Cancer cells escape p53’s tumor suppression through ablation of ZDHHC1-mediated p53 palmitoylation
The inactivation of tumor-suppressor genes contributes heavily to oncogenesis. The mutation of TP53 has been well-studied and recognized as a major factor in the development of tumors. Yet other means of p53 inactivation has not been well-elucidated. We previously identified a hypermethylated gene Z...
Gespeichert in:
| Veröffentlicht in: | Oncogene 2021-09, Vol.40 (35), p.5416-5426 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 5426 |
|---|---|
| container_issue | 35 |
| container_start_page | 5416 |
| container_title | Oncogene |
| container_volume | 40 |
| creator | Tang, Jun Peng, Weiyan Feng, Yixiao Le, Xin Wang, Kang Xiang, Qin Li, Lili Wang, Yan Xu, Can Mu, Junhao Xu, Ke Ji, Ping Tao, Qian Huang, Ailong Deng, Chu-Xia Lin, Yong Xiang, Tingxiu |
| description | The inactivation of tumor-suppressor genes contributes heavily to oncogenesis. The mutation of TP53 has been well-studied and recognized as a major factor in the development of tumors. Yet other means of p53 inactivation has not been well-elucidated. We previously identified a hypermethylated gene
ZDHHC1
that suppresses tumor growth when the expression was restored, but the specific mechanism was yet to be found. The protein product of
ZDHHC1
is an S-palmitoyltransferase and we have identified p53 as a substrate for ZDHHC1-mediated palmitoylation, specifically at the C135, C176, and C275 residues. The novel form of post-translational modification of p53 is required for the nuclear translocation of the tumor suppressor. p53 recruited DNMT3A to
ZDHHC1
promoter and is responsible for the hypermethylation of
ZDHHC1
. The epigenetic feedback loop formed by ZDHHC1 and p53 sheds light on the inactivation of p53 without the presence of genetic mutations. |
| doi_str_mv | 10.1038/s41388-021-01949-5 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_swepu</sourceid><recordid>TN_cdi_swepub_primary_oai_swepub_ki_se_460383</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A674103161</galeid><sourcerecordid>A674103161</sourcerecordid><originalsourceid>FETCH-LOGICAL-c579t-8891ab645d535dab47db26fec598059313954adc660f495e44d5ad15d8b49f893</originalsourceid><addsrcrecordid>eNp9ks1u1DAUhS0EokPhBVigSGzYuPg_9gapGn4GqRIb2LCxHNuZcUniYCeg7niNvl6fBIcZWgYhlEWie79z7XtyAHiK0RlGVL7MDFMpISIYIqyYgvweWGFWC8i5YvfBCimOoCKUnIBHOV8ihGqFyENwQhmRhNRsBdzaDNanyvquy5XP1oy-Gjm9-XGdq2nuY6ryPI7J5xziUE27FOftrjJNZ6alENvq8-vNZo1h710wk3eLuhpN14cpXu2px-BBa7rsnxzep-DT2zcf1xt48eHd-_X5BbS8VhOUUmHTCMYdp9yZhtWuIaL1liuJuKKYKs6Ms0KglinuGXPcOMydbJhqpaKnAO7n5u9-nBs9ptCbdKWjCfpQ-lK-vGai-EcL_2rPl065vvXDlEx3JDvuDGGnt_GblsV5TJYDXxwGpPh19nnSfciLlWbwcc6a8LIJoUzUBX3-F3oZ5zQUOwolJFW0RviO2prO6zC0sZxrl6H6XNSs_HYsFursH1R5nO-DjYNvQ6kfCcheYFPMOfn2dkeM9JIlvc-SLlnSv7KkeRE9-9OdW8nv8BSAHuwurWHr091K_xn7E-M01Ks</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2568393701</pqid></control><display><type>article</type><title>Cancer cells escape p53’s tumor suppression through ablation of ZDHHC1-mediated p53 palmitoylation</title><source>MEDLINE</source><source>SpringerLink Journals</source><source>SWEPUB Freely available online</source><creator>Tang, Jun ; Peng, Weiyan ; Feng, Yixiao ; Le, Xin ; Wang, Kang ; Xiang, Qin ; Li, Lili ; Wang, Yan ; Xu, Can ; Mu, Junhao ; Xu, Ke ; Ji, Ping ; Tao, Qian ; Huang, Ailong ; Deng, Chu-Xia ; Lin, Yong ; Xiang, Tingxiu</creator><creatorcontrib>Tang, Jun ; Peng, Weiyan ; Feng, Yixiao ; Le, Xin ; Wang, Kang ; Xiang, Qin ; Li, Lili ; Wang, Yan ; Xu, Can ; Mu, Junhao ; Xu, Ke ; Ji, Ping ; Tao, Qian ; Huang, Ailong ; Deng, Chu-Xia ; Lin, Yong ; Xiang, Tingxiu</creatorcontrib><description>The inactivation of tumor-suppressor genes contributes heavily to oncogenesis. The mutation of TP53 has been well-studied and recognized as a major factor in the development of tumors. Yet other means of p53 inactivation has not been well-elucidated. We previously identified a hypermethylated gene
