miR-199a modulates cisplatin resistance in ovarian cancer by targeting Hif1α
Resistance to chemotherapy is a primary problem for the effective treatment of ovarian cancer. Recently, increasing evidence has demonstrated that miRNAs modulate many important molecular pathways involved in chemotherapy. Previous studies demonstrated that miR-199a affected ovarian cancer cell resi...
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| description | Resistance to chemotherapy is a primary problem for the effective treatment of ovarian cancer. Recently, increasing evidence has demonstrated that miRNAs modulate many important molecular pathways involved in chemotherapy. Previous studies demonstrated that miR-199a affected ovarian cancer cell resistance to cisplatin (DDP). However, the role of miR-199a and its target genes in determination of ovarian cancer sensitivity to DDP remains unclear. Quantitative reverse transcription polymerase chain reaction was used to detect the expression levels of miR-199a in ovarian cancer tissues and C13* and OV2008 cell lines. After transfection of miR-199a mimic or inhibitor, flow cytometry was used to detect cell apoptosis exposed to DDP. Enzyme-linked immunosorbent assay and Western blot assay were applied to detect tumor necrosis factor-α levels and protein expression levels of Bax, Fas, Fas-associated death domain, and caspase-8. The results indicated that the expression of miR-199a was downregulated and hypoxia-inducible factor 1α (Hif1α) upregulated in the ovarian tumors compared with those in the corresponding normal tissues. Besides, the expression levels of miR-199a were significantly higher in OV2008 cells compared with those in C13* cells. Moreover, suppression of Hif1α reversed the inhibiting function of miR-199a inhibitor on DDP-induced apoptosis in the OV2008 cells. However, overexpression of both miR-199a and Hif1α reduced DDP-induced apoptosis in C13* cells. In conclusion, miR-199a may change DDP resistance in ovarian cancer by regulating Hif1α. |
| doi_str_mv | 10.2147/OTT.S145833 |
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| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5731338</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1980103939</sourcerecordid><originalsourceid>FETCH-LOGICAL-c372t-7853b534407a10d985a662189da5fcc86e719d93a7511774e4a69a98e1ac418b3</originalsourceid><addsrcrecordid>eNpdkclKA0EQhhtRTIyevMuAF0FGe5teLoIEN4gIGs9NpacTO8wSu2cEH8sX8ZlsMYp6qu3jp6p-hPYJPqGEy9O76fTkgfBCMbaBhoRIlQvN8OavfIB2YlxiLISifBsNqKZSMM2G6Lb29znRGrK6LfsKOhcz6-MqZb7Jgos-dtBYl6WqfYHgocnsZyNks9esg7BwCVxk135O3t920dYcquj21nGEHi8vpuPrfHJ3dTM-n-SWSdrlUhVsVjDOsQSCS60KEIISpUso5tYq4STRpWYgi3SC5I6D0KCVI2A5UTM2Qmdfuqt-VrvSuqYLUJlV8DWEV9OCN38njX8yi_bFFJIRxlQSOFoLhPa5d7EztY_WVRU0ru2jIVphgtOHdEIP_6HLtg9NOs9QymlBsUi_HKHjL8qGNsbg5j_LEGw-bTLJJrO2KdEHv_f_Yb99YR_u8o0b</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2242520676</pqid></control><display><type>article</type><title>miR-199a modulates cisplatin resistance in ovarian cancer by targeting Hif1α</title><source>Taylor & Francis Open Access</source><source>DOVE Medical Press Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>PubMed Central Open Access</source><creator>Feng, Xue ; Liu, Ning ; Deng, Suo ; Zhang, Dandan ; Wang, Kexin ; Lu, Meisong</creator><creatorcontrib>Feng, Xue ; Liu, Ning ; Deng, Suo ; Zhang, Dandan ; Wang, Kexin ; Lu, Meisong</creatorcontrib><description>Resistance to chemotherapy is a primary problem for the effective treatment of ovarian cancer. Recently, increasing evidence has demonstrated that miRNAs modulate many important molecular pathways involved in chemotherapy. Previous studies demonstrated that miR-199a