MicroRNA-338-3p suppresses ovarian cancer cells growth and metastasis: implication of Wnt/catenin beta and MEK/ERK signaling pathways
Downregulation of microRNA-338-3p (miR-338-3p) was detected in many malignant tumors, which indicated miR-338-3p might serve as a role of antioncogene in those cancers. The present study aimed to explore the roles of miR-338-3p in the growth and metastasis of ovarian cancer cells and elaborate the u...
Gespeichert in:
Veröffentlicht in: | Journal of experimental & clinical cancer research 2019-12, Vol.38 (1), p.494-494 |
---|---|
Hauptverfasser: | , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 494 |
---|---|
container_issue | 1 |
container_start_page | 494 |
container_title | Journal of experimental & clinical cancer research |
container_volume | 38 |
creator | Zhang, Ruitao Shi, Huirong Ren, Fang Feng, Wei Cao, Yuan Li, Gailing Liu, Zheying Ji, Pengcheng Zhang, Minghui |
description | Downregulation of microRNA-338-3p (miR-338-3p) was detected in many malignant tumors, which indicated miR-338-3p might serve as a role of antioncogene in those cancers. The present study aimed to explore the roles of miR-338-3p in the growth and metastasis of ovarian cancer cells and elaborate the underlying possible molecular mechanism.
Multiply biomedical databases query and KEGG pathway enrichment assay were used to infilter possible target genes and downstream pathways regulated by miR-338-3p. Overexpression miR-338-3p lentiviral vectors were transfected into ovarian cancer OVCAR-3 and OVCAR-8 cells, cell proliferation, migration and invasion were analyzed by MTT, colony formation, transwell, Matrigel assay and xenograft mouse model. One 3'-untranslated regions (UTRs) binding target gene of miR-338-3p, MACC1 (MET transcriptional regulator MACC1), and its regulated gene MET and downstream signaling pathway activities were examined by western blot.
Biomedical databases query indicated that miR-338-3p could target MACC1 gene and regulate Met, downstream Wnt/Catenin beta and MEK/ERK pathways. Rescue of miR-338-3p could inhibit the proliferation, migration and invasion of ovarian cancer cells, and suppress the growth and metastasis of xenograft tumor. Restoration of miR-338-3p could attenuate MACC1 and Met overexpression induced growth, epithelial to mesenchymal transition (EMT) and activities of Wnt/Catenin beta and MEK/ERK signaling in vitro and in vivo.
The present data indicated that restoration of miR-338-3p could suppress the growth and metastasis of ovarian cancer cells, which might due to the inhibition of proliferation and EMT induced by MACC1, Met and its downstream Wnt/Catenin beta and MEK/ERK signaling pathways. |
doi_str_mv | 10.1186/s13046-019-1494-3 |
format | Article |
fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6916056</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A610311514</galeid><sourcerecordid>A610311514</sourcerecordid><originalsourceid>FETCH-LOGICAL-g435t-fc95f1ade59715423cfb678dd506a1b774f6d7eed95443acaba383fa8ab0c6703</originalsourceid><addsrcrecordid>eNptkm9r1TAUxoso7jr9AL6RgCC-6W7S_Gt8IVzGnco2haH4spymaZvRJjVpN_YB_N7LnVN3RU7gcJLfeQ55kix7SfARIaVYR0IxEzkmKidMsZw-ylZEcpErJcTjbIWpKnKFZXmQPYvxEmNBFFFPswNKSlYoTlfZz3Org7_4vMkpLXM6obhMUzAxmoj8FQQLDmlw2gSkzTBE1AV_PfcIXINGM0NMy8Z3yI7TYDXM1jvkW_TdzetUGWcdqhN2x59vT9fbi1MUbedgsK5DE8z9NdzE59mTFoZoXtznw-zbyfbr8cf87MuHT8ebs7xjlM95qxVvCTSGK0k4K6huayHLpuFYAKmlZK1opDGN4oxR0FADLWkLJdRYC4npYfb-l-601KNptHFzgKGagh0h3FQebLV_4mxfdf6qEooIzEUSeHsvEPyPxcS5Gm3cGQPO-CVWBS2kYgWhRUJf_4Ne-iWki99RJRVcKvGX6mAwlXWtT3P1TrTaCIIpIZywRB39h0rRmNFq70xr0_5ew5sHDb2BYe6jH5bd-8R98NVDR_5Y8fuH0Ft5Er0F</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2328365796</pqid></control><display><type>article</type><title>MicroRNA-338-3p suppresses ovarian cancer cells growth and metastasis: implication of Wnt/catenin beta and MEK/ERK signaling pathways</title><source>MEDLINE</source><source>SpringerLink_现刊</source><source>DOAJ Directory of Open Access Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>PubMed Central Open Access</source><source>Springer Nature OA Free Journals</source><creator>Zhang, Ruitao ; Shi, Huirong ; Ren, Fang ; Feng, Wei ; Cao, Yuan ; Li, Gailing ; Liu, Zheying ; Ji, Pengcheng ; Zhang, Minghui</creator><creatorcontrib>Zhang, Ruitao ; Shi, Huirong ; Ren, Fang ; Feng, Wei ; Cao, Yuan ; Li, Gailing ; Liu, Zheying ; Ji, Pengcheng ; Zhang, Minghui</creatorcontrib><description>Downregulation of microRNA-338-3p (miR-338-3p) was detected in many malignant tumors, which indicated miR-338-3p might serve as a role of antioncogene in those cancers. The present study aimed to explore the roles of miR-338-3p in the growth and metastasis of ovarian cancer cells and elaborate the underlying possible molecular mechanism.
