schliessen

Filtern

 

Bibliotheken

miR‑215 promotes epithelial to mesenchymal transition and proliferation by regulating LEFTY2 in endometrial cancer

Endometrial cancer (EC) is the most common gynecological tumor in developed countries with an increasing incidence. Left‑right determination factor 2 (LEFTY2), a suppressor of cell proliferation and tumor growth, is a negative regulator of EC progression. The roles of LEFTY2 are emerging; however, t... Full description

Journal Title: International journal of molecular medicine September 2018, Vol.42(3), pp.1229-1236
Main Author: Gao, Xiaoxu
Other Authors: Cai, Yan , An, Ruifang
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1791-244X ; PMID: 29845221 Version:1 ; DOI: 10.3892/ijmm.2018.3703
Link: http://pubmed.gov/29845221
Zum Text:
SendSend as email Add to Book BagAdd to Book Bag
Staff View
recordid: medline29845221
title: miR‑215 promotes epithelial to mesenchymal transition and proliferation by regulating LEFTY2 in endometrial cancer
format: Article
creator:
  • Gao, Xiaoxu
  • Cai, Yan
  • An, Ruifang
subjects:
  • Endometrial Neoplasms -- Metabolism
  • Epithelial-Mesenchymal Transition -- Physiology
  • Gene Expression Regulation, Neoplastic -- Physiology
  • Left-Right Determination Factors -- Metabolism
  • Micrornas -- Metabolism
ispartof: International journal of molecular medicine, September 2018, Vol.42(3), pp.1229-1236
description: Endometrial cancer (EC) is the most common gynecological tumor in developed countries with an increasing incidence. Left‑right determination factor 2 (LEFTY2), a suppressor of cell proliferation and tumor growth, is a negative regulator of EC progression. The roles of LEFTY2 are emerging; however, the regulatory mechanisms of its expression have not been well understood. MicroRNA (miR)‑215 as an oncogene serves an important role in tumorigenesis by regulating target genes. In the present study, it was demonstrated that overexpression of miR‑215 promoted epithelial to mesenchymal transition (EMT), colony formation and DNA synthesis in EC HEC‑1A cells and its expression was upregulated in EC tissues. Using online miR target prediction software, it was revealed that LEFTY2 is predicted as a target of miR‑215. Using western blot analysis and immunofluorescence assays, it was demonstrated that overexpression of miR‑215 markedly downregulated LEFTY2 protein expression levels in HEC‑1A cells and LEFTY2 protein expression was downregulated in EC tissues, which was inversely correlated with miR‑215 expression. Furthermore, the present study indicated that overexpression of LEFTY2 protein promoted mesenchymal to epithelial transition and sensitized HEC‑1A cells to cisplatin treatment. In addition, it was revealed that the overexpression of LEFTY2 inhibited colony formation and DNA synthesis in HEC‑1A cells. Thus, miR‑215 may promote EMT and proliferation by regulating LEFTY2 in EC.
language: eng
source:
identifier: E-ISSN: 1791-244X ; PMID: 29845221 Version:1 ; DOI: 10.3892/ijmm.2018.3703
fulltext: fulltext
issn:
  • 1791244X
  • 1791-244X
url: Link


