miR-196a Is Able to Restore the Aggressive Phenotype of Annexin A1 Knock-Out in Pancreatic Cancer Cells by CRISPR/Cas9 Genome Editing
Annexin A1 (ANXA1) is a Ca -binding protein that is involved in pancreatic cancer (PC) progression. It is able to mediate cytoskeletal organization maintaining a malignant phenotype. Our previous studies showed that ANXA1 Knock-Out (KO) MIA PaCa-2 cells partially lost their migratory and invasive ca...
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| Veröffentlicht in: | International journal of molecular sciences 2018-07, Vol.19 (7), p.1967 |
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| creator | Belvedere, Raffaella Saggese, Pasquale Pessolano, Emanuela Memoli, Domenico Bizzarro, Valentina Rizzo, Francesca Parente, Luca Weisz, Alessandro Petrella, Antonello |
| description | Annexin A1 (ANXA1) is a Ca
-binding protein that is involved in pancreatic cancer (PC) progression. It is able to mediate cytoskeletal organization maintaining a malignant phenotype. Our previous studies showed that ANXA1 Knock-Out (KO) MIA PaCa-2 cells partially lost their migratory and invasive capabilities and also the metastatization process appeared affected in vivo. Here, we investigated the microRNA (miRNA) profile in ANXA1 KO cells finding that the modification in miRNA expression suggests the significant involvement of ANXA1 in PC development. In this study, we focused on miR-196a which appeared down modulated in absence of ANXA1. This miRNA is a well known oncogenic factor in several tumour models and it is able to trigger the agents of the epithelial to mesenchymal transition (EMT), like ANXA1. Our results show that the reintroduction in ANXA1 KO cells of miR-196a through the mimic sequence restored the early aggressive phenotype of MIA PaCa-2. Then, ANXA1 seems to support the expression of miR-196a and its role. On the other hand, this miRNA is able to mediate cytoskeletal dynamics and other protein functions promoting PC cell migration and invasion. This work describes the correlation between ANXA1 and specific miRNA sequences, particularly miR-196a. These results could lead to further information on ANXA1 intracellular role in PC, explaining other aspects that are apart from its tumorigenic behaviour. |
| doi_str_mv | 10.3390/ijms19071967 |
| format | Article |
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-binding protein that is involved in pancreatic cancer (PC) progression. It is able to mediate cytoskeletal organization maintaining a malignant phenotype. Our previous studies showed that ANXA1 Knock-Out (KO) MIA PaCa-2 cells partially lost their migratory and invasive capabilities and also the metastatization process appeared affected in vivo. Here, we investigated the microRNA (miRNA) profile in ANXA1 KO cells finding that the modification in miRNA expression suggests the significant involvement of ANXA1 in PC development. In this study, we focused on miR-196a which appeared down modulated in absence of ANXA1. This miRNA is a well known oncogenic factor in several tumour models and it is able to trigger the agents of the epithelial to mesenchymal transition (EMT), like ANXA1. Our results show that the reintroduction in ANXA1 KO cells of miR-196a through the mimic sequence restored the early aggressive phenotype of MIA PaCa-2. Then, ANXA1 seems to support the expression of miR-196a and its role. On the other hand, this miRNA is able to mediate cytoskeletal dynamics and other protein functions promoting PC cell migration and invasion. This work describes the correlation between ANXA1 and specific miRNA sequences, particularly miR-196a. These results could lead to further information on ANXA1 intracellular role in PC, explaining other aspects that are apart from its tumorigenic behaviour.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms19071967</identifier><identifier>PMID: 29986379</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Annexin A1 - genetics ; Calcium ions ; Calcium-binding protein ; Cell adhesion & migration ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; CRISPR ; CRISPR-Cas Systems ; Cytoskeleton ; Disease Progression ; Epithelial-Mesenchymal Transition ; Gene Editing ; Gene Expression Regulation, Neoplastic ; Gene Knockout Techniques ; Genome editing ; Genomes ; Genotype & phenotype ; Humans ; In vivo methods and tests ; Invasiveness ; Mesenchyme ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Pancreatic cancer ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - pathology ; Phenotypes ; Proteins ; Tumors</subject><ispartof>International journal of molecular sciences, 2018-07, Vol.19 (7), p.1967</ispartof><rights>2018. This work is licensed under https://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><rights>2018 by the authors. 