The p53 Family Members p63 and p73 Roles in the Metastatic Dissemination: Interactions with microRNAs and TGFβ Pathway
TP53 (TP53), p73 (TP73), and p63 (TP63) are members of the p53 transcription factor family, which has many activities spanning from embryonic development through to tumor suppression. The utilization of two promoters and alternative mRNA splicing has been shown to yield numerous isoforms in p53, p63...
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| Veröffentlicht in: | Cancers 2022-12, Vol.14 (23), p.5948 |
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| creator | Rodriguez Calleja, Lidia Lavaud, Melanie Tesfaye, Robel Brounais-Le-Royer, Bénédicte Baud'huin, Marc Georges, Steven Lamoureux, François Verrecchia, Franck Ory, Benjamin |
| description | TP53 (TP53), p73 (TP73), and p63 (TP63) are members of the p53 transcription factor family, which has many activities spanning from embryonic development through to tumor suppression. The utilization of two promoters and alternative mRNA splicing has been shown to yield numerous isoforms in p53, p63, and p73. TAp73 is thought to mediate apoptosis as a result of nuclear accumulation following chemotherapy-induced DNA damage, according to a number of studies. Overexpression of the nuclear ΔNp63 and ΔNp73 isoforms, on the other hand, suppresses TAp73's pro-apoptotic activity in human malignancies, potentially leading to metastatic spread or inhibition. Another well-known pathway that has been associated to metastatic spread is the TGF pathway. TGFs are a family of structurally related polypeptide growth factors that regulate a variety of cellular functions including cell proliferation, lineage determination, differentiation, motility, adhesion, and cell death, making them significant players in development, homeostasis, and wound repair. Various studies have already identified several interactions between the p53 protein family and the TGFb pathway in the context of tumor growth and metastatic spread, beginning to shed light on this enigmatic intricacy. |
| doi_str_mv | 10.3390/cancers14235948 |
| format | Article |
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The utilization of two promoters and alternative mRNA splicing has been shown to yield numerous isoforms in p53, p63, and p73. TAp73 is thought to mediate apoptosis as a result of nuclear accumulation following chemotherapy-induced DNA damage, according to a number of studies. Overexpression of the nuclear ΔNp63 and ΔNp73 isoforms, on the other hand, suppresses TAp73's pro-apoptotic activity in human malignancies, potentially leading to metastatic spread or inhibition. Another well-known pathway that has been associated to metastatic spread is the TGF pathway. TGFs are a family of structurally related polypeptide growth factors that regulate a variety of cellular functions including cell proliferation, lineage determination, differentiation, motility, adhesion, and cell death, making them significant players in development, homeostasis, and wound repair. Various studies have already identified several interactions between the p53 protein family and the TGFb pathway in the context of tumor growth and metastatic spread, beginning to shed light on this enigmatic intricacy.</description><identifier>ISSN: 2072-6694</identifier><identifier>EISSN: 2072-6694</identifier><identifier>DOI: 10.3390/cancers14235948</identifier><identifier>PMID: 36497429</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Alternative splicing ; Apoptosis ; Biochemistry, Molecular Biology ; Cancer ; Cell cycle ; Cell death ; Cell differentiation ; Cell proliferation ; Chemotherapy ; DNA damage ; Embryogenesis ; Gene expression ; Genomes ; Genomics ; Growth factors ; Head & neck cancer ; Homeostasis ; Isoforms ; Life Sciences ; Malignancy ; Metastases ; Metastasis ; MicroRNAs ; miRNA ; Mutation ; p53 Protein ; Proteins ; Radiation therapy ; Review ; Tumor suppression ; Tumors ; Wound healing</subject><ispartof>Cancers, 2022-12, Vol.14 (23), p.5948</ispartof><rights>COPYRIGHT 2022 MDPI AG</rights><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c452t-55668829befe15af3867a43c4a840940b4589fed8f099a7c5587508c00115db13</citedby><cites>FETCH-LOGICAL-c452t-55668829befe15af3867a43c4a840940b4589fed8f099a7c5587508c00115db13</cites><orcidid>0000-0002-4556-9853 ; 0000-0002-2622-7356 ; 0000-0003-4920-2554 ; 0000-0003-2358-219X</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/PMC9741383/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9741383/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,886,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36497429$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-04425141$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Rodriguez