affected ovarian cancer cell resistance to cisplatin (DDP). However, the role of miR-199a and its target genes in determination of ovarian cancer sensitivity to DDP remains unclear. Quantitative reverse transcription polymerase chain reaction was used to detect the expression levels of miR-199a in ovarian cancer tissues and C13* and OV2008 cell lines. After transfection of miR-199a mimic or inhibitor, flow cytometry was used to detect cell apoptosis exposed to DDP. Enzyme-linked immunosorbent assay and Western blot assay were applied to detect tumor necrosis factor-α levels and protein expression levels of Bax, Fas, Fas-associated death domain, and caspase-8. The results indicated that the expression of miR-199a was downregulated and hypoxia-inducible factor 1α (Hif1α) upregulated in the ovarian tumors compared with those in the corresponding normal tissues. Besides, the expression levels of miR-199a were significantly higher in OV2008 cells compared with those in C13* cells. Moreover, suppression of Hif1α reversed the inhibiting function of miR-199a inhibitor on DDP-induced apoptosis in the OV2008 cells. However, overexpression of both miR-199a and Hif1α reduced DDP-induced apoptosis in C13* cells. In conclusion, miR-199a may change DDP resistance in ovarian cancer by regulating Hif1α.</description><identifier>ISSN: 1178-6930</identifier><identifier>EISSN: 1178-6930</identifier><identifier>DOI: 10.2147/OTT.S145833</identifier><identifier>PMID: 29276393</identifier><language>eng</language><publisher>New Zealand: Taylor & Francis Ltd</publisher><subject>Apoptosis ; BAX protein ; Binding sites ; Bone surgery ; Cancer therapies ; Caspase-8 ; Chemotherapy ; Chronic obstructive pulmonary disease ; Cisplatin ; Enzyme-linked immunosorbent assay ; Enzymes ; Flow cytometry ; Hypoxia ; Hypoxia-inducible factor 1a ; Hypoxia-inducible factors ; Immunoglobulins ; MicroRNAs ; Original Research ; Ovarian cancer ; Proteins ; Reverse transcription ; Transfection ; Tumor cell lines ; Tumor necrosis factor-TNF ; Womens health</subject><ispartof>OncoTargets and therapy, 2017-01, Vol.10, p.5899-5906</ispartof><rights>2017. This work is licensed under https://creativecommons.org/licenses/by-nc/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2017 Feng et al. This work is published and licensed by Dove Medical Press Limited 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-7853b534407a10d985a662189da5fcc86e719d93a7511774e4a69a98e1ac418b3</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/PMC5731338/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5731338/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,3849,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29276393$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Feng, Xue</creatorcontrib><creatorcontrib>Liu, Ning</creatorcontrib><creatorcontrib>Deng, Suo</creatorcontrib><creatorcontrib>Zhang, Dandan</creatorcontrib><creatorcontrib>Wang, Kexin</creatorcontrib><creatorcontrib>Lu, Meisong</creatorcontrib><title>miR-199a modulates cisplatin resistance in ovarian cancer by targeting Hif1α</title><title>OncoTargets and therapy</title><addtitle>Onco Targets Ther</addtitle><description>Resistance to chemotherapy is a primary problem for the effective treatment of ovarian cancer. Recently, increasing evidence has demonstrated that miRNAs modulate many important molecular pathways involved in chemotherapy. Previous studies demonstrated that miR-199a affected ovarian cancer cell resistance to cisplatin (DDP). However, the role of miR-199a and its target genes in determination of ovarian cancer sensitivity to DDP remains unclear. Quantitative reverse transcription polymerase