Overexpression of Long Noncoding RNA H19 Downregulates miR-140-5p and Activates PI3K/AKT Signaling Pathway to Promote Invasion, Migration and Epithelial-Mesenchymal Transition of Ovarian Cancer Cells
Objective. The abnormal expression of LncRNA H19 and miR-140-5p has been linked to ovarian cancer (OC). Whether H19 directly regulates miR-140-5p in ovarian cancer cells has been unclear. In this study, we deeply explored the relationship between H19 and miR-140-5p in ovarian cancer and the mechanis...
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| description | Objective. The abnormal expression of LncRNA H19 and miR-140-5p has been linked to ovarian cancer (OC). Whether H19 directly regulates miR-140-5p in ovarian cancer cells has been unclear. In this study, we deeply explored the relationship between H19 and miR-140-5p in ovarian cancer and the mechanism of action in regulating OC progression. Methods. A total of 66 patients with OC admitted to the hospital from June 2017 to June 2019 were selected as the research group (RG), and meanwhile, 60 cases of healthy subjects were selected as the control group (CG). In addition, OC cells and normal ovarian epithelial cells were used to detect H19 and miR-140-5p expression levels and to analyze the effect of H19 on OC cells. The activation of the PI3K/AKT pathway and downstream proteins were analyzed by western blot. Results. H19 was highly expressed while miR-140-5p was lowly expressed in OC patients and cell lines (P |
| doi_str_mv | 10.1155/2021/6619730 |
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| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8238588</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A696883945</galeid><sourcerecordid>A696883945</sourcerecordid><originalsourceid>FETCH-LOGICAL-c476t-3c55c8a2b59575b3c98b3814012e162725b2634a9edd7906baf124f1eff66c293</originalsourceid><addsrcrecordid>eNp9kkFv0zAUxyMEYtPYjTOyxJGFxnbsxhekqgxWrVurUc7Wi-OknhK72G7LPiFfi4SWAhd8sa330-89W_8keY2z9xgzNiIZwSPOsRjT7FlyTijOU45z_Px0pvQsuQzhMetXgXkm-MvkjOaE9dfiPPmx2Gmvv2-8DsE4i1yN5s426N5Z5SrTnx7uJ-gGC_TR7a3XzbaFqAPqzEOK8yxlGwS2QhMVze5XYTmjt6PJ7Qp9MY2FdjAsIa738ISiQ0vvOhc1mtkdDP2u0J1pPMSh9eC53pi41q2BNr3TQVu1fuqgRSsPNph4HHCxA2_AoilYpT2a6rYNr5IXNbRBXx73i-Trp-vV9CadLz7PppN5qvIxjylVjKkCSMkEG7OSKlGUtOgfgonGnIwJKwmnOQhdVWOR8RJqTPIa67rmXBFBL5IPB-9mW3a6UtpGD63ceNOBf5IOjPy3Ys1aNm4nC0ILVhS94O1R4N23rQ5RPrqt738qSMLygog8y9gfqoFWS2Nr18tUZ4KSEy547xH5QF0dKOVdCF7XpzlwJod8yCEf8piPHn_z9-wn-HcaeuDdAVgbW8He_F_3E0tFwpQ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2548294005</pqid></control><display><type>article</type><title>Overexpression of Long Noncoding RNA H19 Downregulates miR-140-5p and Activates PI3K/AKT Signaling Pathway to Promote Invasion, Migration and Epithelial-Mesenchymal Transition of Ovarian Cancer Cells</title><source>Open Access: PubMed Central</source><source>MEDLINE</source><source>PubMed Central Open Access</source><source>Wiley Online Library Open Access</source><source>Alma/SFX Local Collection</source><creator>Xu, Hao ; Ding, Yuan ; Yang, Xiangying</creator><contributor>Yi, Ming ; Ming Yi</contributor><creatorcontrib>Xu, Hao ; Ding, Yuan ; Yang, Xiangying ; Yi, Ming ; Ming Yi</creatorcontrib><description>Objective. The abnormal expression of LncRNA H19 and miR-140-5p has been linked to ovarian cancer (OC). Whether H19 directly regulates miR-140-5p in ovarian cancer cells has been unclear. In this study, we deeply explored the relationship between H19 and miR-140-5p in ovarian cancer and the mechanism of action in regulating OC progression. Methods. A total of 66 patients with OC admitted to the hospital from June 2017 to June 2019 were selected as the research group (RG), and meanwhile, 60 cases of healthy subjects were selected as the control group (CG). In addition, OC cells and normal ovarian epithelial cells were used to detect H19 and miR-140-5p expression levels and to analyze the effect of H19 on OC cells. The activation of the PI3K/AKT pathway and downstream proteins were analyzed by western blot. Results. H19 was highly expressed while miR-140-5p was lowly expressed in OC patients and cell lines (P<0.050). The proliferation, invasion, migration ability, and epithelial-mesenchymal transition (EMT) of OC cells were reduced after inhibiting H19 expression, and the apoptosis rate was increased. Transfection of cells with miR-140-5p mimics brought opposite effects. Online prediction and dual-luciferase reporter (DLR) confirmed that H19 directly binds miR-140-5p. Western blot assay indicated overexpression activated the PI3K/AKT signaling pathway in OC cells. Moreover, overexpression promoted tumor growth in nude mice and was suppressed by PI3K inhibitor. Conclusion. LncRNA H19 downregulation of miR-140-5p to activate the PI3K/AKT signaling pathway and promote the proliferation, invasion, migration and EMT of OC.