Bioengineered miRNA-1291 prodrug therapy in pancreatic cancer cells and patient-derived xenograft mouse models
Our recent studies have revealed that microRNA-1291 (miR-1291) is downregulated in pancreatic cancer (PC) specimens and restoration of miR-1291 inhibits tumorigenesis of PC cells. This study is to assess the efficacy and underlying mechanism of our bioengineered miR-1291 prodrug monotherapy and comb...
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| Veröffentlicht in: | Cancer letters 2019-02, Vol.442, p.82-90 |
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| container_title | Cancer letters |
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| creator | Tu, Mei-Juan Ho, Pui Yan Zhang, Qian-Yu Jian, Chao Qiu, Jing-Xin Kim, Edward J. Bold, Richard J. Gonzalez, Frank J. Bi, Huichang Yu, Ai-Ming |
| description | Our recent studies have revealed that microRNA-1291 (miR-1291) is downregulated in pancreatic cancer (PC) specimens and restoration of miR-1291 inhibits tumorigenesis of PC cells. This study is to assess the efficacy and underlying mechanism of our bioengineered miR-1291 prodrug monotherapy and combined treatment with chemotherapy. AT-rich interacting domain protein 3B (ARID3B) was verified as a new target for miR-1291, and miR-1291 prodrug was processed to mature miR-1291 in PC cells which surprisingly upregulated ARID3B mRNA and protein levels. Co-administration of miR-1291 with gemcitabine plus nab-paclitaxel (Gem-nP) largely increased the levels of apoptosis, DNA damage and mitotic arrest in PC cells, compared to mono-drug treatment. Consequently, miR-1291 prodrug improved cell sensitivity to Gem-nP. Furthermore, systemic administration of in vivo-jetPEI-formulated miR-1291 prodrug suppressed tumor growth in both PANC-1 xenograft and PC patients derived xenograft (PDX) mouse models to comparable degrees as Gem-nP alone, while combination treatment reduced tumor growth more ubiquitously and to the greatest degrees (70–90%), compared to monotherapy. All treatments were well tolerated in mice. In conclusion, biologic miR-1291 prodrug has therapeutic potential as a monotherapy for PC, and a sensitizing agent to chemotherapy.
•Bioengineered miR-1291 prodrug sensitizes pancreatic cancer cells to chemotherapy.•Induction of apoptosis by miR-1291 is associated with the upregulation of ARID3B.•MiR-1291 alone suppresses tumor growth in PANC-1 xenograft and PDX mouse models.•MiR-1291 augments the efficacy of chemotherapy for pancreatic cancer in vivo. |
| doi_str_mv | 10.1016/j.canlet.2018.10.038 |
| format | Article |
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•Bioengineered miR-1291 prodrug sensitizes pancreatic cancer cells to chemotherapy.•Induction of apoptosis by miR-1291 is associated with the upregulation of ARID3B.•MiR-1291 alone suppresses tumor growth in PANC-1 xenograft and PDX mouse models.•MiR-1291 augments the efficacy of chemotherapy for pancreatic cancer in vivo.</description><identifier>ISSN: 0304-3835</identifier><identifier>EISSN: 1872-7980</identifier><identifier>DOI: 10.1016/j.canlet.2018.10.038</identifier><identifier>PMID: 30389433</identifier><language>eng</language><publisher>Ireland: Elsevier B.V</publisher><subject>Albumins - pharmacology ; Animal models ; Animals ; Antineoplastic Combined Chemotherapy Protocols - pharmacology ; Apoptosis ; Apoptosis - drug effects ; ARID3B ; Bioengineering ; Cancer therapies ; Cell cycle ; Cell Cycle Checkpoints - drug effects ; Cell growth ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Chemotherapy ; Combined treatment ; Deoxycytidine - analogs & derivatives ; Deoxycytidine - pharmacology ; DNA damage ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Dose-Response Relationship, Drug ; Female ; Gemcitabine ; Gemcitabine plus nab-paclitaxel ; Gene Expression Regulation, Neoplastic ; Humans ; Mice, Inbred NOD ; Mice, Nude ; Mice, SCID ; Mice, Transgenic ; MicroRNAs - genetics ; MicroRNAs - metabolism ; MicroRNAs - pharmacology ; miR-1291 ; miRNA ; mRNA ; Paclitaxel ; Paclitaxel - pharmacology ; Pancreatic cancer ; Pancreatic Neoplasms - drug therapy ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - metabolism ; Pancreatic Neoplasms - pathology ; Patients ; PDX model ; Pheochromocytoma cells ; Prodrugs - pharmacology ; Proteins ; Signal Transduction - drug effects ; Tumor Burden - drug effects ; Tumorigenesis ; Xenograft Model Antitumor Assays ; Xenografts</subject><ispartof>Cancer letters, 2019-02, Vol.442, p.82-90</ispartof><rights>2018 Elsevier B.V.