Multiply biomedical databases query and KEGG pathway enrichment assay were used to infilter possible target genes and downstream pathways regulated by miR-338-3p. Overexpression miR-338-3p lentiviral vectors were transfected into ovarian cancer OVCAR-3 and OVCAR-8 cells, cell proliferation, migration and invasion were analyzed by MTT, colony formation, transwell, Matrigel assay and xenograft mouse model. One 3'-untranslated regions (UTRs) binding target gene of miR-338-3p, MACC1 (MET transcriptional regulator MACC1), and its regulated gene MET and downstream signaling pathway activities were examined by western blot.
Biomedical databases query indicated that miR-338-3p could target MACC1 gene and regulate Met, downstream Wnt/Catenin beta and MEK/ERK pathways. Rescue of miR-338-3p could inhibit the proliferation, migration and invasion of ovarian cancer cells, and suppress the growth and metastasis of xenograft tumor. Restoration of miR-338-3p could attenuate MACC1 and Met overexpression induced growth, epithelial to mesenchymal transition (EMT) and activities of Wnt/Catenin beta and MEK/ERK signaling in vitro and in vivo.
The present data indicated that restoration of miR-338-3p could suppress the growth and metastasis of ovarian cancer cells, which might due to the inhibition of proliferation and EMT induced by MACC1, Met and its downstream Wnt/Catenin beta and MEK/ERK signaling pathways.</description><identifier>ISSN: 0392-9078</identifier><identifier>ISSN: 1756-9966</identifier><identifier>EISSN: 1756-9966</identifier><identifier>DOI: 10.1186/s13046-019-1494-3</identifier><identifier>PMID: 31842953</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Analysis ; Animals ; Binding sites ; Biotechnology ; Cancer cells ; Cancer metastasis ; Cell adhesion & migration ; Cell culture ; Cell cycle ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Down-Regulation ; Epithelial-Mesenchymal Transition ; Female ; Gene Expression Regulation, Neoplastic ; Genes ; Growth ; Humans ; Manufacturers ; MAP Kinase Signaling System ; Metastasis ; Mice ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; Neoplasm Metastasis ; Neoplasm Transplantation ; Ovarian cancer ; Ovarian Neoplasms - genetics ; Ovarian Neoplasms - metabolism ; Ovarian Neoplasms - pathology ; Proteins ; Proto-Oncogene Proteins c-met - genetics ; Proto-Oncogene Proteins c-met - metabolism ; Software ; Stem cells ; Trans-Activators - genetics ; Trans-Activators - metabolism ; Transcription (Genetics) ; Tumors ; Variance analysis ; Wnt Signaling Pathway</subject><ispartof>Journal of experimental & clinical cancer research, 2019-12, Vol.38 (1), p.494-494</ispartof><rights>COPYRIGHT 2019 BioMed Central Ltd.</rights><rights>2019. 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). 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0000-0001-5610-9433</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/PMC6916056/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6916056/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31842953$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Ruitao</creatorcontrib><creatorcontrib>Shi, Huirong</creatorcontrib><creatorcontrib>Ren, Fang</creatorcontrib><creatorcontrib>Feng, Wei</creatorcontrib><creatorcontrib>Cao, Yuan</creatorcontrib><creatorcontrib>Li, Gailing</creatorcontrib><creatorcontrib>Liu, Zheying</creatorcontrib><creatorcontrib>Ji, Pengcheng</creatorcontrib><creatorcontrib>Zhang, Minghui</creatorcontrib><title>MicroRNA-338-3p suppresses ovarian cancer cells growth and metastasis: implication of Wnt/catenin beta and MEK/ERK signaling pathways</title><title>Journal of experimental & clinical cancer research</title><addtitle>J Exp Clin Cancer Res</addtitle><description>Downregulation of microRNA-338-3p (miR-338-3p) was detected in many malignant tumors, which indicated miR-338-3p might serve as a role of antioncogene in those cancers. The present study aimed to explore the roles of miR-338-3p in the growth and metastasis of ovarian cancer cells and elaborate the underlying possible molecular mechanism.
