A miR-146a-5p/TRAF6/NF-kB p65 axis regulates pancreatic cancer chemoresistance: functional validation and clinical significance
: Dysregulated microRNA (miRNA) expression in cancer can act as a key factor that modifies biological processes, including chemoresistance. Our study aimed to identify the miRNAs associated with gemcitabine (GEM) resistance in pancreatic ductal adenocarcinoma (PDAC) and to explore the potential mech...
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| Veröffentlicht in: | Theranostics 2020-01, Vol.10 (9), p.3967-3979 |
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| creator | Meng, Qingcai Liang, Chen Hua, Jie Zhang, Bo Liu, Jiang Zhang, Yiyin Wei, Miaoyan Yu, Xianjun Xu, Jin Shi, Si |
| description | : Dysregulated microRNA (miRNA) expression in cancer can act as a key factor that modifies biological processes, including chemoresistance. Our study aimed to identify the miRNAs associated with gemcitabine (GEM) resistance in pancreatic ductal adenocarcinoma (PDAC) and to explore the potential mechanisms.
: The miRNA microarray was used to identify miRNAs associated with GEM resistance. Quantitative real-time PCR was used to examine miR-146a-5p expression in paired PDAC and adjacent normal tissues. Bioinformatics analysis, luciferase reporter assays, and chromatin immunoprecipitation assays were used to confirm tumor necrosis factor receptor-associated factor 6 (TRAF6) as a direct target of miR-146a-5p and to explore the potential transcription factor binding and regulation by miR-146a-5p.
and
experiments were performed to investigate the mechanisms.
: MiR-146a-5p expression was significantly decreased in PDAC tissues compared with adjacent normal tissues, and miR-146a-5p expression correlated with prognosis in PDAC patients. Functional studies indicated that miR-146a-5p suppressed PDAC cell proliferation and sensitized PDAC cells to GEM chemotherapy by targeting the 3'-untranslated region (3'-UTR) of TRAF6. MiR-146a-5p was also observed to downregulate the TRAF6/NF-κB p65/P-gp axis, which regulates PDAC cell growth and chemoresistance.
: Taken together, the results indicate that the miR-146a-5p/TRAF6/NF-κB p65 axis drives pancreatic chemoresistance by regulating P-gp, suggesting that miR-146a-5p may be utilized as a new therapeutic target and prognostic marker in PDAC patients. |
| doi_str_mv | 10.7150/thno.40566 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7086345</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2598253692</sourcerecordid><originalsourceid>FETCH-LOGICAL-c406t-4c2f0c7daf1d5ce0a3be49fabf6cf58ea186639a3e23e66a2ed534e7f8b35ed13</originalsourceid><addsrcrecordid>eNpdkU1r3DAQhk1paUKaS39AEfRSCs7q23IPhU3ItoHQQkjPYlYe7Sq1ZVeyQ3vqX483XySZy3w9vAzzFsV7Ro8qpuhi3Mb-SFKl9atinxlhykpL-vpJvVcc5nxF55CU16x-W-wJzrlWgu8X_5ekCxclkxpKNSwuL5YrvfixKn8fk0ErAn9DJgk3UwsjZjJAdAlhDI64ucRE3Ba7PmEOedwNvhA_RTeGPkJLrqENDewaArEhrg0xuHmewyYGH24V3hVvPLQZD-_zQfFrdXp58r08__nt7GR5XjpJ9VhKxz11VQOeNcohBbFGWXtYe-28MgjMaC1qEMgFag0cGyUkVt6shcKGiYPi653uMK07bBzGMUFrhxQ6SP9sD8E-38SwtZv-2lbUaCHVLPDpXiD1fybMo-1Cdti2ELGfsuXCSCNoXVcz-vEFetVPaf7ITKnacCV0zWfq8x3lUp9zQv94DKN2Z63dWWtvrZ3hD0_Pf0QfjBQ3YzCgwA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2598253692</pqid></control><display><type>article</type><title>A miR-146a-5p/TRAF6/NF-kB p65 axis regulates pancreatic cancer chemoresistance: functional validation and clinical significance</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>PubMed Central Open Access</source><creator>Meng, Qingcai ; Liang, Chen ; Hua, Jie ; Zhang, Bo ; Liu, Jiang ; Zhang, Yiyin ; Wei, Miaoyan ; Yu, Xianjun ; Xu, Jin ; Shi, Si</creator><creatorcontrib>Meng, Qingcai ; Liang, Chen ; Hua, Jie ; Zhang, Bo ; Liu, Jiang ; Zhang, Yiyin ; Wei, Miaoyan ; Yu, Xianjun ; Xu, Jin ; Shi, Si</creatorcontrib><description>: Dysregulated microRNA (miRNA) expression in cancer can act as a key factor that modifies biological processes, including chemoresistance. Our study aimed to identify the miRNAs associated with gemcitabine (GEM) resistance in pancreatic ductal adenocarcinoma (PDAC) and to explore the potential mechanisms.
