CRISPR/Cas9 nanoeditor of double knockout large fragments of E6 and E7 oncogenes for reversing drugs resistance in cervical cancer
Drug resistance of tumor cells is always a headache problem in clinical treatment. In order to combat chemotherapy-resistance in cervical cancer and improve treatment effect, we design a CRISPR/Cas9 nanoeditor to knock out two key oncogenes E6 and E7 that lead to drug tolerance. Meanwhile, the delet...
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| Veröffentlicht in: | Journal of nanobiotechnology 2021-08, Vol.19 (1), p.231-231, Article 231 |
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| creator | Li, Xianhuang Guo, Mingming Hou, Bei Zheng, Bin Wang, Zhiyun Huang, Mengqian Xu, Yanan Chang, Jin Wang, Tao |
| description | Drug resistance of tumor cells is always a headache problem in clinical treatment. In order to combat chemotherapy-resistance in cervical cancer and improve treatment effect, we design a CRISPR/Cas9 nanoeditor to knock out two key oncogenes E6 and E7 that lead to drug tolerance. Meanwhile, the deletion of these two oncogenes can effectively reactivate p53 and pRB signaling pathways that inhibit the growth of tumor cells. Our results demonstrated the nanoeditor could simultaneously delete two oncogenes, and the size of DNA fragments knocked out reaches an unprecedented 563 bp. After the preparation of cationic liposomes combined with chemotherapy drug docetaxel (DOC), this nanosystem can significantly inhibit the drug tolerance of cancer cells and improve the therapeutic effect of cervical cancer. Therefore, this study provides a promising strategy for the treatment of cervical cancer by combining chemotherapy and double-target gene therapy. This strategy can also be applied in other disease models to customize personalized anti-tumor strategies by simply changing chemotherapy drugs and targeted genes. |
| doi_str_mv | 10.1186/s12951-021-00970-w |
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In order to combat chemotherapy-resistance in cervical cancer and improve treatment effect, we design a CRISPR/Cas9 nanoeditor to knock out two key oncogenes E6 and E7 that lead to drug tolerance. Meanwhile, the deletion of these two oncogenes can effectively reactivate p53 and pRB signaling pathways that inhibit the growth of tumor cells. Our results demonstrated the nanoeditor could simultaneously delete two oncogenes, and the size of DNA fragments knocked out reaches an unprecedented 563 bp. After the preparation of cationic liposomes combined with chemotherapy drug docetaxel (DOC), this nanosystem can significantly inhibit the drug tolerance of cancer cells and improve the therapeutic effect of cervical cancer. Therefore, this study provides a promising strategy for the treatment of cervical cancer by combining chemotherapy and double-target gene therapy. This strategy can also be applied in other disease models to customize personalized anti-tumor strategies by simply changing chemotherapy drugs and targeted genes.</description><identifier>ISSN: 1477-3155</identifier><identifier>EISSN: 1477-3155</identifier><identifier>DOI: 10.1186/s12951-021-00970-w</identifier><identifier>PMID: 34353334</identifier><language>eng</language><publisher>LONDON: Springer Nature</publisher><subject>Animals ; Apoptosis ; Apoptosis - drug effects ; Biotechnology & Applied Microbiology ; Cancer ; Cancer therapies ; Care and treatment ; Cervical cancer ; Cervix ; Chemotherapy ; CRISPR ; CRISPR-Cas Systems ; CRISPR/Cas9 ; Cytotoxicity ; Deoxyribonucleic acid ; Disease Models, Animal ; DNA ; Drug resistance ; Drug Resistance, Neoplasm ; Drug tolerance ; Drugs ; Female ; Fragments ; Gene expression ; Gene Knockout Techniques ; Gene Targeting ; Gene therapy ; Genetic Therapy ; Health aspects ; Health services ; HeLa Cells ; Human papillomavirus ; Humans ; Life Sciences & Biomedicine ; Management ; Mice ; Mice, Nude ; Microscopy ; Nanoeditor ; Nanomedicine ; Nanoparticles ; Nanoscience & Nanotechnology ; Oncogene deletion ; Oncogenes ; Oncogenes - genetics ; p53 Protein ; Plasmids ; Science & Technology ; Science & Technology - Other Topics ; Tumor cells ; Tumors ; Uterine Cervical Neoplasms - genetics ; Uterine Cervical Neoplasms - therapy</subject><ispartof>Journal of nanobiotechnology, 2021-08, Vol.19 (1), p.231-231, Article 231</ispartof><rights>2021. The Author(s).</rights><rights>COPYRIGHT 2021 BioMed Central Ltd.</rights><rights>2021. This work is licensed 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><rights>The Author(s) 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>17</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000681749600001</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c597t-e7160e365009ffcc25d8e58eede4d5b4ac811c4da8fa51311addf04cbfa9bf53</citedby><cites>FETCH-LOGICAL-c597t-e7160e365009ffcc25d8e58eede4d5b4ac811c4da8fa51311addf04cbfa9bf53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8340365/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8340365/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2115,27928,27929,39262,53795,53797</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34353334$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Xianhuang</creatorcontrib><creatorcontrib>Guo, Mingming</creatorcontrib><creatorcontrib>Hou, Bei</creatorcontrib><creatorcontrib>Zheng, Bin</creatorcontrib><creatorcontrib>Wang, Zhiyun</creatorcontrib><creatorcontrib>Huang, Mengqian</creatorcontrib><creatorcontrib>Xu, Yanan</creatorcontrib><creatorcontrib>Chang, Jin</creatorcontrib><creatorcontrib>Wang, Tao</creatorcontrib><title>CRISPR/Cas9 nanoeditor of double knockout large fragments of E6 and E7 oncogenes for reversing drugs resistance in cervical cancer</title><title>Journal