KLF7 promotes neuroblastoma differentiation through the GTPase signaling pathway by upregulating neuroblast differentiation‐associated protein AHNAKs and glycerophosphodiesterase GDPD5
The arrest of neural crest‐derived sympathoadrenal neuroblast differentiation contributes to neuroblastoma formation, and overriding this blocked differentiation is a clear strategy for treating high‐risk neuroblastoma. A better understanding of neuroblast or neuroblastoma differentiation is essenti...
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| creator | Qiao, Shupei Jia, Ying Xie, Li Jing, Wenwen Xia, Yang Song, Yue Zhang, Jiahui Cao, Tianhua Song, Huilin Meng, Lingdi Shi, Lei Zhang, Xue |
| description | The arrest of neural crest‐derived sympathoadrenal neuroblast differentiation contributes to neuroblastoma formation, and overriding this blocked differentiation is a clear strategy for treating high‐risk neuroblastoma. A better understanding of neuroblast or neuroblastoma differentiation is essential for developing new therapeutic approaches. It has been proposed that Krueppel‐like factor 7 (KLF7) is a neuroblastoma super‐enhancer‐associated transcription factor gene. Moreover, KLF7 was found to be intensely active in postmitotic neuroblasts of the developing nervous system during embryogenesis. However, the role of KLF7 in the differentiation of neuroblast or neuroblastoma is unknown. Here, we find a strong association between high KLF7 expression and favorable clinical outcomes in neuroblastoma. KLF7 induces differentiation of neuroblastoma cells independently of the retinoic acid (RA) pathway and acts cooperatively with RA to induce neuroblastoma differentiation. KLF7 alters the GTPase activity and multiple differentiation‐related genes by binding directly to the promoters of neuroblast differentiation‐associated protein (AHNAK and AHNAK2) and glycerophosphodiester phosphodiesterase domain‐containing protein 5 (GDPD5) and regulating their expression. Furthermore, we also observe that silencing KLF7 in neuroblastoma cells promotes the adrenergic‐to‐mesenchymal transition accompanied by changes in enhancer‐mediated gene expression. Our results reveal that KLF7 is an inducer of neuroblast or neuroblastoma differentiation with prognostic significance and potential therapeutic value.
KLF7 binds directly to the promoters of neuroblast differentiation‐associated proteins (AHNAK and AHNAK2) and GDPD5 and regulates their expression to influence the GTPase activity, subsequently inducing neuroblastoma differentiation. Depletion of KLF7 in neuroblastoma cells promotes the adrenergic‐to‐mesenchymal transition accompanied by changes in enhancer‐mediated gene expression. |
| doi_str_mv | 10.1111/febs.17208 |
| format | Article |
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KLF7 binds directly to the promoters of neuroblast differentiation‐associated proteins (AHNAK and AHNAK2) and GDPD5 and regulates their expression to influence the GTPase activity, subsequently inducing neuroblastoma differentiation. Depletion of KLF7 in neuroblastoma cells promotes the adrenergic‐to‐mesenchymal transition accompanied by changes in enhancer‐mediated gene expression.</description><identifier>ISSN: 1742-464X</identifier><identifier>ISSN: 1742-4658</identifier><identifier>EISSN: 1742-4658</identifier><identifier>DOI: 10.1111/febs.17208</identifier><identifier>PMID: 38924469</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Adrenal glands ; Cell Differentiation ; Cell Line, Tumor ; Differentiation ; Embryogenesis ; Embryonic growth stage ; Gene expression ; Gene Expression Regulation, Neoplastic ; Glycerophosphodiester phosphodiesterase ; GTP Phosphohydrolases - genetics ; GTP Phosphohydrolases - metabolism ; GTPase activity ; Humans ; KLF7 ; Kruppel-Like Transcription Factors - genetics ; Kruppel-Like Transcription Factors - metabolism ; Nervous system ; Neural crest ; neuroblast differentiation‐associated protein AHNAKs ; Neuroblastoma ; Neuroblastoma - genetics ; Neuroblastoma - metabolism ; Neuroblastoma - pathology ; neuroblastoma differentiation ; Neuroblasts ; Phosphoric Diester Hydrolases - genetics ; Phosphoric Diester Hydrolases - metabolism ; Proteins ; Retinoic acid ; Signal Transduction ; Sympathetic nervous system ; Tretinoin - metabolism ; Tretinoin - pharmacology ; Up-Regulation</subject><ispartof>The FEBS journal, 2024-09, Vol.291 (17), p.3870-3888</ispartof><rights>2024 Federation of European Biochemical Societies.