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...

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Veröffentlicht in:Journal of experimental & clinical cancer research 2019-12, Vol.38 (1), p.494-494
Hauptverfasser: Zhang, Ruitao, Shi, Huirong, Ren, Fang, Feng, Wei, Cao, Yuan, Li, Gailing, Liu, Zheying, Ji, Pengcheng, Zhang, Minghui
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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.
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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 &amp; 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 &amp; 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”). 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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. 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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 &amp; 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>
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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
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