Calleja, Lidia</creatorcontrib><creatorcontrib>Lavaud, Melanie</creatorcontrib><creatorcontrib>Tesfaye, Robel</creatorcontrib><creatorcontrib>Brounais-Le-Royer, Bénédicte</creatorcontrib><creatorcontrib>Baud'huin, Marc</creatorcontrib><creatorcontrib>Georges, Steven</creatorcontrib><creatorcontrib>Lamoureux, François</creatorcontrib><creatorcontrib>Verrecchia, Franck</creatorcontrib><creatorcontrib>Ory, Benjamin</creatorcontrib><title>The p53 Family Members p63 and p73 Roles in the Metastatic Dissemination: Interactions with microRNAs and TGFβ Pathway</title><title>Cancers</title><addtitle>Cancers (Basel)</addtitle><description>TP53 (TP53), p73 (TP73), and p63 (TP63) are members of the p53 transcription factor family, which has many activities spanning from embryonic development through to tumor suppression. The utilization of two promoters and alternative mRNA splicing has been shown to yield numerous isoforms in p53, p63, and p73. TAp73 is thought to mediate apoptosis as a result of nuclear accumulation following chemotherapy-induced DNA damage, according to a number of studies. Overexpression of the nuclear ΔNp63 and ΔNp73 isoforms, on the other hand, suppresses TAp73's pro-apoptotic activity in human malignancies, potentially leading to metastatic spread or inhibition. Another well-known pathway that has been associated to metastatic spread is the TGF pathway. TGFs are a family of structurally related polypeptide growth factors that regulate a variety of cellular functions including cell proliferation, lineage determination, differentiation, motility, adhesion, and cell death, making them significant players in development, homeostasis, and wound repair. Various studies have already identified several interactions between the p53 protein family and the TGFb pathway in the context of tumor growth and metastatic spread, beginning to shed light on this enigmatic intricacy.</description><subject>Alternative splicing</subject><subject>Apoptosis</subject><subject>Biochemistry, Molecular Biology</subject><subject>Cancer</subject><subject>Cell cycle</subject><subject>Cell death</subject><subject>Cell differentiation</subject><subject>Cell proliferation</subject><subject>Chemotherapy</subject><subject>DNA damage</subject><subject>Embryogenesis</subject><subject>Gene expression</subject><subject>Genomes</subject><subject>Genomics</subject><subject>Growth factors</subject><subject>Head & neck cancer</subject><subject>Homeostasis</subject><subject>Isoforms</subject><subject>Life Sciences</subject><subject>Malignancy</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>MicroRNAs</subject><subject>miRNA</subject><subject>Mutation</subject><subject>p53 Protein</subject><subject>Proteins</subject><subject>Radiation therapy</subject><subject>Review</subject><subject>Tumor suppression</subject><subject>Tumors</subject><subject>Wound healing</subject><issn>2072-6694</issn><issn>2072-6694</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptUsFuGyEQRVWrJnJz7q1C6qU9OIEFFuihkpXWSSSnrSL3jFiWzRLtgrvgWP6tfEi-qWydpolVEIIZ3ryBNwPAW4yOCZHoxGhv7BAxLQiTVLwAhwXixbQsJX355HwAjmK8QXkQgnnJX4MDUlLJaSEPwWbZWrhiBM5177otvLR9lTnhqiRQ-xquOIFXobMROg9Txl7apGPSyRn4xcVoe-ezEfwneOGTHbQZjQg3LrWwd2YIV99m8Q_V8mx-fwd_6NRu9PYNeNXoLtqjh30Cfs6_Lk_Pp4vvZxens8XUUFakKWNlKUQhK9tYzHRDRMk1JYZqQZGkqKJMyMbWokFSam4YE5whYRDCmNUVJhPwece7Wle9rY31adCdWg2u18NWBe3U8xvvWnUdblXWBxNBMsHHHUG7F3Y-W6jRhygtGKb4dkz24SHZEH6tbUyqd9HYrtPehnVUBWe5BCQXL0Pf70FvwnrwWYqMooJhImX5D3WtO6ucb0J-oxlJ1YxngTgZ1wQc_weVZ52rY4K3jcv-ZwEnu4BcnhgH2zx-DCM1tpbaa60c8e6pjI_4v41EfgO4sMfk</recordid><startdate>20221201</startdate><enddate>20221201</enddate><creator>Rodriguez Calleja, Lidia</creator><creator>Lavaud, Melanie</creator><creator>Tesfaye, Robel</creator><creator>Brounais-Le-Royer, Bénédicte</creator><creator>Baud'huin, Marc</creator><creator>Georges, Steven</creator><creator>Lamoureux, François</creator><creator>Verrecchia, Franck</creator><creator>Ory, Benjamin</creator><general>MDPI AG</general><general>MDPI</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</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>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>1XC</scope><scope>VOOES</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-4556-9853</orcidid><orcidid>https://orcid.org/0000-0002-2622-7356</orcidid><orcidid>https://orcid.org/0000-0003-4920-2554</orcidid><orcidid>https://orcid.org/0000-0003-2358-219X</orcidid></search><sort><creationdate>20221201</creationdate><title>The