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2021/6619730</identifier><identifier>PMID: 34250088</identifier><language>eng</language><publisher>United States: Hindawi</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Animals ; Apoptosis ; Base Sequence ; Biomedical research ; Cancer ; Carcinogenesis - genetics ; Carcinogenesis - pathology ; Cell activation ; Cell differentiation ; Cell Line, Tumor ; Cell Movement - genetics ; Cell proliferation ; Cellular signal transduction ; Development and progression ; Down-Regulation - genetics ; Epithelial cells ; Epithelial-Mesenchymal Transition - genetics ; Epithelium ; Experiments ; Female ; Flow cytometry ; Gene Expression Regulation, Neoplastic ; Genetic aspects ; Health aspects ; Humans ; Medical prognosis ; Mesenchyme ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Neoplasm Invasiveness ; Oncology, Experimental ; Ovarian cancer ; Ovarian Neoplasms - genetics ; Ovarian Neoplasms - pathology ; Phosphatidylinositol 3-Kinases - metabolism ; Protein kinases ; Proteins ; Proto-Oncogene Proteins c-akt - metabolism ; RNA ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Signal Transduction ; Signaling ; Stem cells ; Transfection ; Tumors</subject><ispartof>BioMed research international, 2021, Vol.2021 (1), p.6619730</ispartof><rights>Copyright © 2021 Hao Xu et al.</rights><rights>COPYRIGHT 2021 John Wiley & Sons, Inc.</rights><rights>Copyright © 2021 Hao Xu et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2021 Hao Xu et al. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c476t-3c55c8a2b59575b3c98b3814012e162725b2634a9edd7906baf124f1eff66c293</citedby><cites>FETCH-LOGICAL-c476t-3c55c8a2b59575b3c98b3814012e162725b2634a9edd7906baf124f1eff66c293</cites><orcidid>0000-0002-6393-2230</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/PMC8238588/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8238588/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4009,27902,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34250088$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Yi, Ming</contributor><contributor>Ming Yi</contributor><creatorcontrib>Xu, Hao</creatorcontrib><creatorcontrib>Ding, Yuan</creatorcontrib><creatorcontrib>Yang, Xiangying</creatorcontrib><title>Overexpression of Long Noncoding RNA H19 Downregulates miR-140-5p and Activates PI3K/AKT Signaling Pathway to Promote Invasion, Migration and Epithelial-Mesenchymal Transition of Ovarian Cancer Cells</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>Objective. The abnormal expression of LncRNA H19 and miR-140-5p has been linked to ovarian cancer (OC). Whether H19 directly regulates miR-140-5p in ovarian cancer cells has been unclear. In this study, we deeply explored the relationship between H19 and miR-140-5p in ovarian cancer and the mechanism of action in regulating OC progression. Methods. A total of 66 patients with OC admitted to the hospital from June 2017 to June 2019 were selected as the research group (RG), and meanwhile, 60 cases of healthy subjects were selected as the control group (CG). In addition, OC cells and normal ovarian epithelial cells were used to detect H19 and miR-140-5p expression levels and to analyze the effect of H19 on OC cells. The activation of the PI3K/AKT pathway and downstream proteins were analyzed by western blot. Results. H19 was highly expressed while miR-140-5p was lowly expressed in OC patients and cell lines (P<0.050). The proliferation, invasion, migration ability, and epithelial-mesenchymal transition (EMT) of OC cells were reduced after inhibiting H19 expression, and the apoptosis rate was increased. Transfection of cells with miR-140-5p mimics brought opposite effects. Online prediction and dual-luciferase reporter (DLR) confirmed that H19 directly binds miR-140-5p. Western blot assay indicated overexpression activated the PI3K/AKT signaling pathway in OC cells. Moreover, overexpression promoted tumor growth in nude mice and was suppressed by PI3K inhibitor. Conclusion. LncRNA H19 downregulation of miR-140-5p to activate the PI3K/AKT signaling pathway and promote the proliferation, invasion, migration and EMT of OC.