chain reaction was used to detect the expression levels of miR-199a in ovarian cancer tissues and C13* and OV2008 cell lines. After transfection of miR-199a mimic or inhibitor, flow cytometry was used to detect cell apoptosis exposed to DDP. Enzyme-linked immunosorbent assay and Western blot assay were applied to detect tumor necrosis factor-α levels and protein expression levels of Bax, Fas, Fas-associated death domain, and caspase-8. The results indicated that the expression of miR-199a was downregulated and hypoxia-inducible factor 1α (Hif1α) upregulated in the ovarian tumors compared with those in the corresponding normal tissues. Besides, the expression levels of miR-199a were significantly higher in OV2008 cells compared with those in C13* cells. Moreover, suppression of Hif1α reversed the inhibiting function of miR-199a inhibitor on DDP-induced apoptosis in the OV2008 cells. However, overexpression of both miR-199a and Hif1α reduced DDP-induced apoptosis in C13* cells. In conclusion, miR-199a may change DDP resistance in ovarian cancer by regulating Hif1α.</description><subject>Apoptosis</subject><subject>BAX protein</subject><subject>Binding sites</subject><subject>Bone surgery</subject><subject>Cancer therapies</subject><subject>Caspase-8</subject><subject>Chemotherapy</subject><subject>Chronic obstructive pulmonary disease</subject><subject>Cisplatin</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Enzymes</subject><subject>Flow cytometry</subject><subject>Hypoxia</subject><subject>Hypoxia-inducible factor 1a</subject><subject>Hypoxia-inducible factors</subject><subject>Immunoglobulins</subject><subject>MicroRNAs</subject><subject>Original Research</subject><subject>Ovarian cancer</subject><subject>Proteins</subject><subject>Reverse transcription</subject><subject>Transfection</subject><subject>Tumor cell lines</subject><subject>Tumor necrosis factor-TNF</subject><subject>Womens health</subject><issn>1178-6930</issn><issn>1178-6930</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkclKA0EQhhtRTIyevMuAF0FGe5teLoIEN4gIGs9NpacTO8wSu2cEH8sX8ZlsMYp6qu3jp6p-hPYJPqGEy9O76fTkgfBCMbaBhoRIlQvN8OavfIB2YlxiLISifBsNqKZSMM2G6Lb29znRGrK6LfsKOhcz6-MqZb7Jgos-dtBYl6WqfYHgocnsZyNks9esg7BwCVxk135O3t920dYcquj21nGEHi8vpuPrfHJ3dTM-n-SWSdrlUhVsVjDOsQSCS60KEIISpUso5tYq4STRpWYgi3SC5I6D0KCVI2A5UTM2Qmdfuqt-VrvSuqYLUJlV8DWEV9OCN38njX8yi_bFFJIRxlQSOFoLhPa5d7EztY_WVRU0ru2jIVphgtOHdEIP_6HLtg9NOs9QymlBsUi_HKHjL8qGNsbg5j_LEGw-bTLJJrO2KdEHv_f_Yb99YR_u8o0b</recordid><startdate>20170101</startdate><enddate>20170101</enddate><creator>Feng, Xue</creator><creator>Liu, Ning</creator><creator>Deng, Suo</creator><creator>Zhang, Dandan</creator><creator>Wang, Kexin</creator><creator>Lu, Meisong</creator><general>Taylor & Francis Ltd</general><general>Dove Medical Press</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M2O</scope><scope>M7P</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></search><sort><creationdate>20170101</creationdate><title>miR-199a modulates cisplatin resistance in ovarian cancer by targeting Hif1α</title><author>Feng, Xue ; Liu, Ning ; Deng, Suo ; Zhang, Dandan ; Wang, Kexin ; Lu, Meisong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-7853b534407a10d985a662189da5fcc86e719d93a7511774e4a69a98e1ac418b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Apoptosis</topic><topic>BAX protein</topic><topic>Binding sites</topic><topic>Bone surgery</topic><topic>Cancer therapies</topic><topic>Caspase-8</topic><topic>Chemotherapy</topic><topic>Chronic obstructive pulmonary disease</topic><topic>Cisplatin</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Enzymes</topic><topic>Flow cytometry</topic><topic>Hypoxia</topic><topic>Hypoxia-inducible