</rights><rights>Copyright © 2024 Federation of European Biochemical Societies</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0009-0004-0249-0581</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Ffebs.17208$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Ffebs.17208$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38924469$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Qiao, Shupei</creatorcontrib><creatorcontrib>Jia, Ying</creatorcontrib><creatorcontrib>Xie, Li</creatorcontrib><creatorcontrib>Jing, Wenwen</creatorcontrib><creatorcontrib>Xia, Yang</creatorcontrib><creatorcontrib>Song, Yue</creatorcontrib><creatorcontrib>Zhang, Jiahui</creatorcontrib><creatorcontrib>Cao, Tianhua</creatorcontrib><creatorcontrib>Song, Huilin</creatorcontrib><creatorcontrib>Meng, Lingdi</creatorcontrib><creatorcontrib>Shi, Lei</creatorcontrib><creatorcontrib>Zhang, Xue</creatorcontrib><title>KLF7 promotes neuroblastoma differentiation through the GTPase signaling pathway by upregulating neuroblast differentiation‐associated protein AHNAKs and glycerophosphodiesterase GDPD5</title><title>The FEBS journal</title><addtitle>FEBS J</addtitle><description>The arrest of neural crest‐derived sympathoadrenal neuroblast differentiation contributes to neuroblastoma formation, and overriding this blocked differentiation is a clear strategy for treating high‐risk neuroblastoma. A better understanding of neuroblast or neuroblastoma differentiation is essential for developing new therapeutic approaches. It has been proposed that Krueppel‐like factor 7 (KLF7) is a neuroblastoma super‐enhancer‐associated transcription factor gene. Moreover, KLF7 was found to be intensely active in postmitotic neuroblasts of the developing nervous system during embryogenesis. However, the role of KLF7 in the differentiation of neuroblast or neuroblastoma is unknown. Here, we find a strong association between high KLF7 expression and favorable clinical outcomes in neuroblastoma. KLF7 induces differentiation of neuroblastoma cells independently of the retinoic acid (RA) pathway and acts cooperatively with RA to induce neuroblastoma differentiation. KLF7 alters the GTPase activity and multiple differentiation‐related genes by binding directly to the promoters of neuroblast differentiation‐associated protein (AHNAK and AHNAK2) and glycerophosphodiester phosphodiesterase domain‐containing protein 5 (GDPD5) and regulating their expression. Furthermore, we also observe that silencing KLF7 in neuroblastoma cells promotes the adrenergic‐to‐mesenchymal transition accompanied by changes in enhancer‐mediated gene expression. Our results reveal that KLF7 is an inducer of neuroblast or neuroblastoma differentiation with prognostic significance and potential therapeutic value.
KLF7 binds directly to the promoters of neuroblast differentiation‐associated proteins (AHNAK and AHNAK2) and GDPD5 and regulates their expression to influence the GTPase activity, subsequently inducing neuroblastoma differentiation. Depletion of KLF7 in neuroblastoma cells promotes the adrenergic‐to‐mesenchymal transition accompanied by changes in enhancer‐mediated gene expression.</description><subject>Adrenal glands</subject><subject>Cell Differentiation</subject><subject>Cell Line, Tumor</subject><subject>Differentiation</subject><subject>Embryogenesis</subject><subject>Embryonic growth stage</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Glycerophosphodiester phosphodiesterase</subject><subject>GTP Phosphohydrolases - genetics</subject><subject>GTP Phosphohydrolases - metabolism</subject><subject>GTPase activity</subject><subject>Humans</subject><subject>KLF7</subject><subject>Kruppel-Like Transcription Factors - genetics</subject><subject>Kruppel-Like Transcription Factors - metabolism</subject><subject>Nervous system</subject><subject>Neural crest</subject><subject>neuroblast differentiation‐associated protein AHNAKs</subject><subject>Neuroblastoma</subject><subject>Neuroblastoma - genetics</subject><subject>Neuroblastoma - metabolism</subject><subject>Neuroblastoma - pathology</subject><subject>neuroblastoma differentiation</subject><subject>Neuroblasts</subject><subject>Phosphoric Diester Hydrolases - genetics</subject><subject>Phosphoric Diester Hydrolases - metabolism</subject><subject>Proteins</subject><subject>Retinoic acid</subject><subject>Signal Transduction</subject><subject>Sympathetic nervous system</subject><subject>Tretinoin - metabolism</subject><subject>Tretinoin - pharmacology</subject><subject>Up-Regulation</subject><issn>1742-464X</issn><issn>1742-4658</issn><issn>1742-4658</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkUFO3DAUhqOqVaHQTQ9QWeqmm6F2Ysf2cgrMgBi1SFCpu8hxnjNGSRzsRCi7HqHn4TicBGegVMKS9Z7tz79_-U-STwQfkTi-GSjDEeEpFm-SfcJpuqA5E29fevp7L_kQwg3GGaNSvk_2MiFTSnO5n9xfbFYc9d61boCAOhi9KxsVBtcqVFljwEM3WDVY16Fh691Yb2MFtL6-VAFQsHWnGtvVqFfD9k5NqJzQ2HuoxyZeivv_JV_rPfz5q0JwOq6gmj0MYDu0PPuxvAhIdRWqm0mDd_3WhTgrC2EAP7-6Prk8YYfJO6OaAB-f60Hya3V6fXy22Pxcnx8vN4s-JUQsJDccVxkXLK04yzGXkApRsUxUoswNECYYx8wQTTU3pWGa6KykNNNSg8hldpB8fdKNDm_H6KFobdDQNKoDN4YiwzzlUpId-uUVeuNGHz8oUoRQygXGM_X5mRrLFqqi97ZVfir-pRIB8gTc2Qaml3OCiznvYs672OVdrE6_X-267BFub6LR</recordid><startdate>202409</startdate><enddate>202409</enddate><creator>Qiao, Shupei</creator><creator>Jia, Ying</creator><creator>Xie, Li</creator><creator>Jing, Wenwen</creator><creator>Xia, Yang</creator><creator>Song, Yue</creator><creator>Zhang, Jiahui</creator><creator>Cao, Tianhua</creator><creator>Song, Huilin</creator><creator>Meng, Lingdi</creator><creator>Shi, Lei</creator><creator>Zhang, Xue</creator><general>Blackwell Publishing Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0009-0004-0249-0581</orcidid></search><sort><creationdate>202409</creationdate><title>KLF7 promotes neuroblastoma differentiation through the GTPase signaling pathway by upregulating neuroblast differentiation‐associated protein AHNAKs and glycerophosphodiesterase GDPD5</title><author>Qiao, Shupei ; 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A better understanding of neuroblast or neuroblastoma differentiation is essential for developing new therapeutic approaches. It has been proposed that Krueppel‐like factor 7 (KLF7) is a neuroblastoma super‐enhancer‐associated transcription factor gene. Moreover, KLF7 was found to be intensely active in postmitotic neuroblasts of the developing nervous system during embryogenesis. However, the role of KLF7 in the differentiation of neuroblast or neuroblastoma is unknown. Here, we find a strong association between high KLF7 expression and favorable clinical outcomes in neuroblastoma. KLF7 induces differentiation of neuroblastoma cells independently of the retinoic acid (RA) pathway and acts cooperatively with RA to induce neuroblastoma differentiation. KLF7 alters the GTPase activity and multiple differentiation‐related genes by binding directly to the promoters of neuroblast differentiation‐associated protein (AHNAK and AHNAK2) and glycerophosphodiester phosphodiesterase domain‐containing protein 5 (GDPD5) and regulating their expression. Furthermore, we also observe that silencing KLF7 in neuroblastoma cells promotes the adrenergic‐to‐mesenchymal transition accompanied by changes in enhancer‐mediated gene expression. Our results reveal that KLF7 is an inducer of neuroblast or neuroblastoma differentiation with prognostic significance and potential therapeutic value.
KLF7 binds directly to the promoters of neuroblast differentiation‐associated proteins (AHNAK and AHNAK2) and GDPD5 and regulates their expression to influence the GTPase activity, subsequently inducing neuroblastoma differentiation. Depletion of KLF7 in neuroblastoma cells promotes the adrenergic‐to‐mesenchymal transition accompanied by changes in enhancer‐mediated gene expression.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>38924469</pmid><doi>10.1111/febs.17208</doi><tpages>19</tpages><orcidid>https://orcid.org/0009-0004-0249-0581</orcidid></addata></record> |
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| subjects | Adrenal glands Cell Differentiation Cell Line, Tumor Differentiation Embryogenesis Embryonic growth stage Gene expression Gene Expression Regulation, Neoplastic Glycerophosphodiester phosphodiesterase GTP Phosphohydrolases - genetics GTP Phosphohydrolases - metabolism GTPase activity Humans KLF7 Kruppel-Like Transcription Factors - genetics Kruppel-Like Transcription Factors - metabolism Nervous system Neural crest neuroblast differentiation‐associated protein AHNAKs Neuroblastoma Neuroblastoma - genetics Neuroblastoma - metabolism Neuroblastoma - pathology neuroblastoma differentiation Neuroblasts Phosphoric Diester Hydrolases - genetics Phosphoric Diester Hydrolases - metabolism Proteins Retinoic acid Signal Transduction Sympathetic nervous system Tretinoin - metabolism Tretinoin - pharmacology Up-Regulation |
| title | KLF7 promotes neuroblastoma differentiation through the GTPase signaling pathway by upregulating neuroblast differentiation‐associated protein AHNAKs and glycerophosphodiesterase GDPD5 |
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