https://doi.org/10.3390/ijms23052851 kostenfrei https://doaj.org/article/2edfc8e5255c4499ae57bbf7b61c2b47 kostenfrei https://www.mdpi.com/1422-0067/23/5/2851 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 23 2022 5, p 2851
language	English
source	In International Journal of Molecular Sciences 23(2022), 5, p 2851 volume:23 year:2022 number:5, p 2851
sourceStr	In International Journal of Molecular Sciences 23(2022), 5, p 2851 volume:23 year:2022 number:5, p 2851
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Musashi Notch stem cells endometriosis apoptosis HES-1 Biology (General) Chemistry
isfreeaccess_bool	true
container_title	International Journal of Molecular Sciences
authorswithroles_txt_mv	Theresa Strauß @@aut@@ Burkhard Greve @@aut@@ Michael Gabriel @@aut@@ Nurjannah Achmad @@aut@@ Dhanusha Schwan @@aut@@ Nancy Adriana Espinoza-Sanchez @@aut@@ Antonio Simone Laganà @@aut@@ Ludwig Kiesel @@aut@@ Matti Poutanen @@aut@@ Martin Götte @@aut@@ Sebastian Daniel Schäfer @@aut@@
publishDateDaySort_date	2022-01-01T00:00:00Z
hierarchy_top_id	316340715
id	DOAJ004682068
language_de	englisch
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callnumber-first	Q - Science
author	Theresa Strauß
spellingShingle	Theresa Strauß misc QH301-705.5 misc QD1-999 misc Musashi misc Notch misc stem cells misc endometriosis misc apoptosis misc HES-1 misc Biology (General) misc Chemistry Impact of Musashi-1 and Musashi-2 Double Knockdown on Notch Signaling and the Pathogenesis of Endometriosis
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topic_title	QH301-705.5 QD1-999 Impact of Musashi-1 and Musashi-2 Double Knockdown on Notch Signaling and the Pathogenesis of Endometriosis Musashi Notch stem cells endometriosis apoptosis HES-1
topic	misc QH301-705.5 misc QD1-999 misc Musashi misc Notch misc stem cells misc endometriosis misc apoptosis misc HES-1 misc Biology (General) misc Chemistry
topic_unstemmed	misc QH301-705.5 misc QD1-999 misc Musashi misc Notch misc stem cells misc endometriosis misc apoptosis misc HES-1 misc Biology (General) misc Chemistry
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title	Impact of Musashi-1 and Musashi-2 Double Knockdown on Notch Signaling and the Pathogenesis of Endometriosis
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title_full	Impact of Musashi-1 and Musashi-2 Double Knockdown on Notch Signaling and the Pathogenesis of Endometriosis
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author_browse	Theresa Strauß Burkhard Greve Michael Gabriel Nurjannah Achmad Dhanusha Schwan Nancy Adriana Espinoza-Sanchez Antonio Simone Laganà Ludwig Kiesel Matti Poutanen Martin Götte Sebastian Daniel Schäfer
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title_sort	impact of musashi-1 and musashi-2 double knockdown on notch signaling and the pathogenesis of endometriosis
callnumber	QH301-705.5
title_auth	Impact of Musashi-1 and Musashi-2 Double Knockdown on Notch Signaling and the Pathogenesis of Endometriosis
abstract	The stem cell marker and RNA-binding protein Musashi-1 is overexpressed in endometriosis. Musashi-1-siRNA knockdown in Ishikawa cells altered the expression of stem cell related genes, such as OCT-4. To investigate the role of both human Musashi homologues (MSI-1 and MSI-2) in the pathogenesis of endometriosis, immortalized endometriotic 12-Z cells and primary endometriotic stroma cells were treated with Musashi-1- and Musashi-2-siRNA. Subsequently, the impact on cell proliferation, cell apoptosis, cell necrosis, spheroid formation, stem cell phenotype and the Notch signaling pathway was studied in vitro. Using the ENDOMET Turku Endometriosis database, the gene expression of stem cell markers and Notch signaling pathway constituents were analyzed according to localization of the endometriosis lesions. The database analysis demonstrated that expression of Musashi and Notch pathway-related genes are dysregulated in patients with endometriosis. Musashi-1/2-double-knockdown increased apoptosis and necrosis and reduced stem cell gene expression, cell proliferation, and the formation of spheroids. Musashi silencing increased the expression of the anti-proliferation mediator p21. Our findings suggest the therapeutic potential of targeting the Musashi–Notch axis. We conclude that the Musashi genes have an impact on Notch signaling and the pathogenesis of endometriosis through the downregulation of proliferation, stemness characteristics and the upregulation of apoptosis, necrosis and of the cell cycle regulator p21.