of nanobiotechnology</title><addtitle>J NANOBIOTECHNOL</addtitle><addtitle>J Nanobiotechnology</addtitle><description>Drug resistance of tumor cells is always a headache problem in clinical treatment. In order to combat chemotherapy-resistance in cervical cancer and improve treatment effect, we design a CRISPR/Cas9 nanoeditor to knock out two key oncogenes E6 and E7 that lead to drug tolerance. Meanwhile, the deletion of these two oncogenes can effectively reactivate p53 and pRB signaling pathways that inhibit the growth of tumor cells. Our results demonstrated the nanoeditor could simultaneously delete two oncogenes, and the size of DNA fragments knocked out reaches an unprecedented 563 bp. After the preparation of cationic liposomes combined with chemotherapy drug docetaxel (DOC), this nanosystem can significantly inhibit the drug tolerance of cancer cells and improve the therapeutic effect of cervical cancer. Therefore, this study provides a promising strategy for the treatment of cervical cancer by combining chemotherapy and double-target gene therapy. This strategy can also be applied in other disease models to customize personalized anti-tumor strategies by simply changing chemotherapy drugs and targeted genes.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Biotechnology & Applied Microbiology</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Care and treatment</subject><subject>Cervical cancer</subject><subject>Cervix</subject><subject>Chemotherapy</subject><subject>CRISPR</subject><subject>CRISPR-Cas Systems</subject><subject>CRISPR/Cas9</subject><subject>Cytotoxicity</subject><subject>Deoxyribonucleic acid</subject><subject>Disease Models, Animal</subject><subject>DNA</subject><subject>Drug resistance</subject><subject>Drug Resistance, Neoplasm</subject><subject>Drug tolerance</subject><subject>Drugs</subject><subject>Female</subject><subject>Fragments</subject><subject>Gene expression</subject><subject>Gene Knockout Techniques</subject><subject>Gene Targeting</subject><subject>Gene therapy</subject><subject>Genetic Therapy</subject><subject>Health aspects</subject><subject>Health services</subject><subject>HeLa Cells</subject><subject>Human papillomavirus</subject><subject>Humans</subject><subject>Life Sciences & Biomedicine</subject><subject>Management</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Microscopy</subject><subject>Nanoeditor</subject><subject>Nanomedicine</subject><subject>Nanoparticles</subject><subject>Nanoscience & Nanotechnology</subject><subject>Oncogene deletion</subject><subject>Oncogenes</subject><subject>Oncogenes - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Journal of nanobiotechnology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Xianhuang</au><au>Guo, Mingming</au><au>Hou, Bei</au><au>Zheng, Bin</au><au>Wang, Zhiyun</au><au>Huang, Mengqian</au><au>Xu, Yanan</au><au>Chang, Jin</au><au>Wang, Tao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CRISPR/Cas9 nanoeditor of double knockout large fragments of E6 and E7 oncogenes for reversing drugs resistance in cervical cancer</atitle><jtitle>Journal of nanobiotechnology</jtitle><stitle>J NANOBIOTECHNOL</stitle><addtitle>J Nanobiotechnology</addtitle><date>2021-08-05</date><risdate>2021</risdate><volume>19</volume><issue>1</issue><spage>231</spage><epage>231</epage><pages>231-231</pages><artnum>231</artnum><issn>1477-3155</issn><eissn>1477-3155</eissn><abstract>Drug resistance of tumor cells is always a headache problem in clinical treatment. In order to combat chemotherapy-resistance in cervical cancer and improve treatment effect, we design a CRISPR/Cas9 nanoeditor to knock out two key oncogenes E6 and E7 that lead to drug tolerance. Meanwhile, the deletion of these two oncogenes can effectively reactivate p53 and pRB signaling pathways that inhibit the growth of tumor cells. Our results demonstrated the nanoeditor could simultaneously delete two oncogenes, and the size of DNA fragments knocked out reaches an unprecedented 563 bp. After the preparation of cationic liposomes combined with chemotherapy drug docetaxel (DOC), this nanosystem can significantly inhibit the drug tolerance of cancer cells and improve the therapeutic effect of cervical cancer. Therefore, this study provides a promising strategy for the treatment of cervical cancer by combining chemotherapy and double-target gene therapy. This strategy can also be applied in other disease models to customize personalized anti-tumor strategies by simply changing chemotherapy drugs and targeted genes.</abstract><cop>LONDON</cop><pub>Springer Nature</pub><pmid>34353334</pmid><doi>10.1186/s12951-021-00970-w</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Apoptosis Apoptosis - drug effects Biotechnology & Applied Microbiology Cancer Cancer therapies Care and treatment Cervical cancer Cervix Chemotherapy CRISPR CRISPR-Cas Systems CRISPR/Cas9 Cytotoxicity Deoxyribonucleic acid Disease Models, Animal DNA Drug resistance Drug Resistance, Neoplasm Drug tolerance Drugs Female Fragments Gene expression Gene Knockout Techniques Gene Targeting Gene therapy Genetic Therapy Health aspects Health services HeLa Cells Human papillomavirus Humans Life Sciences & Biomedicine Management Mice Mice, Nude Microscopy Nanoeditor Nanomedicine Nanoparticles Nanoscience & Nanotechnology Oncogene deletion Oncogenes Oncogenes - genetics p53 Protein Plasmids Science & Technology Science & Technology - Other Topics Tumor cells Tumors Uterine Cervical Neoplasms - genetics Uterine Cervical Neoplasms - therapy |
| title | CRISPR/Cas9 nanoeditor of double knockout large fragments of E6 and E7 oncogenes for reversing drugs resistance in cervical cancer |
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