ZDHHC1
that suppresses tumor growth when the expression was restored, but the specific mechanism was yet to be found. The protein product of
ZDHHC1
is an S-palmitoyltransferase and we have identified p53 as a substrate for ZDHHC1-mediated palmitoylation, specifically at the C135, C176, and C275 residues. The novel form of post-translational modification of p53 is required for the nuclear translocation of the tumor suppressor. p53 recruited DNMT3A to
ZDHHC1
promoter and is responsible for the hypermethylation of
ZDHHC1
. The epigenetic feedback loop formed by ZDHHC1 and p53 sheds light on the inactivation of p53 without the presence of genetic mutations.</description><identifier>ISSN: 0950-9232</identifier><identifier>ISSN: 1476-5594</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/s41388-021-01949-5</identifier><identifier>PMID: 34282274</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/109 ; 13/2 ; 13/31 ; 14/19 ; 631/67/1857 ; 631/80/458 ; 64/60 ; 82/1 ; 82/51 ; 82/80 ; 82/83 ; Ablation ; Acyltransferases - genetics ; Animals ; Apoptosis ; Cancer ; Cell Biology ; Cell Line, Tumor ; Development and progression ; DNA (Cytosine-5-)-Methyltransferases - genetics ; DNA (Cytosine-5-)-Methyltransferases - metabolism ; DNA Methylation ; Epigenetic inheritance ; Epigenetics ; Gene Expression Regulation, Neoplastic ; Gene mutations ; Genetic aspects ; Human Genetics ; Humans ; Internal Medicine ; Lipoylation ; Medicine ; Medicine & Public Health ; Mice ; Mutation ; Neoplasms - genetics ; Neoplasms - metabolism ; Neoplasms - pathology ; Nuclear transport ; Oncology ; Oncology, Experimental ; Palmitoylation ; Palmitoyltransferase ; Post-translation ; Post-translational modification ; Promoter Regions, Genetic ; Protein Processing, Post-Translational ; Tumor proteins ; Tumor suppressor genes ; Tumor Suppressor Protein p53 - genetics ; Tumor Suppressor Protein p53 - metabolism ; Tumorigenesis ; Tumors</subject><ispartof>Oncogene, 2021-09, Vol.40 (35), p.5416-5426</ispartof><rights>The Author(s) 2021</rights><rights>2021. The Author(s).</rights><rights>COPYRIGHT 2021 Nature Publishing Group</rights><rights>The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c579t-8891ab645d535dab47db26fec598059313954adc660f495e44d5ad15d8b49f893</citedby><cites>FETCH-LOGICAL-c579t-8891ab645d535dab47db26fec598059313954adc660f495e44d5ad15d8b49f893</cites><orcidid>0000-0001-5401-1803 ; 0000-0001-8033-3902 ; 0000-0001-5383-4808 ; 0000-0003-4589-0599</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/s41388-021-01949-5$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/s41388-021-01949-5$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,550,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34282274$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:147121118$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Tang, Jun</creatorcontrib><creatorcontrib>Peng, Weiyan</creatorcontrib><creatorcontrib>Feng, Yixiao</creatorcontrib><creatorcontrib>Le, Xin</creatorcontrib><creatorcontrib>Wang, Kang</creatorcontrib><creatorcontrib>Xiang, Qin</creatorcontrib><creatorcontrib>Li, Lili</creatorcontrib><creatorcontrib>Wang, Yan</creatorcontrib><creatorcontrib>Xu, Can</creatorcontrib><creatorcontrib>Mu, Junhao</creatorcontrib><creatorcontrib>Xu, Ke</creatorcontrib><creatorcontrib>Ji, Ping</creatorcontrib><creatorcontrib>Tao, Qian</creatorcontrib><creatorcontrib>Huang, Ailong</creatorcontrib><creatorcontrib>Deng, Chu-Xia</creatorcontrib><creatorcontrib>Lin, Yong</creatorcontrib><creatorcontrib>Xiang, Tingxiu</creatorcontrib><title>Cancer cells escape p53’s tumor suppression through ablation of ZDHHC1-mediated p53 palmitoylation</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>The inactivation of tumor-suppressor genes contributes heavily to oncogenesis. The mutation of TP53 has been well-studied and recognized as a major factor in the development of tumors. Yet other means of p53 inactivation has not been well-elucidated. We previously identified a hypermethylated gene
