Dergi makalesi Açık Erişim
Kucuksayan, Hakan; Akgun, Sakir; Ozes, Osman Nidai; Alikanoglu, Arsenal Sezgin; Yildiz, Mustafa; Dal, Egemen; Akca, Hakan
<?xml version='1.0' encoding='utf-8'?> <resource xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns="http://datacite.org/schema/kernel-4" xsi:schemaLocation="http://datacite.org/schema/kernel-4 http://schema.datacite.org/meta/kernel-4.1/metadata.xsd"> <identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/75021</identifier> <creators> <creator> <creatorName>Kucuksayan, Hakan</creatorName> <givenName>Hakan</givenName> <familyName>Kucuksayan</familyName> <affiliation>Pamukkale Univ, Sch Med, Med Biol Dept, Denizli, Turkey</affiliation> </creator> <creator> <creatorName>Akgun, Sakir</creatorName> <givenName>Sakir</givenName> <familyName>Akgun</familyName> <affiliation>Pamukkale Univ, Sch Med, Med Biol Dept, Denizli, Turkey</affiliation> </creator> <creator> <creatorName>Ozes, Osman Nidai</creatorName> <givenName>Osman Nidai</givenName> <familyName>Ozes</familyName> <affiliation>ALTAY Biopharma, San Bruno, CA USA</affiliation> </creator> <creator> <creatorName>Alikanoglu, Arsenal Sezgin</creatorName> <givenName>Arsenal Sezgin</givenName> <familyName>Alikanoglu</familyName> <affiliation>Antalya Training & Res Hosp, Pathol Dept, Antalya, Turkey</affiliation> </creator> <creator> <creatorName>Yildiz, Mustafa</creatorName> <givenName>Mustafa</givenName> <familyName>Yildiz</familyName> <affiliation>Antalya Training & Res Hosp, Med Oncol, Antalya, Turkey</affiliation> </creator> <creator> <creatorName>Dal, Egemen</creatorName> <givenName>Egemen</givenName> <familyName>Dal</familyName> <affiliation>Pamukkale Univ, Fac Med, Denizli, Turkey</affiliation> </creator> <creator> <creatorName>Akca, Hakan</creatorName> <givenName>Hakan</givenName> <familyName>Akca</familyName> <affiliation>Pamukkale Univ, Sch Med, Med Biol Dept, Denizli, Turkey</affiliation> </creator> </creators> <titles> <title>Tgf-Beta-Smad-Mir-520E Axis Regulates Nsclc Metastasis Through A Tgfbr2-Mediated Negative-Feedback Loop</title> </titles> <publisher>Aperta</publisher> <publicationYear>2019</publicationYear> <dates> <date dateType="Issued">2019-01-01</date> </dates> <resourceType resourceTypeGeneral="Text">Journal article</resourceType> <alternateIdentifiers> <alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/75021</alternateIdentifier> </alternateIdentifiers> <relatedIdentifiers> <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1093/carcin/bgy166</relatedIdentifier> </relatedIdentifiers> <rightsList> <rights rightsURI="http://www.opendefinition.org/licenses/cc-by">Creative Commons Attribution</rights> <rights rightsURI="info:eu-repo/semantics/openAccess">Open Access</rights> </rightsList> <descriptions> <description descriptionType="Abstract">Transforming growth factor-beta (TGF-beta) pathway plays crucial roles during the carcinogenesis and metastasis. TGF-beta receptor 2 (TGFBR2) is a key molecule for the regulation of TGF-beta pathway and frequently downregulated or lost in several cancer types including non-small cell lung cancer (NSCLC), and TGF-beta pathway is often regulated by negative-feedback mechanisms, but little is known about the mechanism of TGFBR2 downregulation in NSCLC. Here, we found that the expression of miR-520e is upregulated in metastatic tumor tissues compared with non-metastatic ones, and its expression is inversely correlated with that of TGFBR2 in clinical samples. We also discovered that TGF-beta dramatically increased the expression of miR-520e, which targeted and downregulated TGFBR2, and the suppression of miR-520e significantly impaired TGF-beta-induced TGFBR2 downregulation. Chromatin immunoprecipitation-PCR experiments further showed that miR-520e is transcriptionally induced by SMAD2/3 in response to TGF-beta. Our findings reveal a novel negative-feedback mechanism in TGF-beta signaling and the expression level of miR-520e could be a predictive biomarker for NSCLC metastasis.</description> </descriptions> </resource>
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