p53 Family Members p63 and p73 Roles in the Metastatic Dissemination: Interactions with microRNAs and TGFβ Pathway</title><author>Rodriguez Calleja, Lidia ; Lavaud, Melanie ; Tesfaye, Robel ; Brounais-Le-Royer, Bénédicte ; Baud'huin, Marc ; Georges, Steven ; Lamoureux, François ; Verrecchia, Franck ; Ory, Benjamin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c452t-55668829befe15af3867a43c4a840940b4589fed8f099a7c5587508c00115db13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Alternative splicing</topic><topic>Apoptosis</topic><topic>Biochemistry, Molecular Biology</topic><topic>Cancer</topic><topic>Cell cycle</topic><topic>Cell death</topic><topic>Cell differentiation</topic><topic>Cell proliferation</topic><topic>Chemotherapy</topic><topic>DNA damage</topic><topic>Embryogenesis</topic><topic>Gene expression</topic><topic>Genomes</topic><topic>Genomics</topic><topic>Growth factors</topic><topic>Head & neck cancer</topic><topic>Homeostasis</topic><topic>Isoforms</topic><topic>Life Sciences</topic><topic>Malignancy</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>MicroRNAs</topic><topic>miRNA</topic><topic>Mutation</topic><topic>p53 Protein</topic><topic>Proteins</topic><topic>Radiation therapy</topic><topic>Review</topic><topic>Tumor suppression</topic><topic>Tumors</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rodriguez Calleja, Lidia</creatorcontrib><creatorcontrib>Lavaud, Melanie</creatorcontrib><creatorcontrib>Tesfaye, Robel</creatorcontrib><creatorcontrib>Brounais-Le-Royer, Bénédicte</creatorcontrib><creatorcontrib>Baud'huin, Marc</creatorcontrib><creatorcontrib>Georges, Steven</creatorcontrib><creatorcontrib>Lamoureux, François</creatorcontrib><creatorcontrib>Verrecchia, Franck</creatorcontrib><creatorcontrib>Ory, Benjamin</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>Biological Sciences</collection><collection>ProQuest research library</collection><collection>ProQuest Biological Science Journals</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</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>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancers</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rodriguez Calleja, Lidia</au><au>Lavaud, Melanie</au><au>Tesfaye, Robel</au><au>Brounais-Le-Royer, Bénédicte</au><au>Baud'huin, Marc</au><au>Georges, Steven</au><au>Lamoureux, François</au><au>Verrecchia, Franck</au><au>Ory, Benjamin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The p53 Family Members p63 and p73 Roles in the Metastatic Dissemination: Interactions with microRNAs and TGFβ Pathway</atitle><jtitle>Cancers</jtitle><addtitle>Cancers (Basel)</addtitle><date>2022-12-01</date><risdate>2022</risdate><volume>14</volume><issue>23</issue><spage>5948</spage><pages>5948-</pages><issn>2072-6694</issn><eissn>2072-6694</eissn><abstract>TP53 (TP53), p73 (TP73), and p63 (TP63) are members of the p53 transcription factor family, which has many activities spanning from embryonic development through to tumor suppression. The utilization of two promoters and alternative mRNA splicing has been shown to yield numerous isoforms in p53, p63, and p73. TAp73 is thought to mediate apoptosis as a result of nuclear accumulation following chemotherapy-induced DNA damage, according to a number of studies. Overexpression of the nuclear ΔNp63 and ΔNp73 isoforms, on the other hand, suppresses TAp73's pro-apoptotic activity in human malignancies, potentially leading to metastatic spread or inhibition. Another well-known pathway that has been associated to metastatic spread is the TGF pathway. TGFs are a family of structurally related polypeptide growth factors that regulate a variety of cellular functions including cell proliferation, lineage determination, differentiation, motility, adhesion, and cell death, making them significant players in development, homeostasis, and wound repair. 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| subjects | Alternative splicing Apoptosis Biochemistry, Molecular Biology Cancer Cell cycle Cell death Cell differentiation Cell proliferation Chemotherapy DNA damage Embryogenesis Gene expression Genomes Genomics Growth factors Head & neck cancer Homeostasis Isoforms Life Sciences Malignancy Metastases Metastasis MicroRNAs miRNA Mutation p53 Protein Proteins Radiation therapy Review Tumor suppression Tumors Wound healing |
| title | The p53 Family Members p63 and p73 Roles in the Metastatic Dissemination: Interactions with microRNAs and TGFβ Pathway |
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