CRISPR-Cas9 mediated CD133 knockout inhibits colon cancer invasion through reduced epithelial-mesenchymal transition
We previously reported that CD133, as a putative cancer stem cell marker, plays an important role in cell proliferation and invasion in colon cancer. To understand the role of CD133 expression in colon cancer, we evaluated the inhibitory effect of CD133 in colon cancer cells. In this study, we gener...
Gespeichert in:
| Veröffentlicht in: | PloS one 2019-08, Vol.14 (8), p.e0220860-e0220860 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | e0220860 |
|---|---|
| container_issue | 8 |
| container_start_page | e0220860 |
| container_title | PloS one |
| container_volume | 14 |
| creator | Li, Wanlu Cho, Mee-Yon Lee, Suji Jang, Mirae Park, Junsoo Park, Rackhyun |
| description | We previously reported that CD133, as a putative cancer stem cell marker, plays an important role in cell proliferation and invasion in colon cancer. To understand the role of CD133 expression in colon cancer, we evaluated the inhibitory effect of CD133 in colon cancer cells. In this study, we generated CD133knockout colon cancer cells (LoVo) using the CRISPR-Cas9 gene editing system. CD133+ colon cancer cells (LoVo) were infected with the lentiviral vector carrying CD133 gRNA and purified cell by culturing single cell colonies. CD133knockout cells was validated by western blot and flow cytometry analysis. In functional study, we observed a significant reduction in cell proliferation and colony formation in CRISPR-Cas9 mediated CD133 knockout cells in compare with control (P < 0.001). We also found the anticancer effect of stattic was dependent on CD133 expression in colon cancer cells. Although CD133knockout cells could not completely block the tumorigenic property, they showed remarkable inhibitory effects on the ability of cell migration and invasion (P < 0.001). In addition, we examined the epithelial mesenchymal transition (EMT)-related protein expression by western blot. The result clearly showed a loss of vimentin expression in CD133knockout cells. Therefore, CRISPR-Cas9 mediated CD133knockout can be an effective treatment modality for CD133+ colon cancer through reducing the characteristics of cancer stem cells. |
| doi_str_mv | 10.1371/journal.pone.0220860 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_plos_</sourceid><recordid>TN_cdi_plos_journals_2270188485</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A595927368</galeid><doaj_id>oai_doaj_org_article_bf4ad50586224dc0bdb21f41a5a57d58</doaj_id><sourcerecordid>A595927368</sourcerecordid><originalsourceid>FETCH-LOGICAL-c692t-f50ea1d6ba6fbc80a2a3e78754050ce4dc18f34f670a9a1674616f9c2890571b3</originalsourceid><addsrcrecordid>eNqNk01v1DAQhiMEoqXwDxBEQkJwyOKP2HEuSNXytVKloi1wtSaOs3HrjbexU9F_j8Om1Qb1gHJIPH7edzJjT5K8xGiBaYE_XLqh78Audq7TC0QIEhw9So5xSUnGCaKPD76PkmfeXyLEqOD8aXJEMS1pmePjJCzXq4vv62wJvky3ujYQdJ0uP2FK06vOqSs3hNR0ralM8Kly1nWpgk7pPkZvwJu4Dm3vhk2b9roeVFTrnQmttgZsttVed6q93YJNQw-dNyEqnidPGrBev5jeJ8nPL59_LL9lZ-dfV8vTs0zxkoSsYUgDrnkFvKmUQECA6kIULEcMKZ3XCouG5g0vEJSAeZFzzJtSEVEiVuCKniSv974767ycGuYlIQXCQuSCRWK1J2oHl3LXmy30t9KBkX8Drt9I6INRVsuqyaFmiAlOSEyNqroiuMkxMGBFzUT0-jhlG6rYSaW7WLGdmc53OtPKjbuRnIsCcxwN3k0GvbsetA9ya7zS1kKn3bD_b4SKQoy53vyDPlzdRG0gFmC6xsW8ajSVp6xkJSkoH70WD1DxqfXWqHi7GhPjM8H7mSAyQf8OGxi8l6uL9f-z57_m7NsDttVgQ-udHcYr4-dgvgdV77zvdXPfZIzkOBx33ZDjcMhpOKLs1eEB3YvupoH-AQQYCiI</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2270188485</pqid></control><display><type>article</type><title>CRISPR-Cas9 mediated CD133 knockout inhibits colon cancer invasion through reduced epithelial-mesenchymal transition</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Public Library of Science (PLoS)</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><creator>Li, Wanlu ; Cho, Mee-Yon ; Lee, Suji ; Jang, Mirae ; Park, Junsoo ; Park, Rackhyun</creator><contributor>Ahmad, Aamir</contributor><creatorcontrib>Li, Wanlu ; Cho, Mee-Yon ; Lee, Suji ; Jang, Mirae ; Park, Junsoo ; Park, Rackhyun ; Ahmad, Aamir</creatorcontrib><description>We previously reported that CD133, as a putative cancer stem cell marker, plays an important role in cell proliferation and invasion in colon cancer. To understand the role of CD133 expression in colon cancer, we evaluated the inhibitory effect of CD133 in colon cancer cells. In this study, we generated CD133knockout colon cancer cells (LoVo) using the CRISPR-Cas9 gene editing system. CD133+ colon cancer cells (LoVo) were infected with the lentiviral vector carrying CD133 gRNA and purified cell by culturing single cell colonies. CD133knockout cells was validated by western blot and flow cytometry analysis. In functional study, we observed a significant reduction in cell proliferation and colony formation in CRISPR-Cas9 mediated CD133 knockout cells in compare with control (P < 0.001). We also found the anticancer effect of stattic was dependent on CD133 expression in colon cancer cells. Although CD133knockout cells could not completely block the tumorigenic property, they showed remarkable inhibitory effects on the ability of cell migration and invasion (P < 0.001). In addition, we examined the epithelial mesenchymal transition (EMT)-related protein expression by western blot. The result clearly showed a loss of vimentin expression in CD133knockout cells. Therefore, CRISPR-Cas9 mediated CD133knockout can be an effective treatment modality for CD133+ colon cancer through reducing the characteristics of cancer stem cells.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0220860</identifier><identifier>PMID: 31393941</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>AC133 Antigen - deficiency ; AC133 Antigen - genetics ; AC133 Antigen - pharmacology ; Anticancer properties ; Biology and Life Sciences ; Cancer cells ; Cancer research ; Care and treatment ; Cell adhesion & migration ; Cell differentiation ; Cell growth ; Cell migration ; Cell Proliferation ; Colon ; Colon cancer ; Colonic Neoplasms - genetics ; Colonic Neoplasms - pathology ; Colonic Neoplasms - therapy ; Colonies ; Colorectal cancer ; CRISPR ; CRISPR-Cas Systems - genetics ; CRISPR-Cas technology ; Cyclic S-Oxides - pharmacology ; EDTA ; Engineering and Technology ; Epithelial-Mesenchymal Transition - genetics ; Flow cytometry ; Gene Knockout Techniques - methods ; Genes ; Genetic aspects ; Genetic modification ; Genome editing ; Genomes ; gRNA ; Health aspects ; Humans ; Medicine ; Medicine and Health Sciences ; Mesenchyme ; Metastasis ; Methylene blue ; Neoplasm Invasiveness - prevention & control ; Neoplastic Stem Cells ; Pathology ; Social Sciences ; Stem cells ; Testing ; Tumor Cells, Cultured ; Vimentin ; Vimentin - metabolism</subject><ispartof>PloS one, 2019-08, Vol.14 (8), p.e0220860-e0220860</ispartof><rights>COPYRIGHT 2019 Public Library of Science</rights><rights>2019 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2019 Li et al 2019 Li et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-f50ea1d6ba6fbc80a2a3e78754050ce4dc18f34f670a9a1674616f9c2890571b3</citedby><cites>FETCH-LOGICAL-c692t-f50ea1d6ba6fbc80a2a3e78754050ce4dc18f34f670a9a1674616f9c2890571b3</cites><orcidid>0000-0002-7955-4211</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/PMC6687161/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6687161/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31393941$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Ahmad, Aamir</contributor><creatorcontrib>Li, Wanlu</creatorcontrib><creatorcontrib>Cho, Mee-Yon</creatorcontrib><creatorcontrib>Lee, Suji</creatorcontrib><creatorcontrib>Jang, Mirae</creatorcontrib><creatorcontrib>Park, Junsoo</creatorcontrib><creatorcontrib>Park, Rackhyun</creatorcontrib><title>CRISPR-Cas9 