@attributes
ID1418538436
RANK0.07
NO1
SEARCH_ENGINEprimo_central_multiple_fe
SEARCH_ENGINE_TYPEPrimo Central Search Engine
LOCALfalse
PrimoNMBib
record
control
sourcerecordid29845221
sourceidmedline
recordidTN_medline29845221
sourceformatXML
sourcesystemOther
pqid2047291221
galeid553760917
display
typearticle
titlemiR‑215 promotes epithelial to mesenchymal transition and proliferation by regulating LEFTY2 in endometrial cancer
creatorGao, Xiaoxu ; Cai, Yan ; An, Ruifang
ispartofInternational journal of molecular medicine, September 2018, Vol.42(3), pp.1229-1236
identifier
subjectEndometrial Neoplasms -- Metabolism ; Epithelial-Mesenchymal Transition -- Physiology ; Gene Expression Regulation, Neoplastic -- Physiology ; Left-Right Determination Factors -- Metabolism ; Micrornas -- Metabolism
descriptionEndometrial cancer (EC) is the most common gynecological tumor in developed countries with an increasing incidence. Left‑right determination factor 2 (LEFTY2), a suppressor of cell proliferation and tumor growth, is a negative regulator of EC progression. The roles of LEFTY2 are emerging; however, the regulatory mechanisms of its expression have not been well understood. MicroRNA (miR)‑215 as an oncogene serves an important role in tumorigenesis by regulating target genes. In the present study, it was demonstrated that overexpression of miR‑215 promoted epithelial to mesenchymal transition (EMT), colony formation and DNA synthesis in EC HEC‑1A cells and its expression was upregulated in EC tissues. Using online miR target prediction software, it was revealed that LEFTY2 is predicted as a target of miR‑215. Using western blot analysis and immunofluorescence assays, it was demonstrated that overexpression of miR‑215 markedly downregulated LEFTY2 protein expression levels in HEC‑1A cells and LEFTY2 protein expression was downregulated in EC tissues, which was inversely correlated with miR‑215 expression. Furthermore, the present study indicated that overexpression of LEFTY2 protein promoted mesenchymal to epithelial transition and sensitized HEC‑1A cells to cisplatin treatment. In addition, it was revealed that the overexpression of LEFTY2 inhibited colony formation and DNA synthesis in HEC‑1A cells. Thus, miR‑215 may promote EMT and proliferation by regulating LEFTY2 in EC.
languageeng
source
version7
lds50peer_reviewed
links
openurl$$Topenurl_article
backlink$$Uhttp://pubmed.gov/29845221$$EView_this_record_in_MEDLINE/PubMed
openurlfulltext$$Topenurlfull_article
addlink$$Uhttp://exlibris-pub.s3.amazonaws.com/aboutMedline.html$$EView_the_MEDLINE/PubMed_Copyright_Statement
search
creatorcontrib
0Gao, Xiaoxu
1Cai, Yan
2An, Ruifang
titlemiR‑215 promotes epithelial to mesenchymal transition and proliferation by regulating LEFTY2 in endometrial cancer
descriptionEndometrial cancer (EC) is the most common gynecological tumor in developed countries with an increasing incidence. Left‑right determination factor 2 (LEFTY2), a suppressor of cell proliferation and tumor growth, is a negative regulator of EC progression. The roles of LEFTY2 are emerging; however, the regulatory mechanisms of its expression have not been well understood. MicroRNA (miR)‑215 as an oncogene serves an important role in tumorigenesis by regulating target genes. In the present study, it was demonstrated that overexpression of miR‑215 promoted epithelial to mesenchymal transition (EMT), colony formation and DNA synthesis in EC HEC‑1A cells and its expression was upregulated in EC tissues. Using online miR target prediction software, it was revealed that LEFTY2 is predicted as a target of miR‑215. Using western blot analysis and immunofluorescence assays, it was demonstrated that overexpression of miR‑215 markedly downregulated LEFTY2 protein expression levels in HEC‑1A cells and LEFTY2 protein expression was downregulated in EC tissues, which was inversely correlated with miR‑215 expression. Furthermore, the present study indicated that overexpression of LEFTY2 protein promoted mesenchymal to epithelial transition and sensitized HEC‑1A cells to cisplatin treatment. In addition, it was revealed that the overexpression of LEFTY2 inhibited colony formation and DNA synthesis in HEC‑1A cells. Thus, miR‑215 may promote EMT and proliferation by regulating LEFTY2 in EC.
subject
0Endometrial Neoplasms -- Metabolism
1Epithelial-Mesenchymal Transition -- Physiology
2Gene Expression Regulation, Neoplastic -- Physiology
3Left-Right Determination Factors -- Metabolism
4Micrornas -- Metabolism
general
029845221
1English
2MEDLINE/PubMed (U.S. National Library of Medicine)
310.3892/ijmm.2018.3703
4MEDLINE/PubMed (NLM)
sourceidmedline
recordidmedline29845221
issn
01791244X
11791-244X
rsrctypearticle
creationdate2018
addtitleInternational journal of molecular medicine
searchscope
0medline
1nlm_medline
2MEDLINE
scope
0medline
1nlm_medline
2MEDLINE
lsr41201809
citationpf 1229 vol 42 issue 3
startdate20180901
enddate20180931
lsr30VSR-Enriched:[issn, pqid, galeid]
sort
titlemiR‑215 promotes epithelial to mesenchymal transition and proliferation by regulating LEFTY2 in endometrial cancer
authorGao, Xiaoxu ; Cai, Yan ; An, Ruifang
creationdate20180900
lso0120180900
facets
frbrgroupid1463549773790709392
frbrtype5
newrecords20190701
languageeng
creationdate2018
topic
0Endometrial Neoplasms–Metabolism
1Epithelial-Mesenchymal Transition–Physiology
2Gene Expression Regulation, Neoplastic–Physiology
3Left-Right Determination Factors–Metabolism
4Micrornas–Metabolism
collectionMEDLINE/PubMed (NLM)
prefilterarticles
rsrctypearticles
creatorcontrib
0Gao, Xiaoxu
1Cai, Yan
2An, Ruifang
jtitleInternational Journal Of Molecular Medicine
toplevelpeer_reviewed
delivery
delcategoryRemote Search Resource
fulltextfulltext
addata
aulast
0Gao
1Cai
2An
aufirst
0Xiaoxu
1Yan
2Ruifang
au
0Gao, Xiaoxu
1Cai, Yan
2An, Ruifang
atitlemiR‑215 promotes epithelial to mesenchymal transition and proliferation by regulating LEFTY2 in endometrial cancer
jtitleInternational journal of molecular medicine
risdate201809
volume42
issue3
spage1229
pages1229-1236
eissn1791-244X
formatjournal
genrearticle
ristypeJOUR
abstractEndometrial cancer (EC) is the most common gynecological tumor in developed countries with an increasing incidence. Left‑right determination factor 2 (LEFTY2), a suppressor of cell proliferation and tumor growth, is a negative regulator of EC progression. The roles of LEFTY2 are emerging; however, the regulatory mechanisms of its expression have not been well understood. MicroRNA (miR)‑215 as an oncogene serves an important role in tumorigenesis by regulating target genes. In the present study, it was demonstrated that overexpression of miR‑215 promoted epithelial to mesenchymal transition (EMT), colony formation and DNA synthesis in EC HEC‑1A cells and its expression was upregulated in EC tissues. Using online miR target prediction software, it was revealed that LEFTY2 is predicted as a target of miR‑215. Using western blot analysis and immunofluorescence assays, it was demonstrated that overexpression of miR‑215 markedly downregulated LEFTY2 protein expression levels in HEC‑1A cells and LEFTY2 protein expression was downregulated in EC tissues, which was inversely correlated with miR‑215 expression. Furthermore, the present study indicated that overexpression of LEFTY2 protein promoted mesenchymal to epithelial transition and sensitized HEC‑1A cells to cisplatin treatment. In addition, it was revealed that the overexpression of LEFTY2 inhibited colony formation and DNA synthesis in HEC‑1A cells. Thus, miR‑215 may promote EMT and proliferation by regulating LEFTY2 in EC.
doi10.3892/ijmm.2018.3703
pmid29845221
issn11073756
oafree_for_read
date2018-09