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Base Sequence</subject><subject>Biomedical research</subject><subject>Cancer</subject><subject>Carcinogenesis - genetics</subject><subject>Carcinogenesis - pathology</subject><subject>Cell activation</subject><subject>Cell differentiation</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Cell proliferation</subject><subject>Cellular signal transduction</subject><subject>Development and progression</subject><subject>Down-Regulation - genetics</subject><subject>Epithelial cells</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Epithelium</subject><subject>Experiments</subject><subject>Female</subject><subject>Flow cytometry</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Medical prognosis</subject><subject>Mesenchyme</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Neoplasm Invasiveness</subject><subject>Oncology, Experimental</subject><subject>Ovarian cancer</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Ovarian Neoplasms - pathology</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Protein kinases</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>RNA</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Signal Transduction</subject><subject>Signaling</subject><subject>Stem cells</subject><subject>Transfection</subject><subject>Tumors</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kkFv0zAUxyMEYtPYjTOyxJGFxnbsxhekqgxWrVurUc7Wi-OknhK72G7LPiFfi4SWAhd8sa330-89W_8keY2z9xgzNiIZwSPOsRjT7FlyTijOU45z_Px0pvQsuQzhMetXgXkm-MvkjOaE9dfiPPmx2Gmvv2-8DsE4i1yN5s426N5Z5SrTnx7uJ-gGC_TR7a3XzbaFqAPqzEOK8yxlGwS2QhMVze5XYTmjt6PJ7Qp9MY2FdjAsIa738ISiQ0vvOhc1mtkdDP2u0J1pPMSh9eC53pi41q2BNr3TQVu1fuqgRSsPNph4HHCxA2_AoilYpT2a6rYNr5IXNbRBXx73i-Trp-vV9CadLz7PppN5qvIxjylVjKkCSMkEG7OSKlGUtOgfgonGnIwJKwmnOQhdVWOR8RJqTPIa67rmXBFBL5IPB-9mW3a6UtpGD63ceNOBf5IOjPy3Ys1aNm4nC0ILVhS94O1R4N23rQ5RPrqt738qSMLygog8y9gfqoFWS2Nr18tUZ4KSEy547xH5QF0dKOVdCF7XpzlwJod8yCEf8piPHn_z9-wn-HcaeuDdAVgbW8He_F_3E0tFwpQ</recordid><startdate>2021</startdate><enddate>2021</enddate><creator>Xu, Hao</creator><creator>Ding, Yuan</creator><creator>Yang, Xiangying</creator><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><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>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</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>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-6393-2230</orcidid></search><sort><creationdate>2021</creationdate><title>Overexpression of Long Noncoding RNA H19 Downregulates miR-140-5p and Activates PI3K/AKT Signaling Pathway to Promote Invasion, Migration and Epithelial-Mesenchymal Transition of Ovarian Cancer Cells</title><author>Xu, Hao ; Ding, Yuan ; Yang, Xiangying</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c476t-3c55c8a2b59575b3c98b3814012e162725b2634a9edd7906baf124f1eff66c293</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Base Sequence</topic><topic>Biomedical research</topic><topic>Cancer</topic><topic>Carcinogenesis - genetics</topic><topic>Carcinogenesis - pathology</topic><topic>Cell activation</topic><topic>Cell differentiation</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - genetics</topic><topic>Cell proliferation</topic><topic>Cellular signal transduction</topic><topic>Development and progression</topic><topic>Down-Regulation - genetics</topic><topic>Epithelial cells</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Epithelium</topic><topic>Experiments</topic><topic>Female</topic><topic>Flow cytometry</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Medical prognosis</topic><topic>Mesenchyme</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Neoplasm Invasiveness</topic><topic>Oncology, Experimental</topic><topic>Ovarian cancer</topic><topic>Ovarian Neoplasms - genetics</topic><topic>Ovarian Neoplasms - pathology</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Protein kinases</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>RNA</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Signal