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Regulation of ZMYND8 to Treat Cancer
Zinc finger myeloid, nervy, and deformed epidermal autoregulatory factor 1-type containing 8 (Zinc finger MYND-type containing 8, ZMYND8) is a transcription factor, a histone H3-interacting protein, and a putative chromatin reader/effector that plays an essential role in regulating transcription dur...
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Published in: | Molecules (Basel, Switzerland) Switzerland), 2021-02, Vol.26 (4), p.1083 |
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description | Zinc finger myeloid, nervy, and deformed epidermal autoregulatory factor 1-type containing 8 (Zinc finger MYND-type containing 8, ZMYND8) is a transcription factor, a histone H3-interacting protein, and a putative chromatin reader/effector that plays an essential role in regulating transcription during normal cellular growth. Mutations and altered expression of ZMYND8 are associated with the development and progression of cancer. Increased expression of ZMYND8 is linked to breast, prostate, colorectal, and cervical cancers. It exerts pro-oncogenic effects in breast and prostate cancers, and it promotes angiogenesis in zebrafish, as well as in breast and prostate cancers. In contrast, downregulation of ZMYND8 is also reported in breast, prostate, and nasopharyngeal cancers. ZMYND8 acts as a tumor suppressor in breast and prostate cancers, and it inhibits tumor growth by promoting differentiation; inhibiting proliferation, cell-cycle progression, invasiveness, and metastasis; and maintaining the epithelial phenotype in various types of cancers. These data together suggest that ZMYND8 is important in tumorigenesis; however, the existing data are contradictory. More studies are necessary to clarify the exact role of ZMYND8 in tumorigenesis. In the future, regulation of expression/activity of ZMYND8 and/or its binding partners may become useful in treating cancer. |
doi_str_mv | 10.3390/molecules26041083 |
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Mutations and altered expression of ZMYND8 are associated with the development and progression of cancer. Increased expression of ZMYND8 is linked to breast, prostate, colorectal, and cervical cancers. It exerts pro-oncogenic effects in breast and prostate cancers, and it promotes angiogenesis in zebrafish, as well as in breast and prostate cancers. In contrast, downregulation of ZMYND8 is also reported in breast, prostate, and nasopharyngeal cancers. ZMYND8 acts as a tumor suppressor in breast and prostate cancers, and it inhibits tumor growth by promoting differentiation; inhibiting proliferation, cell-cycle progression, invasiveness, and metastasis; and maintaining the epithelial phenotype in various types of cancers. These data together suggest that ZMYND8 is important in tumorigenesis; however, the existing data are contradictory. More studies are necessary to clarify the exact role of ZMYND8 in tumorigenesis. In the future, regulation of expression/activity of ZMYND8 and/or its binding partners may become useful in treating cancer.</description><identifier>ISSN: 1420-3049</identifier><identifier>EISSN: 1420-3049</identifier><identifier>DOI: 10.3390/molecules26041083</identifier><identifier>PMID: 33670804</identifier><language>eng</language><publisher>Switzerland: MDPI</publisher><subject>Animals ; Carcinogenesis - metabolism ; Carcinogenesis - pathology ; DNA Damage ; epigenetic regulation ; Histones - metabolism ; Humans ; Models, Biological ; Neoplasms - drug therapy ; pro-oncogenic effects ; Review ; tumor suppression ; Tumor Suppressor Proteins - chemistry ; Tumor Suppressor Proteins - metabolism ; tumorigenesis ; ZMYND8</subject><ispartof>Molecules (Basel, Switzerland), 2021-02, Vol.26 (4), p.1083</ispartof><rights>2021 by the authors. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c531t-4796f9fec1082110f1ce14e54aafa6d1c9a66ebc99a85dee3e7906d214985a423</citedby><cites>FETCH-LOGICAL-c531t-4796f9fec1082110f1ce14e54aafa6d1c9a66ebc99a85dee3e7906d214985a423</cites><orcidid>0000-0002-0906-5367 ; 0000-0002-7913-6415</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7923094/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7923094/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33670804$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Yun</creatorcontrib><creatorcontrib>Tsai, Ya-Hui</creatorcontrib><creatorcontrib>Tseng, Sheng-Hong</creatorcontrib><title>Regulation of ZMYND8 to Treat Cancer</title><title>Molecules (Basel, Switzerland)</title><addtitle>Molecules</addtitle><description>Zinc finger myeloid, nervy, and deformed epidermal autoregulatory factor 1-type containing 8 (Zinc finger MYND-type containing 8, ZMYND8) is a transcription factor, a histone H3-interacting protein, and a putative chromatin reader/effector that plays an essential role in regulating transcription during normal cellular growth. Mutations and altered expression of ZMYND8 are associated with the development and progression of cancer. Increased expression of ZMYND8 is linked to breast, prostate, colorectal, and cervical cancers. It exerts pro-oncogenic effects in breast and prostate cancers, and it promotes angiogenesis in zebrafish, as well as in breast and prostate cancers. In contrast, downregulation of ZMYND8 is also reported in breast, prostate, and nasopharyngeal cancers. ZMYND8 acts as a tumor suppressor in breast and prostate cancers, and it inhibits tumor growth by promoting differentiation; inhibiting proliferation, cell-cycle progression, invasiveness, and metastasis; and maintaining the epithelial phenotype in various types of cancers. These data together suggest that ZMYND8 is important in tumorigenesis; however, the existing data are contradictory. More studies are necessary to clarify the exact role of ZMYND8 in tumorigenesis. In the future, regulation of expression/activity of ZMYND8 and/or its binding partners may become useful in treating cancer.