abstractGer	The stem cell marker and RNA-binding protein Musashi-1 is overexpressed in endometriosis. Musashi-1-siRNA knockdown in Ishikawa cells altered the expression of stem cell related genes, such as OCT-4. To investigate the role of both human Musashi homologues (MSI-1 and MSI-2) in the pathogenesis of endometriosis, immortalized endometriotic 12-Z cells and primary endometriotic stroma cells were treated with Musashi-1- and Musashi-2-siRNA. Subsequently, the impact on cell proliferation, cell apoptosis, cell necrosis, spheroid formation, stem cell phenotype and the Notch signaling pathway was studied in vitro. Using the ENDOMET Turku Endometriosis database, the gene expression of stem cell markers and Notch signaling pathway constituents were analyzed according to localization of the endometriosis lesions. The database analysis demonstrated that expression of Musashi and Notch pathway-related genes are dysregulated in patients with endometriosis. Musashi-1/2-double-knockdown increased apoptosis and necrosis and reduced stem cell gene expression, cell proliferation, and the formation of spheroids. Musashi silencing increased the expression of the anti-proliferation mediator p21. Our findings suggest the therapeutic potential of targeting the Musashi–Notch axis. We conclude that the Musashi genes have an impact on Notch signaling and the pathogenesis of endometriosis through the downregulation of proliferation, stemness characteristics and the upregulation of apoptosis, necrosis and of the cell cycle regulator p21.
abstract_unstemmed	The stem cell marker and RNA-binding protein Musashi-1 is overexpressed in endometriosis. Musashi-1-siRNA knockdown in Ishikawa cells altered the expression of stem cell related genes, such as OCT-4. To investigate the role of both human Musashi homologues (MSI-1 and MSI-2) in the pathogenesis of endometriosis, immortalized endometriotic 12-Z cells and primary endometriotic stroma cells were treated with Musashi-1- and Musashi-2-siRNA. Subsequently, the impact on cell proliferation, cell apoptosis, cell necrosis, spheroid formation, stem cell phenotype and the Notch signaling pathway was studied in vitro. Using the ENDOMET Turku Endometriosis database, the gene expression of stem cell markers and Notch signaling pathway constituents were analyzed according to localization of the endometriosis lesions. The database analysis demonstrated that expression of Musashi and Notch pathway-related genes are dysregulated in patients with endometriosis. Musashi-1/2-double-knockdown increased apoptosis and necrosis and reduced stem cell gene expression, cell proliferation, and the formation of spheroids. Musashi silencing increased the expression of the anti-proliferation mediator p21. Our findings suggest the therapeutic potential of targeting the Musashi–Notch axis. We conclude that the Musashi genes have an impact on Notch signaling and the pathogenesis of endometriosis through the downregulation of proliferation, stemness characteristics and the upregulation of apoptosis, necrosis and of the cell cycle regulator p21.
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container_issue	5, p 2851
title_short	Impact of Musashi-1 and Musashi-2 Double Knockdown on Notch Signaling and the Pathogenesis of Endometriosis
url	https://doi.org/10.3390/ijms23052851 https://doaj.org/article/2edfc8e5255c4499ae57bbf7b61c2b47 https://www.mdpi.com/1422-0067/23/5/2851 https://doaj.org/toc/1661-6596 https://doaj.org/toc/1422-0067
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Impact of Musashi-1 and Musashi-2 Double Knockdown on Notch Signaling and the Pathogenesis of Endometriosis

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Zugang & Verfügbarkeit

Vorhandene Bände

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