factor 1a</topic><topic>Hypoxia-inducible factors</topic><topic>Immunoglobulins</topic><topic>MicroRNAs</topic><topic>Original Research</topic><topic>Ovarian cancer</topic><topic>Proteins</topic><topic>Reverse transcription</topic><topic>Transfection</topic><topic>Tumor cell lines</topic><topic>Tumor necrosis factor-TNF</topic><topic>Womens health</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Feng, Xue</creatorcontrib><creatorcontrib>Liu, Ning</creatorcontrib><creatorcontrib>Deng, Suo</creatorcontrib><creatorcontrib>Zhang, Dandan</creatorcontrib><creatorcontrib>Wang, Kexin</creatorcontrib><creatorcontrib>Lu, Meisong</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech 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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>OncoTargets and therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Feng, Xue</au><au>Liu, Ning</au><au>Deng, Suo</au><au>Zhang, Dandan</au><au>Wang, Kexin</au><au>Lu, Meisong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR-199a modulates cisplatin resistance in ovarian cancer by targeting Hif1α</atitle><jtitle>OncoTargets and therapy</jtitle><addtitle>Onco Targets Ther</addtitle><date>2017-01-01</date><risdate>2017</risdate><volume>10</volume><spage>5899</spage><epage>5906</epage><pages>5899-5906</pages><issn>1178-6930</issn><eissn>1178-6930</eissn><abstract>Resistance to chemotherapy is a primary problem for the effective treatment of ovarian cancer. Recently, increasing evidence has demonstrated that miRNAs modulate many important molecular pathways involved in chemotherapy. Previous studies demonstrated that miR-199a affected ovarian cancer cell resistance to cisplatin (DDP). However, the role of miR-199a and its target genes in determination of ovarian cancer sensitivity to DDP remains unclear. Quantitative reverse transcription polymerase chain reaction was used to detect the expression levels of miR-199a in ovarian cancer tissues and C13* and OV2008 cell lines. After transfection of miR-199a mimic or inhibitor, flow cytometry was used to detect cell apoptosis exposed to DDP. Enzyme-linked immunosorbent assay and Western blot assay were applied to detect tumor necrosis factor-α levels and protein expression levels of Bax, Fas, Fas-associated death domain, and caspase-8. The results indicated that the expression of miR-199a was downregulated and hypoxia-inducible factor 1α (Hif1α) upregulated in the ovarian tumors compared with those in the corresponding normal tissues. Besides, the expression levels of miR-199a were significantly higher in OV2008 cells compared with those in C13* cells. Moreover, suppression of Hif1α reversed the inhibiting function of miR-199a inhibitor on DDP-induced apoptosis in the OV2008 cells. However, overexpression of both miR-199a and Hif1α reduced DDP-induced apoptosis in C13* cells. In conclusion, miR-199a may change DDP resistance in ovarian cancer by regulating Hif1α.</abstract><cop>New Zealand</cop><pub>Taylor & Francis Ltd</pub><pmid>29276393</pmid><doi>10.2147/OTT.S145833</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Apoptosis BAX protein Binding sites Bone surgery Cancer therapies Caspase-8 Chemotherapy Chronic obstructive pulmonary disease Cisplatin Enzyme-linked immunosorbent assay Enzymes Flow cytometry Hypoxia Hypoxia-inducible factor 1a Hypoxia-inducible factors Immunoglobulins MicroRNAs Original Research Ovarian cancer Proteins Reverse transcription Transfection Tumor cell lines Tumor necrosis factor-TNF Womens health |
| title | miR-199a modulates cisplatin resistance in ovarian cancer by targeting Hif1α |
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