</rights><rights>Copyright © 2018 Elsevier B.V. All rights reserved.</rights><rights>Copyright Elsevier Limited Feb 1, 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c491t-c000c249792ff2ed628449206a7ae6a5ae989a38d4f1b567a23205bdcb25eb8e3</citedby><cites>FETCH-LOGICAL-c491t-c000c249792ff2ed628449206a7ae6a5ae989a38d4f1b567a23205bdcb25eb8e3</cites><orcidid>0000-0002-5787-5081 ; 0000-0003-1441-4012</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.canlet.2018.10.038$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30389433$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tu, Mei-Juan</creatorcontrib><creatorcontrib>Ho, Pui Yan</creatorcontrib><creatorcontrib>Zhang, Qian-Yu</creatorcontrib><creatorcontrib>Jian, Chao</creatorcontrib><creatorcontrib>Qiu, Jing-Xin</creatorcontrib><creatorcontrib>Kim, Edward J.</creatorcontrib><creatorcontrib>Bold, Richard J.</creatorcontrib><creatorcontrib>Gonzalez, Frank J.</creatorcontrib><creatorcontrib>Bi, Huichang</creatorcontrib><creatorcontrib>Yu, Ai-Ming</creatorcontrib><title>Bioengineered miRNA-1291 prodrug therapy in pancreatic cancer cells and patient-derived xenograft mouse models</title><title>Cancer letters</title><addtitle>Cancer Lett</addtitle><description>Our recent studies have revealed that microRNA-1291 (miR-1291) is downregulated in pancreatic cancer (PC) specimens and restoration of miR-1291 inhibits tumorigenesis of PC cells. This study is to assess the efficacy and underlying mechanism of our bioengineered miR-1291 prodrug monotherapy and combined treatment with chemotherapy. AT-rich interacting domain protein 3B (ARID3B) was verified as a new target for miR-1291, and miR-1291 prodrug was processed to mature miR-1291 in PC cells which surprisingly upregulated ARID3B mRNA and protein levels. Co-administration of miR-1291 with gemcitabine plus nab-paclitaxel (Gem-nP) largely increased the levels of apoptosis, DNA damage and mitotic arrest in PC cells, compared to mono-drug treatment. Consequently, miR-1291 prodrug improved cell sensitivity to Gem-nP. Furthermore, systemic administration of in vivo-jetPEI-formulated miR-1291 prodrug suppressed tumor growth in both PANC-1 xenograft and PC patients derived xenograft (PDX) mouse models to comparable degrees as Gem-nP alone, while combination treatment reduced tumor growth more ubiquitously and to the greatest degrees (70–90%), compared to monotherapy. All treatments were well tolerated in mice. In conclusion, biologic miR-1291 prodrug has therapeutic potential as a monotherapy for PC, and a sensitizing agent to chemotherapy.
•Bioengineered miR-1291 prodrug sensitizes pancreatic cancer cells to chemotherapy.•Induction of apoptosis by miR-1291 is associated with the upregulation of ARID3B.•MiR-1291 alone suppresses tumor growth in PANC-1 xenograft and PDX mouse models.•MiR-1291 augments the efficacy of chemotherapy for pancreatic cancer in vivo.</description><subject>Albumins - pharmacology</subject><subject>Animal models</subject><subject>Animals</subject><subject>Antineoplastic Combined Chemotherapy Protocols - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>ARID3B</subject><subject>Bioengineering</subject><subject>Cancer therapies</subject><subject>Cell cycle</subject><subject>Cell Cycle Checkpoints - drug effects</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Chemotherapy</subject><subject>Combined treatment</subject><subject>Deoxycytidine - analogs & derivatives</subject><subject>Deoxycytidine - pharmacology</subject><subject>DNA damage</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Dose-Response Relationship, Drug</subject><subject>Female</subject><subject>Gemcitabine</subject><subject>Gemcitabine plus nab-paclitaxel</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Mice, Inbred NOD</subject><subject>Mice, Nude</subject><subject>Mice, SCID</subject><subject>Mice, Transgenic</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>MicroRNAs - pharmacology</subject><subject>miR-1291</subject><subject>miRNA</subject><subject>mRNA</subject><subject>Paclitaxel</subject><subject>Paclitaxel - pharmacology</subject><subject>Pancreatic cancer</subject><subject>Pancreatic Neoplasms - drug therapy</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Patients</subject><subject>PDX model</subject><subject>Pheochromocytoma cells</subject><subject>Prodrugs - pharmacology</subject><subject>Proteins</subject><subject>Signal Transduction - drug effects</subject><subject>Tumor Burden - drug effects</subject><subject>Tumorigenesis</subject><subject>Xenograft Model Antitumor Assays</subject><subject>Xenografts</subject><issn>0304-3835</issn><issn>1872-7980</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9UV1rFDEUDaLYte0_EAn4PGu-ZiZ5EWpRWygWij6HTHJnm2U2GZPM0v57s2yt-uJLAveee87hHITeUrKmhHYftmtrwgRlzQiVdbQmXL5AKyp71vRKkpdoRTgRDZe8PUFvct4SQlrRt6_RCa9YJThfofDJRwgbHwASOLzzd98uGsoUxXOKLi0bXO4hmfkR-4BnE2wCU7zFVdtCwhamKWMTXN0VD6E0DpLfV6YHCHGTzFjwLi4Z6utgymfo1WimDOdP_yn68eXz98ur5ub26_XlxU1jhaKlsdWqZUL1io0jA9cxKYRipDO9gc60BpRUhksnRjq0XW8YZ6QdnB1YC4MEfoo-HnnnZdiBs9VZMpOek9-Z9Kij8frfTfD3ehP3uuOUCsYqwfsnghR_LpCL3sYlhepZM9qRnnIpuooSR5RNMecE47MCJfrQkt7qY0v60NJhWpOvZ-_-dvd89LuWP_ZrZLD3kHS2NV0LziewRbvo_6_wC9ydpwc</recordid><startdate>20190201</startdate><enddate>20190201</enddate><creator>Tu, Mei-Juan</creator><creator>Ho, Pui Yan</creator><creator>Zhang, Qian-Yu</creator><creator>Jian, Chao</creator><creator>Qiu, Jing-Xin</creator><creator>Kim, Edward J.</creator><creator>Bold, Richard J.</creator><creator>Gonzalez, Frank J.</creator><creator>Bi, Huichang</creator><creator>Yu, Ai-Ming</creator><general>Elsevier B.V</general><general>Elsevier Limited</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>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-5787-5081</orcidid><orcidid>https://orcid.org/0000-0003-1441-4012</orcidid></search><sort><creationdate>20190201</creationdate><title>Bioengineered miRNA-1291 prodrug therapy in pancreatic cancer cells and patient-derived xenograft mouse models</title><author>Tu, Mei-Juan ; Ho, Pui Yan ; Zhang, Qian-Yu ; Jian, Chao ; Qiu, Jing-Xin ; Kim, Edward J. ; Bold, Richard J. ; Gonzalez, Frank J. ; Bi, Huichang ; Yu, Ai-Ming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c491t-c000c249792ff2ed628449206a7ae6a5ae989a38d4f1b567a23205bdcb25eb8e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Albumins - pharmacology</topic><topic>Animal models</topic><topic>Animals</topic><topic>Antineoplastic Combined Chemotherapy Protocols - pharmacology</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>ARID3B</topic><topic>Bioengineering</topic><topic>Cancer therapies</topic><topic>Cell cycle</topic><topic>Cell Cycle Checkpoints - drug effects</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Chemotherapy</topic><topic>Combined treatment</topic><topic>Deoxycytidine - analogs & derivatives</topic><topic>Deoxycytidine - pharmacology</topic><topic>DNA damage</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Dose-Response Relationship, Drug</topic><topic>Female</topic><topic>Gemcitabine</topic><topic>Gemcitabine plus nab-paclitaxel</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Mice, Inbred NOD</topic><topic>Mice, Nude</topic><topic>Mice, SCID</topic><topic>Mice, Transgenic</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>MicroRNAs - pharmacology</topic><topic>miR-1291</topic><topic>miRNA</topic><topic>mRNA</topic><topic>Paclitaxel</topic><topic>Paclitaxel - pharmacology</topic><topic>Pancreatic cancer</topic><topic>Pancreatic Neoplasms - drug therapy</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Pancreatic Neoplasms - metabolism</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Patients</topic><topic>PDX model</topic><topic>Pheochromocytoma cells</topic><topic>Prodrugs - pharmacology</topic><topic>Proteins</topic><topic>Signal Transduction - drug effects</topic><topic>Tumor Burden - drug effects</topic><topic>Tumorigenesis</topic><topic>Xenograft Model Antitumor Assays</topic><topic>Xenografts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tu, Mei-Juan</creatorcontrib><creatorcontrib>Ho, Pui Yan</creatorcontrib><creatorcontrib>Zhang, Qian-Yu</creatorcontrib><creatorcontrib>Jian, Chao</creatorcontrib><creatorcontrib>Qiu, Jing-Xin</creatorcontrib><creatorcontrib>Kim, Edward J.