Inhibition of MTA2 and MTA3 induces mesendoderm specification of human embryonic stem cells
Fully understanding the regulatory network under the pluripotency of embryonic stem cells (ESC) is a prerequisite for their safe application. Here, we addressed the characteristics of metastasis-associated (MTA) family members in human ESCs and found that knockdown of the expression of MTA2 and MTA3...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2021-05, Vol.552, p.142-149 |
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| creator | You, Yu Cui, Yandi Li, Yuting Zhang, Meng Wang, Xin Ji, Junxiang Zhang, Xinbao Zhou, Min Zhang, Zhonglin Ye, Shou-Dong Wang, Xiaoxiao |
| description | Fully understanding the regulatory network under the pluripotency of embryonic stem cells (ESC) is a prerequisite for their safe application. Here, we addressed the characteristics of metastasis-associated (MTA) family members in human ESCs and found that knockdown of the expression of MTA2 and MTA3, but not MTA1, would induce differentiation. High-throughput sequence and quantitative real-time PCR showed that the decreased MTA2 or MTA3 gene transcript mainly led to the emergence of mesendoderm associated markers. Finally, based on the chemical small molecule library screening, we observed that addition of ID8, a specific inhibitor of the dual-specificity tyrosine phosphorylation-regulated kinases (DYRKs), was able to impair the differentiation phenotype induced by MTA2 and MTA3 reduction. Functional assay showed that ID8 could mediate differentiation caused by MTA2 or MTA3 knockdown mainly through inhibition of DYRK4 activity. Therefore, our finding provides the evidence that the functions of MTA family genes in human ESCs are different. Revealing the function of MTA in ESCs with different pluripotency states will help us better understand and apply stem cells.
•MTA2 and MTA3 are essential for hESC maintenance•Suppression of MTA2 and MTA3 directs hESCs differentiation into endoderm and mesoderm cells.•Addition of ID8 can rescue the differentiation phenotype induced by MTA2 or MTA3 downregulation.•ID8 functions in MTA2 and MTA3 knockdown hESCs mainly through inhibition of DYRK4 |
| doi_str_mv | 10.1016/j.bbrc.2021.03.030 |
| format | Article |
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•MTA2 and MTA3 are essential for hESC maintenance•Suppression of MTA2 and MTA3 directs hESCs differentiation into endoderm and mesoderm cells.•Addition of ID8 can rescue the differentiation phenotype induced by MTA2 or MTA3 downregulation.•ID8 functions in MTA2 and MTA3 knockdown hESCs mainly through inhibition of DYRK4</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2021.03.030</identifier><identifier>PMID: 33744762</identifier><language>eng</language><publisher>SAN DIEGO: Elsevier Inc</publisher><subject><![CDATA[Animals ; Biochemistry & Molecular Biology ; Biophysics ; Cell Differentiation - genetics ; Cell Line ; DYRK ; Dyrk Kinases ; Endoderm ; Endoderm - cytology ; Endoderm - metabolism ; Enzyme Inhibitors - pharmacology ; Gene Expression Profiling - methods ; Gene Expression Regulation ; Histone Deacetylases - genetics ; Histone Deacetylases - metabolism ; Human embryonic stem cells ; Human Embryonic Stem Cells - cytology ; Human Embryonic Stem Cells - metabolism ; Humans ; ID8 ; Life Sciences & Biomedicine ; Mesoderm ; Mesoderm - cytology ; Mesoderm - metabolism ; MTA ; Neoplasm Proteins - antagonists & inhibitors ; Neoplasm Proteins - genetics ; Neoplasm Proteins - metabolism ; Protein Serine-Threonine Kinases - antagonists & inhibitors ; Protein Serine-Threonine Kinases - genetics ; Protein Serine-Threonine Kinases - metabolism ; Protein-Tyrosine Kinases - antagonists & inhibitors ; Protein-Tyrosine Kinases - genetics ; Protein-Tyrosine Kinases - metabolism ; Repressor Proteins - antagonists & inhibitors ; Repressor Proteins - genetics ; Repressor Proteins - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; RNA Interference ; Science & Technology]]></subject><ispartof>Biochemical and biophysical research communications, 2021-05, Vol.552, p.142-149</ispartof><rights>2021 Elsevier Inc.