Multiply biomedical databases query and KEGG pathway enrichment assay were used to infilter possible target genes and downstream pathways regulated by miR-338-3p. Overexpression miR-338-3p lentiviral vectors were transfected into ovarian cancer OVCAR-3 and OVCAR-8 cells, cell proliferation, migration and invasion were analyzed by MTT, colony formation, transwell, Matrigel assay and xenograft mouse model. One 3'-untranslated regions (UTRs) binding target gene of miR-338-3p, MACC1 (MET transcriptional regulator MACC1), and its regulated gene MET and downstream signaling pathway activities were examined by western blot.
Biomedical databases query indicated that miR-338-3p could target MACC1 gene and regulate Met, downstream Wnt/Catenin beta and MEK/ERK pathways. Rescue of miR-338-3p could inhibit the proliferation, migration and invasion of ovarian cancer cells, and suppress the growth and metastasis of xenograft tumor. Restoration of miR-338-3p could attenuate MACC1 and Met overexpression induced growth, epithelial to mesenchymal transition (EMT) and activities of Wnt/Catenin beta and MEK/ERK signaling in vitro and in vivo.
The present data indicated that restoration of miR-338-3p could suppress the growth and metastasis of ovarian cancer cells, which might due to the inhibition of proliferation and EMT induced by MACC1, Met and its downstream Wnt/Catenin beta and MEK/ERK signaling pathways.</description><subject>Analysis</subject><subject>Animals</subject><subject>Binding sites</subject><subject>Biotechnology</subject><subject>Cancer cells</subject><subject>Cancer metastasis</subject><subject>Cell adhesion & migration</subject><subject>Cell culture</subject><subject>Cell cycle</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Down-Regulation</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes</subject><subject>Growth</subject><subject>Humans</subject><subject>Manufacturers</subject><subject>MAP Kinase Signaling System</subject><subject>Metastasis</subject><subject>Mice</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>Neoplasm Metastasis</subject><subject>Neoplasm Transplantation</subject><subject>Ovarian cancer</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Ovarian Neoplasms - metabolism</subject><subject>Ovarian Neoplasms - pathology</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-met - genetics</subject><subject>Proto-Oncogene Proteins c-met - metabolism</subject><subject>Software</subject><subject>Stem cells</subject><subject>Trans-Activators - genetics</subject><subject>Trans-Activators - metabolism</subject><subject>Transcription (Genetics)</subject><subject>Tumors</subject><subject>Variance analysis</subject><subject>Wnt Signaling Pathway</subject><issn>0392-9078</issn><issn>1756-9966</issn><issn>1756-9966</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNptkm9r1TAUxoso7jr9AL6RgCC-6W7S_Gt8IVzGnco2haH4spymaZvRJjVpN_YB_N7LnVN3RU7gcJLfeQ55kix7SfARIaVYR0IxEzkmKidMsZw-ylZEcpErJcTjbIWpKnKFZXmQPYvxEmNBFFFPswNKSlYoTlfZz3Org7_4vMkpLXM6obhMUzAxmoj8FQQLDmlw2gSkzTBE1AV_PfcIXINGM0NMy8Z3yI7TYDXM1jvkW_TdzetUGWcdqhN2x59vT9fbi1MUbedgsK5DE8z9NdzE59mTFoZoXtznw-zbyfbr8cf87MuHT8ebs7xjlM95qxVvCTSGK0k4K6huayHLpuFYAKmlZK1opDGN4oxR0FADLWkLJdRYC4npYfb-l-601KNptHFzgKGagh0h3FQebLV_4mxfdf6qEooIzEUSeHsvEPyPxcS5Gm3cGQPO-CVWBS2kYgWhRUJf_4Ne-iWki99RJRVcKvGX6mAwlXWtT3P1TrTaCIIpIZywRB39h0rRmNFq70xr0_5ew5sHDb2BYe6jH5bd-8R98NVDR_5Y8fuH0Ft5Er0F</recordid><startdate>20191216</startdate><enddate>20191216</enddate><creator>Zhang, Ruitao</creator><creator>Shi, Huirong</creator><creator>Ren, Fang</creator><creator>Feng, Wei</creator><creator>Cao, Yuan</creator><creator>Li, Gailing</creator><creator>Liu, Zheying</creator><creator>Ji, Pengcheng</creator><creator>Zhang, Minghui</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</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>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-5610-9433</orcidid></search><sort><creationdate>20191216</creationdate><title>MicroRNA-338-3p