</creatorcontrib><creatorcontrib>Bold, Richard J.</creatorcontrib><creatorcontrib>Gonzalez, Frank J.</creatorcontrib><creatorcontrib>Bi, Huichang</creatorcontrib><creatorcontrib>Yu, Ai-Ming</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tu, Mei-Juan</au><au>Ho, Pui Yan</au><au>Zhang, Qian-Yu</au><au>Jian, Chao</au><au>Qiu, Jing-Xin</au><au>Kim, Edward J.</au><au>Bold, Richard J.</au><au>Gonzalez, Frank J.</au><au>Bi, Huichang</au><au>Yu, Ai-Ming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bioengineered miRNA-1291 prodrug therapy in pancreatic cancer cells and patient-derived xenograft mouse models</atitle><jtitle>Cancer letters</jtitle><addtitle>Cancer Lett</addtitle><date>2019-02-01</date><risdate>2019</risdate><volume>442</volume><spage>82</spage><epage>90</epage><pages>82-90</pages><issn>0304-3835</issn><eissn>1872-7980</eissn><abstract>Our recent studies have revealed that microRNA-1291 (miR-1291) is downregulated in pancreatic cancer (PC) specimens and restoration of miR-1291 inhibits tumorigenesis of PC cells. This study is to assess the efficacy and underlying mechanism of our bioengineered miR-1291 prodrug monotherapy and combined treatment with chemotherapy. AT-rich interacting domain protein 3B (ARID3B) was verified as a new target for miR-1291, and miR-1291 prodrug was processed to mature miR-1291 in PC cells which surprisingly upregulated ARID3B mRNA and protein levels. Co-administration of miR-1291 with gemcitabine plus nab-paclitaxel (Gem-nP) largely increased the levels of apoptosis, DNA damage and mitotic arrest in PC cells, compared to mono-drug treatment. Consequently, miR-1291 prodrug improved cell sensitivity to Gem-nP. Furthermore, systemic administration of in vivo-jetPEI-formulated miR-1291 prodrug suppressed tumor growth in both PANC-1 xenograft and PC patients derived xenograft (PDX) mouse models to comparable degrees as Gem-nP alone, while combination treatment reduced tumor growth more ubiquitously and to the greatest degrees (70–90%), compared to monotherapy. All treatments were well tolerated in mice. In conclusion, biologic miR-1291 prodrug has therapeutic potential as a monotherapy for PC, and a sensitizing agent to chemotherapy.
•Bioengineered miR-1291 prodrug sensitizes pancreatic cancer cells to chemotherapy.•Induction of apoptosis by miR-1291 is associated with the upregulation of ARID3B.•MiR-1291 alone suppresses tumor growth in PANC-1 xenograft and PDX mouse models.•MiR-1291 augments the efficacy of chemotherapy for pancreatic cancer in vivo.</abstract><cop>Ireland</cop><pub>Elsevier B.V</pub><pmid>30389433</pmid><doi>10.1016/j.canlet.2018.10.038</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-5787-5081</orcidid><orcidid>https://orcid.org/0000-0003-1441-4012</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Cancer letters, 2019-02, Vol.442, p.82-90 |
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| subjects | Albumins - pharmacology Animal models Animals Antineoplastic Combined Chemotherapy Protocols - pharmacology Apoptosis Apoptosis - drug effects ARID3B Bioengineering Cancer therapies Cell cycle Cell Cycle Checkpoints - drug effects Cell growth Cell Line, Tumor Cell Proliferation - drug effects Chemotherapy Combined treatment Deoxycytidine - analogs & derivatives Deoxycytidine - pharmacology DNA damage DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Dose-Response Relationship, Drug Female Gemcitabine Gemcitabine plus nab-paclitaxel Gene Expression Regulation, Neoplastic Humans Mice, Inbred NOD Mice, Nude Mice, SCID Mice, Transgenic MicroRNAs - genetics MicroRNAs - metabolism MicroRNAs - pharmacology miR-1291 miRNA mRNA Paclitaxel Paclitaxel - pharmacology Pancreatic cancer Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - genetics Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology Patients PDX model Pheochromocytoma cells Prodrugs - pharmacology Proteins Signal Transduction - drug effects Tumor Burden - drug effects Tumorigenesis Xenograft Model Antitumor Assays Xenografts |
| title | Bioengineered miRNA-1291 prodrug therapy in pancreatic cancer cells and patient-derived xenograft mouse models |
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