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-ad799506682d9f17358974feb5d812564a79141e38cbf3f4422fe0b31ae7c3623</citedby><cites>FETCH-LOGICAL-c412t-ad799506682d9f17358974feb5d812564a79141e38cbf3f4422fe0b31ae7c3623</cites><orcidid>0000-0002-6945-5295 ; 0000-0003-1783-5015 ; 0000-0003-0455-2083 ; 0000-0002-5222-0705 ; 0000-0001-5290-2709 ; 0000-0003-1040-7288 ; 0000-0002-5036-7869</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/PMC6073506/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6073506/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29986379$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Belvedere, Raffaella</creatorcontrib><creatorcontrib>Saggese, Pasquale</creatorcontrib><creatorcontrib>Pessolano, Emanuela</creatorcontrib><creatorcontrib>Memoli, Domenico</creatorcontrib><creatorcontrib>Bizzarro, Valentina</creatorcontrib><creatorcontrib>Rizzo, Francesca</creatorcontrib><creatorcontrib>Parente, Luca</creatorcontrib><creatorcontrib>Weisz, Alessandro</creatorcontrib><creatorcontrib>Petrella, Antonello</creatorcontrib><title>miR-196a Is Able to Restore the Aggressive Phenotype of Annexin A1 Knock-Out in Pancreatic Cancer Cells by CRISPR/Cas9 Genome Editing</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Annexin A1 (ANXA1) is a Ca
-binding protein that is involved in pancreatic cancer (PC) progression. It is able to mediate cytoskeletal organization maintaining a malignant phenotype. Our previous studies showed that ANXA1 Knock-Out (KO) MIA PaCa-2 cells partially lost their migratory and invasive capabilities and also the metastatization process appeared affected in vivo. Here, we investigated the microRNA (miRNA) profile in ANXA1 KO cells finding that the modification in miRNA expression suggests the significant involvement of ANXA1 in PC development. In this study, we focused on miR-196a which appeared down modulated in absence of ANXA1. This miRNA is a well known oncogenic factor in several tumour models and it is able to trigger the agents of the epithelial to mesenchymal transition (EMT), like ANXA1. Our results show that the reintroduction in ANXA1 KO cells of miR-196a through the mimic sequence restored the early aggressive phenotype of MIA PaCa-2. Then, ANXA1 seems to support the expression of miR-196a and its role. On the other hand, this miRNA is able to mediate cytoskeletal dynamics and other protein functions promoting PC cell migration and invasion. This work describes the correlation between ANXA1 and specific miRNA sequences, particularly miR-196a. These results could lead to further information on ANXA1 intracellular role in PC, explaining other aspects that are apart from its tumorigenic behaviour.</description><subject>Annexin A1 - genetics</subject><subject>Calcium ions</subject><subject>Calcium-binding protein</subject><subject>Cell adhesion & migration</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>CRISPR</subject><subject>CRISPR-Cas Systems</subject><subject>Cytoskeleton</subject><subject>Disease Progression</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>Gene Editing</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Knockout Techniques</subject><subject>Genome editing</subject><subject>Genomes</subject><subject>Genotype & phenotype</subject><subject>Humans</subject><subject>In vivo methods and tests</subject><subject>Invasiveness</subject><subject>Mesenchyme</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Neoplasm Invasiveness</subject><subject>Neoplasm Metastasis</subject><subject>Pancreatic