suppresses ovarian cancer cells growth and metastasis: implication of Wnt/catenin beta and MEK/ERK signaling pathways</title><author>Zhang, Ruitao ; Shi, Huirong ; Ren, Fang ; Feng, Wei ; Cao, Yuan ; Li, Gailing ; Liu, Zheying ; Ji, Pengcheng ; Zhang, Minghui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-g435t-fc95f1ade59715423cfb678dd506a1b774f6d7eed95443acaba383fa8ab0c6703</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>Binding sites</topic><topic>Biotechnology</topic><topic>Cancer cells</topic><topic>Cancer metastasis</topic><topic>Cell adhesion & migration</topic><topic>Cell culture</topic><topic>Cell cycle</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Down-Regulation</topic><topic>Epithelial-Mesenchymal Transition</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes</topic><topic>Growth</topic><topic>Humans</topic><topic>Manufacturers</topic><topic>MAP Kinase Signaling System</topic><topic>Metastasis</topic><topic>Mice</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>Neoplasm Metastasis</topic><topic>Neoplasm Transplantation</topic><topic>Ovarian cancer</topic><topic>Ovarian Neoplasms - genetics</topic><topic>Ovarian Neoplasms - metabolism</topic><topic>Ovarian Neoplasms - pathology</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-met - genetics</topic><topic>Proto-Oncogene Proteins c-met - metabolism</topic><topic>Software</topic><topic>Stem cells</topic><topic>Trans-Activators - genetics</topic><topic>Trans-Activators - metabolism</topic><topic>Transcription (Genetics)</topic><topic>Tumors</topic><topic>Variance analysis</topic><topic>Wnt Signaling Pathway</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Ruitao</creatorcontrib><creatorcontrib>Shi, Huirong</creatorcontrib><creatorcontrib>Ren, Fang</creatorcontrib><creatorcontrib>Feng, Wei</creatorcontrib><creatorcontrib>Cao, Yuan</creatorcontrib><creatorcontrib>Li, Gailing</creatorcontrib><creatorcontrib>Liu, Zheying</creatorcontrib><creatorcontrib>Ji, Pengcheng</creatorcontrib><creatorcontrib>Zhang, Minghui</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of experimental & clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Ruitao</au><au>Shi, Huirong</au><au>Ren, Fang</au><au>Feng, Wei</au><au>Cao, Yuan</au><au>Li, Gailing</au><au>Liu, Zheying</au><au>Ji, Pengcheng</au><au>Zhang, Minghui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MicroRNA-338-3p suppresses ovarian cancer cells growth and metastasis: implication of Wnt/catenin beta and MEK/ERK signaling pathways</atitle><jtitle>Journal of experimental & clinical cancer research</jtitle><addtitle>J Exp Clin Cancer Res</addtitle><date>2019-12-16</date><risdate>2019</risdate><volume>38</volume><issue>1</issue><spage>494</spage><epage>494</epage><pages>494-494</pages><issn>0392-9078</issn><issn>1756-9966</issn><eissn>1756-9966</eissn><abstract>Downregulation of microRNA-338-3p (miR-338-3p) was detected in many malignant tumors, which indicated miR-338-3p might serve as a role of antioncogene in those cancers. The present study aimed to explore the roles of miR-338-3p in the growth and metastasis of ovarian cancer cells and elaborate the underlying possible molecular mechanism.