: The miRNA microarray was used to identify miRNAs associated with GEM resistance. Quantitative real-time PCR was used to examine miR-146a-5p expression in paired PDAC and adjacent normal tissues. Bioinformatics analysis, luciferase reporter assays, and chromatin immunoprecipitation assays were used to confirm tumor necrosis factor receptor-associated factor 6 (TRAF6) as a direct target of miR-146a-5p and to explore the potential transcription factor binding and regulation by miR-146a-5p.
and
experiments were performed to investigate the mechanisms.
: MiR-146a-5p expression was significantly decreased in PDAC tissues compared with adjacent normal tissues, and miR-146a-5p expression correlated with prognosis in PDAC patients. Functional studies indicated that miR-146a-5p suppressed PDAC cell proliferation and sensitized PDAC cells to GEM chemotherapy by targeting the 3'-untranslated region (3'-UTR) of TRAF6. MiR-146a-5p was also observed to downregulate the TRAF6/NF-κB p65/P-gp axis, which regulates PDAC cell growth and chemoresistance.
: Taken together, the results indicate that the miR-146a-5p/TRAF6/NF-κB p65 axis drives pancreatic chemoresistance by regulating P-gp, suggesting that miR-146a-5p may be utilized as a new therapeutic target and prognostic marker in PDAC patients.</description><identifier>ISSN: 1838-7640</identifier><identifier>EISSN: 1838-7640</identifier><identifier>DOI: 10.7150/thno.40566</identifier><identifier>PMID: 32226532</identifier><language>eng</language><publisher>Australia: Ivyspring International Publisher Pty Ltd</publisher><subject>Animals ; Antibodies ; Apoptosis ; Cancer therapies ; Carcinoma, Pancreatic Ductal - drug therapy ; Carcinoma, Pancreatic Ductal - metabolism ; Cell growth ; Cell Line, Tumor ; Cell Proliferation ; Clinical significance ; Drug Resistance, Neoplasm ; Gene Expression Regulation, Neoplastic ; Glycoproteins ; Humans ; Intracellular Signaling Peptides and Proteins - metabolism ; Kinases ; Laboratory animals ; Medical prognosis ; Medical research ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; MicroRNAs ; MicroRNAs - physiology ; Mutagenesis ; Pancreatic cancer ; Pancreatic Neoplasms - drug therapy ; Pancreatic Neoplasms - metabolism ; Protein expression ; Proteins ; Reagents ; Research Paper ; Software ; Survival analysis ; Transcription Factor RelA - metabolism ; Tumorigenesis ; Tumors</subject><ispartof>Theranostics, 2020-01, Vol.10 (9), p.3967-3979</ispartof><rights>The author(s).</rights><rights>2020. This work is published 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>The author(s) 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c406t-4c2f0c7daf1d5ce0a3be49fabf6cf58ea186639a3e23e66a2ed534e7f8b35ed13</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7086345/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7086345/$$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/32226532$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Meng, Qingcai</creatorcontrib><creatorcontrib>Liang, Chen</creatorcontrib><creatorcontrib>Hua, Jie</creatorcontrib><creatorcontrib>Zhang, Bo</creatorcontrib><creatorcontrib>Liu, Jiang</creatorcontrib><creatorcontrib>Zhang, Yiyin</creatorcontrib><creatorcontrib>Wei, Miaoyan</creatorcontrib><creatorcontrib>Yu, Xianjun</creatorcontrib><creatorcontrib>Xu, Jin</creatorcontrib><creatorcontrib>Shi, Si</creatorcontrib><title>A miR-146a-5p/TRAF6/NF-kB p65 axis regulates pancreatic cancer chemoresistance: functional validation and clinical significance</title><title>Theranostics</title><addtitle>Theranostics</addtitle><description>: Dysregulated microRNA (miRNA) expression in cancer can act as a key factor that modifies biological processes, including chemoresistance. Our study aimed to identify the miRNAs associated with gemcitabine (GEM) resistance in pancreatic ductal adenocarcinoma (PDAC) and to explore the potential mechanisms.