ZDHHC1
that suppresses tumor growth when the expression was restored, but the specific mechanism was yet to be found. The protein product of
ZDHHC1
is an S-palmitoyltransferase and we have identified p53 as a substrate for ZDHHC1-mediated palmitoylation, specifically at the C135, C176, and C275 residues. The novel form of post-translational modification of p53 is required for the nuclear translocation of the tumor suppressor. p53 recruited DNMT3A to
ZDHHC1
promoter and is responsible for the hypermethylation of
ZDHHC1
. The epigenetic feedback loop formed by ZDHHC1 and p53 sheds light on the inactivation of p53 without the presence of genetic mutations.</description><subject>13/109</subject><subject>13/2</subject><subject>13/31</subject><subject>14/19</subject><subject>631/67/1857</subject><subject>631/80/458</subject><subject>64/60</subject><subject>82/1</subject><subject>82/51</subject><subject>82/80</subject><subject>82/83</subject><subject>Ablation</subject><subject>Acyltransferases - genetics</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Cancer</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Development and progression</subject><subject>DNA (Cytosine-5-)-Methyltransferases - genetics</subject><subject>DNA (Cytosine-5-)-Methyltransferases - metabolism</subject><subject>DNA Methylation</subject><subject>Epigenetic inheritance</subject><subject>Epigenetics</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene mutations</subject><subject>Genetic aspects</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Lipoylation</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Mutation</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - metabolism</subject><subject>Neoplasms - pathology</subject><subject>Nuclear transport</subject><subject>Oncology</subject><subject>Oncology, Experimental</subject><subject>Palmitoylation</subject><subject>Palmitoyltransferase</subject><subject>Post-translation</subject><subject>Post-translational modification</subject><subject>Promoter Regions, Genetic</subject><subject>Protein Processing, Post-Translational</subject><subject>Tumor proteins</subject><subject>Tumor suppressor genes</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><issn>0950-9232</issn><issn>1476-5594</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><sourceid>D8T</sourceid><recordid>eNp9ks1u1DAUhS0EokPhBVigSGzYuPg_9gapGn4GqRIb2LCxHNuZcUniYCeg7niNvl6fBIcZWgYhlEWie79z7XtyAHiK0RlGVL7MDFMpISIYIqyYgvweWGFWC8i5YvfBCimOoCKUnIBHOV8ihGqFyENwQhmRhNRsBdzaDNanyvquy5XP1oy-Gjm9-XGdq2nuY6ryPI7J5xziUE27FOftrjJNZ6alENvq8-vNZo1h710wk3eLuhpN14cpXu2px-BBa7rsnxzep-DT2zcf1xt48eHd-_X5BbS8VhOUUmHTCMYdp9yZhtWuIaL1liuJuKKYKs6Ms0KglinuGXPcOMydbJhqpaKnAO7n5u9-nBs9ptCbdKWjCfpQ-lK-vGai-EcL_2rPl065vvXDlEx3JDvuDGGnt_GblsV5TJYDXxwGpPh19nnSfciLlWbwcc6a8LIJoUzUBX3-F3oZ5zQUOwolJFW0RviO2prO6zC0sZxrl6H6XNSs_HYsFursH1R5nO-DjYNvQ6kfCcheYFPMOfn2dkeM9JIlvc-SLlnSv7KkeRE9-9OdW8nv8BSAHuwurWHr091K_xn7E-M01Ks</recordid><startdate>20210902</startdate><enddate>20210902</enddate><creator>Tang, Jun</creator><creator>Peng, Weiyan</creator><creator>Feng, Yixiao</creator><creator>Le, Xin</creator><creator>Wang, Kang</creator><creator>Xiang, Qin</creator><creator>Li, Lili</creator><creator>Wang, Yan</creator><creator>Xu, Can</creator><creator>Mu, Junhao</creator><creator>Xu, Ke</creator><creator>Ji, Ping</creator><creator>Tao, Qian</creator><creator>Huang, Ailong</creator><creator>Deng, Chu-Xia</creator><creator>Lin, Yong</creator><creator>Xiang, Tingxiu</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>3V.