Transduction</topic><topic>Signaling</topic><topic>Stem cells</topic><topic>Transfection</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xu, Hao</creatorcontrib><creatorcontrib>Ding, Yuan</creatorcontrib><creatorcontrib>Yang, Xiangying</creatorcontrib><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Middle East & Africa Database</collection><collection>ProQuest Central</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>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>ProQuest Biological Science Journals</collection><collection>ProQuest advanced technologies & aerospace journals</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</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>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xu, Hao</au><au>Ding, Yuan</au><au>Yang, Xiangying</au><au>Yi, Ming</au><au>Ming Yi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overexpression of Long Noncoding RNA H19 Downregulates miR-140-5p and Activates PI3K/AKT Signaling Pathway to Promote Invasion, Migration and Epithelial-Mesenchymal Transition of Ovarian Cancer Cells</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2021</date><risdate>2021</risdate><volume>2021</volume><issue>1</issue><spage>6619730</spage><pages>6619730-</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>Objective. The abnormal expression of LncRNA H19 and miR-140-5p has been linked to ovarian cancer (OC). Whether H19 directly regulates miR-140-5p in ovarian cancer cells has been unclear. In this study, we deeply explored the relationship between H19 and miR-140-5p in ovarian cancer and the mechanism of action in regulating OC progression. Methods. A total of 66 patients with OC admitted to the hospital from June 2017 to June 2019 were selected as the research group (RG), and meanwhile, 60 cases of healthy subjects were selected as the control group (CG). In addition, OC cells and normal ovarian epithelial cells were used to detect H19 and miR-140-5p expression levels and to analyze the effect of H19 on OC cells. The activation of the PI3K/AKT pathway and downstream proteins were analyzed by western blot. Results. H19 was highly expressed while miR-140-5p was lowly expressed in OC patients and cell lines (P<0.050). The proliferation, invasion, migration ability, and epithelial-mesenchymal transition (EMT) of OC cells were reduced after inhibiting H19 expression, and the apoptosis rate was increased. Transfection of cells with miR-140-5p mimics brought opposite effects. Online prediction and dual-luciferase reporter (DLR) confirmed that H19 directly binds miR-140-5p. Western blot assay indicated overexpression activated the PI3K/AKT signaling pathway in OC cells. Moreover, overexpression promoted tumor growth in nude mice and was suppressed by PI3K inhibitor. Conclusion. LncRNA H19 downregulation of miR-140-5p to activate the PI3K/AKT signaling pathway and promote the proliferation, invasion, migration and EMT of OC.</abstract><cop>United States</cop><pub>Hindawi</pub><pmid>34250088</pmid><doi>10.1155/2021/6619730</doi><orcidid>https://orcid.org/0000-0002-6393-2230</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Animals Apoptosis Base Sequence Biomedical research Cancer Carcinogenesis - genetics Carcinogenesis - pathology Cell activation Cell differentiation Cell Line, Tumor Cell Movement - genetics Cell proliferation Cellular signal transduction Development and progression Down-Regulation - genetics Epithelial cells Epithelial-Mesenchymal Transition - genetics Epithelium Experiments Female Flow cytometry Gene Expression Regulation, Neoplastic Genetic aspects Health aspects Humans Medical prognosis Mesenchyme Mice Mice, Inbred BALB C Mice, Nude MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism Neoplasm Invasiveness Oncology, Experimental Ovarian cancer Ovarian Neoplasms - genetics Ovarian Neoplasms - pathology Phosphatidylinositol 3-Kinases - metabolism Protein kinases Proteins Proto-Oncogene Proteins c-akt - metabolism RNA RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Signal Transduction Signaling Stem cells Transfection Tumors |
| title | Overexpression of Long Noncoding RNA H19 Downregulates miR-140-5p and Activates PI3K/AKT Signaling Pathway to Promote Invasion, Migration and Epithelial-Mesenchymal Transition of Ovarian Cancer Cells |
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