: The miRNA microarray was used to identify miRNAs associated with GEM resistance. Quantitative real-time PCR was used to examine miR-146a-5p expression in paired PDAC and adjacent normal tissues. Bioinformatics analysis, luciferase reporter assays, and chromatin immunoprecipitation assays were used to confirm tumor necrosis factor receptor-associated factor 6 (TRAF6) as a direct target of miR-146a-5p and to explore the potential transcription factor binding and regulation by miR-146a-5p.
and
experiments were performed to investigate the mechanisms.
: MiR-146a-5p expression was significantly decreased in PDAC tissues compared with adjacent normal tissues, and miR-146a-5p expression correlated with prognosis in PDAC patients. Functional studies indicated that miR-146a-5p suppressed PDAC cell proliferation and sensitized PDAC cells to GEM chemotherapy by targeting the 3'-untranslated region (3'-UTR) of TRAF6. MiR-146a-5p was also observed to downregulate the TRAF6/NF-κB p65/P-gp axis, which regulates PDAC cell growth and chemoresistance.
: Taken together, the results indicate that the miR-146a-5p/TRAF6/NF-κB p65 axis drives pancreatic chemoresistance by regulating P-gp, suggesting that miR-146a-5p may be utilized as a new therapeutic target and prognostic marker in PDAC patients.</description><subject>Animals</subject><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Cancer therapies</subject><subject>Carcinoma, Pancreatic Ductal - drug therapy</subject><subject>Carcinoma, Pancreatic Ductal - metabolism</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Clinical significance</subject><subject>Drug Resistance, Neoplasm</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Glycoproteins</subject><subject>Humans</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Medical prognosis</subject><subject>Medical research</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>MicroRNAs</subject><subject>MicroRNAs - physiology</subject><subject>Mutagenesis</subject><subject>Pancreatic cancer</subject><subject>Pancreatic Neoplasms - drug therapy</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Reagents</subject><subject>Research Paper</subject><subject>Software</subject><subject>Survival analysis</subject><subject>Transcription Factor RelA - metabolism</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><issn>1838-7640</issn><issn>1838-7640</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkU1r3DAQhk1paUKaS39AEfRSCs7q23IPhU3ItoHQQkjPYlYe7Sq1ZVeyQ3vqX483XySZy3w9vAzzFsV7Ro8qpuhi3Mb-SFKl9atinxlhykpL-vpJvVcc5nxF55CU16x-W-wJzrlWgu8X_5ekCxclkxpKNSwuL5YrvfixKn8fk0ErAn9DJgk3UwsjZjJAdAlhDI64ucRE3Ba7PmEOedwNvhA_RTeGPkJLrqENDewaArEhrg0xuHmewyYGH24V3hVvPLQZD-_zQfFrdXp58r08__nt7GR5XjpJ9VhKxz11VQOeNcohBbFGWXtYe-28MgjMaC1qEMgFag0cGyUkVt6shcKGiYPi653uMK07bBzGMUFrhxQ6SP9sD8E-38SwtZv-2lbUaCHVLPDpXiD1fybMo-1Cdti2ELGfsuXCSCNoXVcz-vEFetVPaf7ITKnacCV0zWfq8x3lUp9zQv94DKN2Z63dWWtvrZ3hD0_Pf0QfjBQ3YzCgwA</recordid><startdate>20200101</startdate><enddate>20200101</enddate><creator>Meng, Qingcai</creator><creator>Liang, Chen</creator><creator>Hua, Jie</creator><creator>Zhang, Bo</creator><creator>Liu, Jiang</creator><creator>Zhang, Yiyin</creator><creator>Wei, Miaoyan</creator><creator>Yu, Xianjun</creator><creator>Xu, Jin</creator><creator>Shi, Si</creator><general>Ivyspring