mediated CD133 knockout inhibits colon cancer invasion through reduced epithelial-mesenchymal transition</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>We previously reported that CD133, as a putative cancer stem cell marker, plays an important role in cell proliferation and invasion in colon cancer. To understand the role of CD133 expression in colon cancer, we evaluated the inhibitory effect of CD133 in colon cancer cells. In this study, we generated CD133knockout colon cancer cells (LoVo) using the CRISPR-Cas9 gene editing system. CD133+ colon cancer cells (LoVo) were infected with the lentiviral vector carrying CD133 gRNA and purified cell by culturing single cell colonies. CD133knockout cells was validated by western blot and flow cytometry analysis. In functional study, we observed a significant reduction in cell proliferation and colony formation in CRISPR-Cas9 mediated CD133 knockout cells in compare with control (P < 0.001). We also found the anticancer effect of stattic was dependent on CD133 expression in colon cancer cells. Although CD133knockout cells could not completely block the tumorigenic property, they showed remarkable inhibitory effects on the ability of cell migration and invasion (P < 0.001). In addition, we examined the epithelial mesenchymal transition (EMT)-related protein expression by western blot. The result clearly showed a loss of vimentin expression in CD133knockout cells. Therefore, CRISPR-Cas9 mediated CD133knockout can be an effective treatment modality for CD133+ colon cancer through reducing the characteristics of cancer stem cells.</description><subject>AC133 Antigen - deficiency</subject><subject>AC133 Antigen - genetics</subject><subject>AC133 Antigen - pharmacology</subject><subject>Anticancer properties</subject><subject>Biology and Life Sciences</subject><subject>Cancer cells</subject><subject>Cancer research</subject><subject>Care and treatment</subject><subject>Cell adhesion & migration</subject><subject>Cell differentiation</subject><subject>Cell growth</subject><subject>Cell migration</subject><subject>Cell Proliferation</subject><subject>Colon</subject><subject>Colon cancer</subject><subject>Colonic Neoplasms - genetics</subject><subject>Colonic Neoplasms - pathology</subject><subject>Colonic Neoplasms - therapy</subject><subject>Colonies</subject><subject>Colorectal cancer</subject><subject>CRISPR</subject><subject>CRISPR-Cas Systems - genetics</subject><subject>CRISPR-Cas technology</subject><subject>Cyclic S-Oxides - pharmacology</subject><subject>EDTA</subject><subject>Engineering and Technology</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Flow cytometry</subject><subject>Gene Knockout Techniques - methods</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic modification</subject><subject>Genome editing</subject><subject>Genomes</subject><subject>gRNA</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Medicine</subject><subject>Medicine and Health Sciences</subject><subject>Mesenchyme</subject><subject>Metastasis</subject><subject>Methylene blue</subject><subject>Neoplasm Invasiveness - prevention & control</subject><subject>Neoplastic Stem Cells</subject><subject>Pathology</subject><subject>Social Sciences</subject><subject>Stem cells</subject><subject>Testing</subject><subject>Tumor Cells, Cultured</subject><subject>Vimentin</subject><subject>Vimentin - metabolism</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk01v1DAQhiMEoqXwDxBEQkJwyOKP2HEuSNXytVKloi1wtSaOs3HrjbexU9F_j8Om1Qb1gHJIPH7edzJjT5K8xGiBaYE_XLqh78Audq7TC0QIEhw9So5xSUnGCaKPD76PkmfeXyLEqOD8aXJEMS1pmePjJCzXq4vv62wJvky3ujYQdJ0uP2FK06vOqSs3hNR0ralM8Kly1nWpgk7pPkZvwJu4Dm3vhk2b9roeVFTrnQmttgZsttVed6q93YJNQw-dNyEqnidPGrBev5jeJ8nPL59_LL9lZ-dfV8vTs0zxkoSsYUgDrnkFvKmUQECA6kIULEcMKZ3XCouG5g0vEJSAeZFzzJtSEVEiVuCKniSv974767ycGuYlIQXCQuSCRWK1J2oHl3LXmy30t9KBkX8Drt9I6INRVsuqyaFmiAlOSEyNqroiuMkxMGBFzUT0-jhlG6rYSaW7WLGdmc53OtPKjbuRnIsCcxwN3k0GvbsetA9ya7zS1kKn3bD_b4SKQoy53vyDPlzdRG0gFmC6xsW8ajSVp6xkJSkoH70WD1DxqfXWqHi7GhPjM8H7mSAyQf8OGxi8l6uL9f-z57_m7NsDttVgQ-udHcYr4-dgvgdV77zvdXPfZIzkOBx33ZDjcMhpOKLs1eEB3YvupoH-AQQYCiI</recordid><startdate>20190808</startdate><enddate>20190808</enddate><creator>Li, Wanlu</creator><creator>Cho, Mee-Yon</creator><creator>Lee, Suji</creator><creator>Jang, Mirae</creator><creator>Park, Junsoo</creator><creator>Park, Rackhyun</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-7955-4211</orcidid></search><sort><creationdate>20190808</creationdate><title>CRISPR-Cas9 mediated CD133 knockout inhibits colon cancer invasion through reduced epithelial-mesenchymal transition</title><author>Li, Wanlu ; Cho, Mee-Yon ; Lee, Suji ; Jang, Mirae ; Park, Junsoo ; Park, Rackhyun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-f50ea1d6ba6fbc80a2a3e78754050ce4dc18f34f670a9a1674616f9c2890571b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>AC133 Antigen - deficiency</topic><topic>AC133 Antigen - genetics</topic><topic>AC133 Antigen - pharmacology</topic><topic>Anticancer properties</topic><topic>Biology and Life Sciences</topic><topic>Cancer cells</topic><topic>Cancer research</topic><topic>Care and treatment</topic><topic>Cell adhesion & migration</topic><topic>Cell differentiation</topic><topic>Cell growth</topic><topic>Cell migration</topic><topic>Cell Proliferation</topic><topic>Colon</topic><topic>Colon cancer</topic><topic>Colonic Neoplasms - genetics</topic><topic>Colonic Neoplasms - pathology</topic><topic>Colonic Neoplasms - therapy</topic><topic>Colonies</topic><topic>Colorectal cancer</topic><topic>CRISPR</topic><topic>CRISPR-Cas Systems - genetics</topic><topic>CRISPR-Cas technology</topic><topic>Cyclic S-Oxides - pharmacology</topic><topic>EDTA</topic><topic>Engineering and Technology</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Flow cytometry</topic><topic>Gene Knockout Techniques - methods</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genetic modification</topic><topic>Genome editing</topic><topic>Genomes</topic><topic>gRNA</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Medicine</topic><topic>Medicine and Health Sciences</topic><topic>Mesenchyme</topic><topic>Metastasis</topic><topic>Methylene blue</topic><topic>Neoplasm Invasiveness - prevention & control</topic><topic>Neoplastic Stem Cells</topic><topic>Pathology</topic><topic>Social Sciences</topic><topic>Stem cells</topic><topic>Testing</topic><topic>Tumor Cells, Cultured</topic><topic>Vimentin</topic><topic>Vimentin - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Wanlu</creatorcontrib><creatorcontrib>Cho, Mee-Yon</creatorcontrib><creatorcontrib>Lee, Suji</creatorcontrib><creatorcontrib>Jang, Mirae</creatorcontrib><creatorcontrib>Park, Junsoo</creatorcontrib><creatorcontrib>Park, Rackhyun</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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 Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</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>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</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>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Wanlu</au><au>Cho, Mee-Yon</au><au>Lee, Suji</au><au>Jang, Mirae</au><au>Park, Junsoo</au><au>Park, Rackhyun</au><au>Ahmad, Aamir</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CRISPR-Cas9 mediated CD133 knockout inhibits colon cancer invasion through reduced epithelial-mesenchymal