</description><subject>Animals</subject><subject>Carcinogenesis - metabolism</subject><subject>Carcinogenesis - pathology</subject><subject>DNA Damage</subject><subject>epigenetic regulation</subject><subject>Histones - metabolism</subject><subject>Humans</subject><subject>Models, Biological</subject><subject>Neoplasms - drug therapy</subject><subject>pro-oncogenic effects</subject><subject>Review</subject><subject>tumor suppression</subject><subject>Tumor Suppressor Proteins - chemistry</subject><subject>Tumor Suppressor Proteins - metabolism</subject><subject>tumorigenesis</subject><subject>ZMYND8</subject><issn>1420-3049</issn><issn>1420-3049</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNplkM1Lw0AQxRdRbK3-AV4kB6_R_UqyexGkfhWqgtSDXpbpZrampNmySQT_e1OrpcXTDPN4v3k8Qk4ZvRBC08uFL9G2JdY8pZJRJfZIn0lOY0Gl3t_ae-SorueUciZZckh6QqQZVVT2yfkLztoSmsJXkXfR--Pb042KGh9NAkITDaGyGI7JgYOyxpPfOSCvd7eT4UM8fr4fDa_HsU0Ea2KZ6dRph7aLwhmjjllkEhMJ4CDNmdWQpji1WoNKckSBmaZp3oXSKgHJxYCM1tzcw9wsQ7GA8GU8FObn4MPMQGgKW6JRgoGVWlOXSSl1ohwA40rnmHGboexYV2vWsp0uMLdYNQHKHeiuUhUfZuY_Taa5oHoFYGuADb6uA7qNl1Gzqt_8q7_znG0_3Tj--hbfIoeByA</recordid><startdate>20210218</startdate><enddate>20210218</enddate><creator>Chen, Yun</creator><creator>Tsai, Ya-Hui</creator><creator>Tseng, Sheng-Hong</creator><general>MDPI</general><general>MDPI AG</general><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>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-0906-5367</orcidid><orcidid>https://orcid.org/0000-0002-7913-6415</orcidid></search><sort><creationdate>20210218</creationdate><title>Regulation of ZMYND8 to Treat Cancer</title><author>Chen, Yun ; Tsai, Ya-Hui ; Tseng, Sheng-Hong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c531t-4796f9fec1082110f1ce14e54aafa6d1c9a66ebc99a85dee3e7906d214985a423</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Carcinogenesis - metabolism</topic><topic>Carcinogenesis - pathology</topic><topic>DNA Damage</topic><topic>epigenetic regulation</topic><topic>Histones - metabolism</topic><topic>Humans</topic><topic>Models, Biological</topic><topic>Neoplasms - drug therapy</topic><topic>pro-oncogenic effects</topic><topic>Review</topic><topic>tumor suppression</topic><topic>Tumor Suppressor Proteins - chemistry</topic><topic>Tumor Suppressor Proteins - metabolism</topic><topic>tumorigenesis</topic><topic>ZMYND8</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Yun</creatorcontrib><creatorcontrib>Tsai, Ya-Hui</creatorcontrib><creatorcontrib>Tseng, Sheng-Hong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Molecules (Basel, Switzerland)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Yun</au><au>Tsai, Ya-Hui</au><au>Tseng, Sheng-Hong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation of ZMYND8 to Treat Cancer</atitle><jtitle>Molecules (Basel, Switzerland)</jtitle><addtitle>Molecules</addtitle><date>2021-02-18</date><risdate>2021</risdate><volume>26</volume><issue>4</issue><spage>1083</spage><pages>1083-</pages><issn>1420-3049</issn><eissn>1420-3049</eissn><abstract>Zinc finger myeloid, nervy, and deformed epidermal autoregulatory factor 1-type containing 8 (Zinc finger MYND-type containing 8, ZMYND8) is a transcription factor, a histone H3-interacting protein, and a putative chromatin reader/effector that plays an essential role in regulating transcription during normal cellular growth. Mutations and altered expression of ZMYND8 are associated with the development and progression of cancer. Increased expression of ZMYND8 is linked to breast, prostate, colorectal, and cervical cancers. It exerts pro-oncogenic effects in breast and prostate cancers, and it promotes angiogenesis in zebrafish, as well as in breast and prostate cancers. In contrast, downregulation of ZMYND8 is also reported in breast, prostate, and nasopharyngeal cancers. ZMYND8 acts as a tumor suppressor in breast and prostate cancers, and it inhibits tumor growth by promoting differentiation; inhibiting proliferation, cell-cycle progression, invasiveness, and metastasis; and maintaining the epithelial phenotype in various types of cancers. These data together suggest that ZMYND8 is important in tumorigenesis; however, the existing data are contradictory. More studies are necessary to clarify the exact role of ZMYND8 in tumorigenesis. 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subjects | Animals Carcinogenesis - metabolism Carcinogenesis - pathology DNA Damage epigenetic regulation Histones - metabolism Humans Models, Biological Neoplasms - drug therapy pro-oncogenic effects Review tumor suppression Tumor Suppressor Proteins - chemistry Tumor Suppressor Proteins - metabolism tumorigenesis ZMYND8 |
title | Regulation of ZMYND8 to Treat Cancer |
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