Multiply biomedical databases query and KEGG pathway enrichment assay were used to infilter possible target genes and downstream pathways regulated by miR-338-3p. Overexpression miR-338-3p lentiviral vectors were transfected into ovarian cancer OVCAR-3 and OVCAR-8 cells, cell proliferation, migration and invasion were analyzed by MTT, colony formation, transwell, Matrigel assay and xenograft mouse model. One 3'-untranslated regions (UTRs) binding target gene of miR-338-3p, MACC1 (MET transcriptional regulator MACC1), and its regulated gene MET and downstream signaling pathway activities were examined by western blot.
Biomedical databases query indicated that miR-338-3p could target MACC1 gene and regulate Met, downstream Wnt/Catenin beta and MEK/ERK pathways. Rescue of miR-338-3p could inhibit the proliferation, migration and invasion of ovarian cancer cells, and suppress the growth and metastasis of xenograft tumor. Restoration of miR-338-3p could attenuate MACC1 and Met overexpression induced growth, epithelial to mesenchymal transition (EMT) and activities of Wnt/Catenin beta and MEK/ERK signaling in vitro and in vivo.
The present data indicated that restoration of miR-338-3p could suppress the growth and metastasis of ovarian cancer cells, which might due to the inhibition of proliferation and EMT induced by MACC1, Met and its downstream Wnt/Catenin beta and MEK/ERK signaling pathways.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>31842953</pmid><doi>10.1186/s13046-019-1494-3</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0001-5610-9433</orcidid><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0392-9078 |
ispartof | Journal of experimental & clinical cancer research, 2019-12, Vol.38 (1), p.494-494 |
issn | 0392-9078 1756-9966 1756-9966 |
language | eng |
recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6916056 |
source | MEDLINE; SpringerLink_现刊; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; PubMed Central Open Access; Springer Nature OA Free Journals |
subjects | Analysis Animals Binding sites Biotechnology Cancer cells Cancer metastasis Cell adhesion & migration Cell culture Cell cycle Cell Line, Tumor Cell Movement Cell Proliferation Down-Regulation Epithelial-Mesenchymal Transition Female Gene Expression Regulation, Neoplastic Genes Growth Humans Manufacturers MAP Kinase Signaling System Metastasis Mice MicroRNA MicroRNAs MicroRNAs - genetics Neoplasm Metastasis Neoplasm Transplantation Ovarian cancer Ovarian Neoplasms - genetics Ovarian Neoplasms - metabolism Ovarian Neoplasms - pathology Proteins Proto-Oncogene Proteins c-met - genetics Proto-Oncogene Proteins c-met - metabolism Software Stem cells Trans-Activators - genetics Trans-Activators - metabolism Transcription (Genetics) Tumors Variance analysis Wnt Signaling Pathway |
title | MicroRNA-338-3p suppresses ovarian cancer cells growth and metastasis: implication of Wnt/catenin beta and MEK/ERK signaling pathways |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-07T14%3A23%3A43IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=MicroRNA-338-3p%20suppresses%20ovarian%20cancer%20cells%20growth%20and%20metastasis:%20implication%20of%20Wnt/catenin%20beta%20and%20MEK/ERK%20signaling%20pathways&rft.jtitle=Journal%20of%20experimental%20&%20clinical%20cancer%20research&rft.au=Zhang,%20Ruitao&rft.date=2019-12-16&rft.volume=38&rft.issue=1&rft.spage=494&rft.epage=494&rft.pages=494-494&rft.issn=0392-9078&rft.eissn=1756-9966&rft_id=info:doi/10.1186/s13046-019-1494-3&rft_dat=%3Cgale_pubme%3EA610311514%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2328365796&rft_id=info:pmid/31842953&rft_galeid=A610311514&rfr_iscdi=true |