cancer</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Phenotypes</subject><subject>Proteins</subject><subject>Tumors</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdUU1v1DAQtRCIfsCNM7LEhUPT-iOJ4wtSFLVl1UpdLXC2HGey6yWxFzupuj-A_42rlmrh5GfNmzfz5iH0gZJzziW5sNsxUkkElaV4hY5pzlhGSCleH-AjdBLjlhDGWSHfoiMmZVVyIY_R79GustSq8SLiuh0ATx6vIE4-JLgBXK_XAWK094CXG3B-2u8A-x7XzsGDdbim-MZ58zO7myec_kvtTAA9WYObBCHgBoYh4naPm9Xi23J10ego8XWSGgFfdnaybv0Oven1EOH983uKflxdfm--Zrd314umvs1MTtmU6U5IWZCyrFgneyp4UUmR99AWXUVZUeZaSJpT4JVpe97nyX4PpOVUgzC8ZPwUfXnS3c3tCJ0BNwU9qF2wow575bVV_1ac3ai1v1clScNImQQ-PwsE_2tOZ1KjjSYZ1A78HBVLx65kWqVK1E__Ubd-Di7ZU4wSmReyoI-CZ08sE3yMAfqXZShRj_mqw3wT_eOhgRfy30D5H0vkn1w</recordid><startdate>20180706</startdate><enddate>20180706</enddate><creator>Belvedere, Raffaella</creator><creator>Saggese, Pasquale</creator><creator>Pessolano, Emanuela</creator><creator>Memoli, Domenico</creator><creator>Bizzarro, Valentina</creator><creator>Rizzo, Francesca</creator><creator>Parente, Luca</creator><creator>Weisz, Alessandro</creator><creator>Petrella, Antonello</creator><general>MDPI AG</general><general>MDPI</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</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>5PM</scope><orcidid>https://orcid.org/0000-0002-6945-5295</orcidid><orcidid>https://orcid.org/0000-0003-1783-5015</orcidid><orcidid>https://orcid.org/0000-0003-0455-2083</orcidid><orcidid>https://orcid.org/0000-0002-5222-0705</orcidid><orcidid>https://orcid.org/0000-0001-5290-2709</orcidid><orcidid>https://orcid.org/0000-0003-1040-7288</orcidid><orcidid>https://orcid.org/0000-0002-5036-7869</orcidid></search><sort><creationdate>20180706</creationdate><title>miR-196a Is Able to Restore the Aggressive Phenotype of Annexin A1 Knock-Out in Pancreatic Cancer Cells by CRISPR/Cas9 Genome Editing</title><author>Belvedere, Raffaella ; 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-binding protein that is involved in pancreatic cancer (PC) progression. It is able to mediate cytoskeletal organization maintaining a malignant phenotype. Our previous studies showed that ANXA1 Knock-Out (KO) MIA PaCa-2 cells partially lost their migratory and invasive capabilities and also the metastatization process appeared affected in vivo. Here, we investigated the microRNA (miRNA) profile in ANXA1 KO cells finding that the modification in miRNA expression suggests the significant involvement of ANXA1 in PC development. In this study, we focused on miR-196a which appeared down modulated in absence of ANXA1. This miRNA is a well known oncogenic factor in several tumour models and it is able to trigger the agents of the epithelial to mesenchymal transition (EMT), like ANXA1. Our results show that the reintroduction in ANXA1 KO cells of miR-196a through the mimic sequence restored the early aggressive phenotype of MIA PaCa-2. Then, ANXA1 seems to support the expression of miR-196a and its role. On the other hand, this miRNA is able to mediate cytoskeletal dynamics and other protein functions promoting PC cell migration and invasion. This work describes the correlation between ANXA1 and specific miRNA sequences, particularly miR-196a. These results could lead to further information on ANXA1 intracellular role in PC, explaining other aspects that are apart from its tumorigenic behaviour.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>29986379</pmid><doi>10.3390/ijms19071967</doi><orcidid>https://orcid.org/0000-0002-6945-5295</orcidid><orcidid>https://orcid.org/0000-0003-1783-5015</orcidid><orcidid>https://orcid.org/0000-0003-0455-2083</orcidid><orcidid>https://orcid.org/0000-0002-5222-0705</orcidid><orcidid>https://orcid.org/0000-0001-5290-2709</orcidid><orcidid>https://orcid.org/0000-0003-1040-7288</orcidid><orcidid>https://orcid.org/0000-0002-5036-7869</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MDPI - Multidisciplinary Digital Publishing Institute; MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Annexin A1 - genetics Calcium ions Calcium-binding protein Cell adhesion & migration Cell Line, Tumor Cell Movement Cell Proliferation CRISPR CRISPR-Cas Systems Cytoskeleton Disease Progression Epithelial-Mesenchymal Transition Gene Editing Gene Expression Regulation, Neoplastic Gene Knockout Techniques Genome editing Genomes Genotype & phenotype Humans In vivo methods and tests Invasiveness Mesenchyme MicroRNAs - genetics MicroRNAs - metabolism miRNA Neoplasm Invasiveness Neoplasm Metastasis Pancreatic cancer Pancreatic Neoplasms - genetics Pancreatic Neoplasms - pathology Phenotypes Proteins Tumors |
| title | miR-196a Is Able to Restore the Aggressive Phenotype of Annexin A1 Knock-Out in Pancreatic Cancer Cells by CRISPR/Cas9 Genome Editing |
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