transition</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2019-08-08</date><risdate>2019</risdate><volume>14</volume><issue>8</issue><spage>e0220860</spage><epage>e0220860</epage><pages>e0220860-e0220860</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>We previously reported that CD133, as a putative cancer stem cell marker, plays an important role in cell proliferation and invasion in colon cancer. To understand the role of CD133 expression in colon cancer, we evaluated the inhibitory effect of CD133 in colon cancer cells. In this study, we generated CD133knockout colon cancer cells (LoVo) using the CRISPR-Cas9 gene editing system. CD133+ colon cancer cells (LoVo) were infected with the lentiviral vector carrying CD133 gRNA and purified cell by culturing single cell colonies. CD133knockout cells was validated by western blot and flow cytometry analysis. In functional study, we observed a significant reduction in cell proliferation and colony formation in CRISPR-Cas9 mediated CD133 knockout cells in compare with control (P < 0.001). We also found the anticancer effect of stattic was dependent on CD133 expression in colon cancer cells. Although CD133knockout cells could not completely block the tumorigenic property, they showed remarkable inhibitory effects on the ability of cell migration and invasion (P < 0.001). In addition, we examined the epithelial mesenchymal transition (EMT)-related protein expression by western blot. The result clearly showed a loss of vimentin expression in CD133knockout cells. Therefore, CRISPR-Cas9 mediated CD133knockout can be an effective treatment modality for CD133+ colon cancer through reducing the characteristics of cancer stem cells.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>31393941</pmid><doi>10.1371/journal.pone.0220860</doi><tpages>e0220860</tpages><orcidid>https://orcid.org/0000-0002-7955-4211</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2019-08, Vol.14 (8), p.e0220860-e0220860 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_2270188485 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | AC133 Antigen - deficiency AC133 Antigen - genetics AC133 Antigen - pharmacology Anticancer properties Biology and Life Sciences Cancer cells Cancer research Care and treatment Cell adhesion & migration Cell differentiation Cell growth Cell migration Cell Proliferation Colon Colon cancer Colonic Neoplasms - genetics Colonic Neoplasms - pathology Colonic Neoplasms - therapy Colonies Colorectal cancer CRISPR CRISPR-Cas Systems - genetics CRISPR-Cas technology Cyclic S-Oxides - pharmacology EDTA Engineering and Technology Epithelial-Mesenchymal Transition - genetics Flow cytometry Gene Knockout Techniques - methods Genes Genetic aspects Genetic modification Genome editing Genomes gRNA Health aspects Humans Medicine Medicine and Health Sciences Mesenchyme Metastasis Methylene blue Neoplasm Invasiveness - prevention & control Neoplastic Stem Cells Pathology Social Sciences Stem cells Testing Tumor Cells, Cultured Vimentin Vimentin - metabolism |
| title | CRISPR-Cas9 mediated CD133 knockout inhibits colon cancer invasion through reduced epithelial-mesenchymal transition |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-04T17%3A53%3A59IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=CRISPR-Cas9%20mediated%20CD133%20knockout%20inhibits%20colon%20cancer%20invasion%20through%20reduced%20epithelial-mesenchymal%20transition&rft.jtitle=PloS%20one&rft.au=Li,%20Wanlu&rft.date=2019-08-08&rft.volume=14&rft.issue=8&rft.spage=e0220860&rft.epage=e0220860&rft.pages=e0220860-e0220860&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0220860&rft_dat=%3Cgale_plos_%3EA595927368%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2270188485&rft_id=info:pmid/31393941&rft_galeid=A595927368&rft_doaj_id=oai_doaj_org_article_bf4ad50586224dc0bdb21f41a5a57d58&rfr_iscdi=true |