International Publisher Pty Ltd</general><general>Ivyspring International Publisher</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>8FI</scope><scope>8FJ</scope><scope>8FK</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>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20200101</creationdate><title>A miR-146a-5p/TRAF6/NF-kB p65 axis regulates pancreatic cancer chemoresistance: functional validation and clinical significance</title><author>Meng, Qingcai ; 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Our study aimed to identify the miRNAs associated with gemcitabine (GEM) resistance in pancreatic ductal adenocarcinoma (PDAC) and to explore the potential mechanisms.
: The miRNA microarray was used to identify miRNAs associated with GEM resistance. Quantitative real-time PCR was used to examine miR-146a-5p expression in paired PDAC and adjacent normal tissues. Bioinformatics analysis, luciferase reporter assays, and chromatin immunoprecipitation assays were used to confirm tumor necrosis factor receptor-associated factor 6 (TRAF6) as a direct target of miR-146a-5p and to explore the potential transcription factor binding and regulation by miR-146a-5p.
and
experiments were performed to investigate the mechanisms.
: MiR-146a-5p expression was significantly decreased in PDAC tissues compared with adjacent normal tissues, and miR-146a-5p expression correlated with prognosis in PDAC patients. Functional studies indicated that miR-146a-5p suppressed PDAC cell proliferation and sensitized PDAC cells to GEM chemotherapy by targeting the 3'-untranslated region (3'-UTR) of TRAF6. MiR-146a-5p was also observed to downregulate the TRAF6/NF-κB p65/P-gp axis, which regulates PDAC cell growth and chemoresistance.
: Taken together, the results indicate that the miR-146a-5p/TRAF6/NF-κB p65 axis drives pancreatic chemoresistance by regulating P-gp, suggesting that miR-146a-5p may be utilized as a new therapeutic target and prognostic marker in PDAC patients.</abstract><cop>Australia</cop><pub>Ivyspring International Publisher Pty Ltd</pub><pmid>32226532</pmid><doi>10.7150/thno.40566</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antibodies Apoptosis Cancer therapies Carcinoma, Pancreatic Ductal - drug therapy Carcinoma, Pancreatic Ductal - metabolism Cell growth Cell Line, Tumor Cell Proliferation Clinical significance Drug Resistance, Neoplasm Gene Expression Regulation, Neoplastic Glycoproteins Humans Intracellular Signaling Peptides and Proteins - metabolism Kinases Laboratory animals Medical prognosis Medical research Mice Mice, Inbred BALB C Mice, Nude MicroRNAs MicroRNAs - physiology Mutagenesis Pancreatic cancer Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - metabolism Protein expression Proteins Reagents Research Paper Software Survival analysis Transcription Factor RelA - metabolism Tumorigenesis Tumors |
| title | A miR-146a-5p/TRAF6/NF-kB p65 axis regulates pancreatic cancer chemoresistance: functional validation and clinical significance |
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