</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>D8T</scope><scope>ZZAVC</scope><orcidid>https://orcid.org/0000-0001-5401-1803</orcidid><orcidid>https://orcid.org/0000-0001-8033-3902</orcidid><orcidid>https://orcid.org/0000-0001-5383-4808</orcidid><orcidid>https://orcid.org/0000-0003-4589-0599</orcidid></search><sort><creationdate>20210902</creationdate><title>Cancer cells escape p53’s tumor suppression through ablation of ZDHHC1-mediated p53 palmitoylation</title><author>Tang, Jun ; Peng, Weiyan ; Feng, Yixiao ; Le, Xin ; Wang, Kang ; Xiang, Qin ; Li, Lili ; Wang, Yan ; Xu, Can ; Mu, Junhao ; Xu, Ke ; Ji, Ping ; Tao, Qian ; Huang, Ailong ; Deng, Chu-Xia ; Lin, Yong ; Xiang, Tingxiu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c579t-8891ab645d535dab47db26fec598059313954adc660f495e44d5ad15d8b49f893</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>13/109</topic><topic>13/2</topic><topic>13/31</topic><topic>14/19</topic><topic>631/67/1857</topic><topic>631/80/458</topic><topic>64/60</topic><topic>82/1</topic><topic>82/51</topic><topic>82/80</topic><topic>82/83</topic><topic>Ablation</topic><topic>Acyltransferases - genetics</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Cancer</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>Development and progression</topic><topic>DNA (Cytosine-5-)-Methyltransferases - genetics</topic><topic>DNA (Cytosine-5-)-Methyltransferases - metabolism</topic><topic>DNA Methylation</topic><topic>Epigenetic inheritance</topic><topic>Epigenetics</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene mutations</topic><topic>Genetic aspects</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Lipoylation</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice</topic><topic>Mutation</topic><topic>Neoplasms - genetics</topic><topic>Neoplasms - metabolism</topic><topic>Neoplasms - pathology</topic><topic>Nuclear transport</topic><topic>Oncology</topic><topic>Oncology, Experimental</topic><topic>Palmitoylation</topic><topic>Palmitoyltransferase</topic><topic>Post-translation</topic><topic>Post-translational modification</topic><topic>Promoter Regions, Genetic</topic><topic>Protein Processing, Post-Translational</topic><topic>Tumor proteins</topic><topic>Tumor suppressor genes</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Tumorigenesis</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tang, Jun</creatorcontrib><creatorcontrib>Peng, Weiyan</creatorcontrib><creatorcontrib>Feng, Yixiao</creatorcontrib><creatorcontrib>Le, Xin</creatorcontrib><creatorcontrib>Wang, Kang</creatorcontrib><creatorcontrib>Xiang, Qin</creatorcontrib><creatorcontrib>Li, Lili</creatorcontrib><creatorcontrib>Wang, Yan</creatorcontrib><creatorcontrib>Xu, Can</creatorcontrib><creatorcontrib>Mu, Junhao</creatorcontrib><creatorcontrib>Xu, Ke</creatorcontrib><creatorcontrib>Ji, Ping</creatorcontrib><creatorcontrib>Tao, Qian</creatorcontrib><creatorcontrib>Huang, Ailong</creatorcontrib><creatorcontrib>Deng, Chu-Xia</creatorcontrib><creatorcontrib>Lin, Yong</creatorcontrib><creatorcontrib>Xiang, Tingxiu</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SwePub Articles full text</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tang, Jun</au><au>Peng, Weiyan</au><au>Feng, Yixiao</au><au>Le, Xin</au><au>Wang, Kang</au><au>Xiang, Qin</au><au>Li, Lili</au><au>Wang, Yan</au><au>Xu, Can</au><au>Mu, Junhao</au><au>Xu, Ke</au><au>Ji, Ping</au><au>Tao, Qian</au><au>Huang, Ailong</au><au>Deng, Chu-Xia</au><au>Lin, Yong</au><au>Xiang, Tingxiu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cancer