</rights><rights>Copyright © 2021 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>2</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000632164800001</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c356t-ded433502ad43a5abafb624f56b7c9638795f518cab33b1a613778452f1a4f053</citedby><cites>FETCH-LOGICAL-c356t-ded433502ad43a5abafb624f56b7c9638795f518cab33b1a613778452f1a4f053</cites><orcidid>0000-0003-1864-8561</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bbrc.2021.03.030$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33744762$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>You, Yu</creatorcontrib><creatorcontrib>Cui, Yandi</creatorcontrib><creatorcontrib>Li, Yuting</creatorcontrib><creatorcontrib>Zhang, Meng</creatorcontrib><creatorcontrib>Wang, Xin</creatorcontrib><creatorcontrib>Ji, Junxiang</creatorcontrib><creatorcontrib>Zhang, Xinbao</creatorcontrib><creatorcontrib>Zhou, Min</creatorcontrib><creatorcontrib>Zhang, Zhonglin</creatorcontrib><creatorcontrib>Ye, Shou-Dong</creatorcontrib><creatorcontrib>Wang, Xiaoxiao</creatorcontrib><title>Inhibition of MTA2 and MTA3 induces mesendoderm specification of human embryonic stem cells</title><title>Biochemical and biophysical research communications</title><addtitle>BIOCHEM BIOPH RES CO</addtitle><addtitle>Biochem Biophys Res Commun</addtitle><description>Fully understanding the regulatory network under the pluripotency of embryonic stem cells (ESC) is a prerequisite for their safe application. Here, we addressed the characteristics of metastasis-associated (MTA) family members in human ESCs and found that knockdown of the expression of MTA2 and MTA3, but not MTA1, would induce differentiation. High-throughput sequence and quantitative real-time PCR showed that the decreased MTA2 or MTA3 gene transcript mainly led to the emergence of mesendoderm associated markers. Finally, based on the chemical small molecule library screening, we observed that addition of ID8, a specific inhibitor of the dual-specificity tyrosine phosphorylation-regulated kinases (DYRKs), was able to impair the differentiation phenotype induced by MTA2 and MTA3 reduction. Functional assay showed that ID8 could mediate differentiation caused by MTA2 or MTA3 knockdown mainly through inhibition of DYRK4 activity. Therefore, our finding provides the evidence that the functions of MTA family genes in human ESCs are different. Revealing the function of MTA in ESCs with different pluripotency states will help us better understand and apply stem cells.
•MTA2 and MTA3 are essential for hESC maintenance•Suppression of MTA2 and MTA3 directs hESCs differentiation into endoderm and mesoderm cells.•Addition of ID8 can rescue the differentiation phenotype induced by MTA2 or MTA3 downregulation.•ID8 functions in MTA2 and MTA3 knockdown hESCs mainly through inhibition of DYRK4</description><subject>Animals</subject><subject>Biochemistry & Molecular Biology</subject><subject>Biophysics</subject><subject>Cell Differentiation - genetics</subject><subject>Cell Line</subject><subject>DYRK</subject><subject>Dyrk Kinases</subject><subject>Endoderm</subject><subject>Endoderm - cytology</subject><subject>Endoderm - metabolism</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Gene Expression Profiling - methods</subject><subject>Gene Expression Regulation</subject><subject>Histone Deacetylases - genetics</subject><subject>Histone Deacetylases - metabolism</subject><subject>Human embryonic stem cells</subject><subject>Human Embryonic Stem Cells - cytology</subject><subject>Human Embryonic Stem Cells - metabolism</subject><subject>Humans</subject><subject>ID8</subject><subject>Life Sciences & Biomedicine</subject><subject>Mesoderm</subject><subject>Mesoderm - cytology</subject><subject>Mesoderm - metabolism</subject><subject>MTA</subject><subject>Neoplasm Proteins - antagonists & inhibitors</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Protein Serine-Threonine Kinases - antagonists & inhibitors</subject><subject>Protein Serine-Threonine Kinases - genetics</subject><subject>Protein Serine-Threonine Kinases - metabolism</subject><subject>Protein-Tyrosine Kinases - antagonists & inhibitors</subject><subject>Protein-Tyrosine Kinases - genetics</subject><subject>Protein-Tyrosine Kinases - metabolism</subject><subject>Repressor Proteins - antagonists & inhibitors</subject><subject>Repressor Proteins - genetics</subject><subject>Repressor Proteins - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA Interference</subject><subject>Science & Technology</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>HGBXW</sourceid><sourceid>EIF</sourceid><recordid>eNqNkcFq3DAQhkVpaLZpX6CHomOheDuSbNmGXsLSpoGUXBII9CAkeUS0rKWtZKfk7StnNzmWwsDM4fsGzS9CPjBYM2Dyy3ZtTLJrDpytQZSCV2TFoIeKM6hfkxUAyIr37O6UvM15C8BYLfs35FSItq5byVfk12W498ZPPgYaHf15c86pDsMyCOrDMFvMdMSMYYgDppHmPVrvvNXPyv086kBxNOkxBm9pnnCkFne7_I6cOL3L-P7Yz8jt9283mx_V1fXF5eb8qrKikVM14FAL0QDXpetGG-2M5LVrpGltL0XX9o1rWGe1EcIwLZlo265uuGO6dtCIM_LpsHef4u8Z86RGn5cX6IBxzoo3IKTknPGC8gNqU8w5oVP75EedHhUDtYSqtmoJVS2hKhCloEgfj_tnM-LwojynWIDPB-APmuiy9RgsvmDLLwjOZN2VCVihu_-nN356SnoT5zAV9etBxRLng8ekjvrgE9pJDdH_65C_fEqn6g</recordid><startdate>20210507</startdate><enddate>20210507</enddate><creator>You, Yu</creator><creator>Cui, Yandi</creator><creator>Li, Yuting</creator><creator>Zhang, Meng</creator><creator>Wang, Xin</creator><creator>Ji, Junxiang</creator><creator>Zhang, Xinbao</creator><creator>Zhou, Min</creator><creator>Zhang, Zhonglin</creator><creator>Ye, Shou-Dong</creator><creator>Wang, Xiaoxiao</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>BLEPL</scope><scope>DTL</scope><scope>HGBXW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-1864-8561</orcidid></search><sort><creationdate>20210507</creationdate><title>Inhibition of MTA2 and MTA3 induces mesendoderm specification of human embryonic stem cells</title><author>You, Yu ; 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Here, we addressed the characteristics of metastasis-associated (MTA) family members in human ESCs and found that knockdown of the expression of MTA2 and MTA3, but not MTA1, would induce differentiation. High-throughput sequence and quantitative real-time PCR showed that the decreased MTA2 or MTA3 gene transcript mainly led to the emergence of mesendoderm associated markers. Finally, based on the chemical small molecule library screening, we observed that addition of ID8, a specific inhibitor of the dual-specificity tyrosine phosphorylation-regulated kinases (DYRKs), was able to impair the differentiation phenotype induced by MTA2 and MTA3 reduction. Functional assay showed that ID8 could mediate differentiation caused by MTA2 or MTA3 knockdown mainly through inhibition of DYRK4 activity. Therefore, our finding provides the evidence that the functions of MTA family genes in human ESCs are different. Revealing the function of MTA in ESCs with different pluripotency states will help us better understand and apply stem cells.
•MTA2 and MTA3 are essential for hESC maintenance•Suppression of MTA2 and MTA3 directs hESCs differentiation into endoderm and mesoderm cells.•Addition of ID8 can rescue the differentiation phenotype induced by MTA2 or MTA3 downregulation.•ID8 functions in MTA2 and MTA3 knockdown hESCs mainly through inhibition of DYRK4</abstract><cop>SAN DIEGO</cop><pub>Elsevier Inc</pub><pmid>33744762</pmid><doi>10.1016/j.bbrc.2021.03.030</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0003-1864-8561</orcidid></addata></record> |
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| subjects | Animals Biochemistry & Molecular Biology Biophysics Cell Differentiation - genetics Cell Line DYRK Dyrk Kinases Endoderm Endoderm - cytology Endoderm - metabolism Enzyme Inhibitors - pharmacology Gene Expression Profiling - methods Gene Expression Regulation Histone Deacetylases - genetics Histone Deacetylases - metabolism Human embryonic stem cells Human Embryonic Stem Cells - cytology Human Embryonic Stem Cells - metabolism Humans ID8 Life Sciences & Biomedicine Mesoderm Mesoderm - cytology Mesoderm - metabolism MTA Neoplasm Proteins - antagonists & inhibitors Neoplasm Proteins - genetics Neoplasm Proteins - metabolism Protein Serine-Threonine Kinases - antagonists & inhibitors Protein Serine-Threonine Kinases - genetics Protein Serine-Threonine Kinases - metabolism Protein-Tyrosine Kinases - antagonists & inhibitors Protein-Tyrosine Kinases - genetics Protein-Tyrosine Kinases - metabolism Repressor Proteins - antagonists & inhibitors Repressor Proteins - genetics Repressor Proteins - metabolism Reverse Transcriptase Polymerase Chain Reaction RNA Interference Science & Technology |
| title | Inhibition of MTA2 and MTA3 induces mesendoderm specification of human embryonic stem cells |
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