cells escape p53’s tumor suppression through ablation of ZDHHC1-mediated p53 palmitoylation</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2021-09-02</date><risdate>2021</risdate><volume>40</volume><issue>35</issue><spage>5416</spage><epage>5426</epage><pages>5416-5426</pages><issn>0950-9232</issn><issn>1476-5594</issn><eissn>1476-5594</eissn><abstract>The inactivation of tumor-suppressor genes contributes heavily to oncogenesis. The mutation of TP53 has been well-studied and recognized as a major factor in the development of tumors. Yet other means of p53 inactivation has not been well-elucidated. We previously identified a hypermethylated gene
ZDHHC1
that suppresses tumor growth when the expression was restored, but the specific mechanism was yet to be found. The protein product of
ZDHHC1
is an S-palmitoyltransferase and we have identified p53 as a substrate for ZDHHC1-mediated palmitoylation, specifically at the C135, C176, and C275 residues. The novel form of post-translational modification of p53 is required for the nuclear translocation of the tumor suppressor. p53 recruited DNMT3A to
ZDHHC1
promoter and is responsible for the hypermethylation of
ZDHHC1
. The epigenetic feedback loop formed by ZDHHC1 and p53 sheds light on the inactivation of p53 without the presence of genetic mutations.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>34282274</pmid><doi>10.1038/s41388-021-01949-5</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0001-5401-1803</orcidid><orcidid>https://orcid.org/0000-0001-8033-3902</orcidid><orcidid>https://orcid.org/0000-0001-5383-4808</orcidid><orcidid>https://orcid.org/0000-0003-4589-0599</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0950-9232 |
| ispartof | Oncogene, 2021-09, Vol.40 (35), p.5416-5426 |
| issn | 0950-9232 1476-5594 1476-5594 |
| language | eng |
| recordid | cdi_swepub_primary_oai_swepub_ki_se_460383 |
| source | MEDLINE; SpringerLink Journals; SWEPUB Freely available online |
| subjects | 13/109 13/2 13/31 14/19 631/67/1857 631/80/458 64/60 82/1 82/51 82/80 82/83 Ablation Acyltransferases - genetics Animals Apoptosis Cancer Cell Biology Cell Line, Tumor Development and progression DNA (Cytosine-5-)-Methyltransferases - genetics DNA (Cytosine-5-)-Methyltransferases - metabolism DNA Methylation Epigenetic inheritance Epigenetics Gene Expression Regulation, Neoplastic Gene mutations Genetic aspects Human Genetics Humans Internal Medicine Lipoylation Medicine Medicine & Public Health Mice Mutation Neoplasms - genetics Neoplasms - metabolism Neoplasms - pathology Nuclear transport Oncology Oncology, Experimental Palmitoylation Palmitoyltransferase Post-translation Post-translational modification Promoter Regions, Genetic Protein Processing, Post-Translational Tumor proteins Tumor suppressor genes Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Tumorigenesis Tumors |
| title | Cancer cells escape p53’s tumor suppression through ablation of ZDHHC1-mediated p53 palmitoylation |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-09T01%3A15%3A54IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_swepu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Cancer%20cells%20escape%20p53%E2%80%99s%20tumor%20suppression%20through%20ablation%20of%20ZDHHC1-mediated%20p53%20palmitoylation&rft.jtitle=Oncogene&rft.au=Tang,%20Jun&rft.date=2021-09-02&rft.volume=40&rft.issue=35&rft.spage=5416&rft.epage=5426&rft.pages=5416-5426&rft.issn=0950-9232&rft.eissn=1476-5594&rft_id=info:doi/10.1038/s41388-021-01949-5&rft_dat=%3Cgale_swepu%3EA674103161%3C/gale_swepu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2568393701&rft_id=info:pmid/34282274&rft_galeid=A674103161&rfr_iscdi=true |