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The effect of medicarpin on PTEN/AKT signal pathway in head and neck squamous cell carcinoma

dc.contributor.authorYiğin, Aysel Kalayci
dc.contributor.authorDonmez, Huseyin
dc.contributor.authorHitit, Mustafa
dc.contributor.authorSeven, Sena
dc.contributor.authorEser, Nadire
dc.contributor.authorKurar, Ercan
dc.contributor.authorSeven, Mehmet
dc.date.accessioned2026-01-04T16:16:49Z
dc.date.issued2022-01-01
dc.description.abstractBackground/Aim: We aimed to investigate the in vitro modulating effects of medicarpin on the PI3K/AKT signal pathway gene expressions in head and neck squamous cell carcinoma (HNSCC). Materials and Methods: The effect of medicarpin on PTEN and other associated genes in the PTEN/AKT signal pathway was investigated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, real-time quantitative polymerase chain reaction, and Western blot analysis in the SCCL-MT1 (HNSCC) and control (HEK-293) cell lines. Results: The IC50 dose was 80 μM as a result of medicarpin treatment on HNSCC cells (P = 0.0006). It was found that PTEN and AKT gene expressions increased after the medicarpin administration while PDK1 gene expression was decreased in SCCL-MT1 cells (P = 0.0002, P = 0.0003, and P = 0.05, respectively). Protein expression results showed that medicarpin-treated cells significantly increased in pAKT (P = 0.024), pPTEN (P = 0.032), and decreased pPDK1 (P = 0.059) in SCCL-MT1. Conclusions: Our data show that medicarpin modulates HNSCC cells by increasing the PTEN and decreasing PDK1 expressions. PDK1 gene expression effects mTOR pathway which may increase AKT gene. Our study suggests that both medicarpin extracts combination with the HNSCC drug may be more effective in cancer treatment. Future prospective studies that integrate molecular and pharmacogenetic studies are crucial for revealing the mechanism and preventive medical efforts.
dc.description.urihttps://doi.org/10.4103/jcrt.jcrt_641_21
dc.description.urihttps://pubmed.ncbi.nlm.nih.gov/35381781
dc.description.urihttps://hdl.handle.net/20.500.12831/8686
dc.identifier.doi10.4103/jcrt.jcrt_641_21
dc.identifier.eissn1998-4138
dc.identifier.endpage184
dc.identifier.issn0973-1482
dc.identifier.openairedoi_dedup___::e4b6800c5b04cc5ab20c7bb4f42e654a
dc.identifier.orcid0000-0001-8549-5564
dc.identifier.orcid0000-0002-9746-0227
dc.identifier.pubmed35381781
dc.identifier.scopus2-s2.0-85127711075
dc.identifier.startpage180
dc.identifier.urihttps://hdl.handle.net/20.500.12597/39399
dc.identifier.volume18
dc.identifier.wos000788081000027
dc.language.isoeng
dc.publisherOvid Technologies (Wolters Kluwer Health)
dc.relation.ispartofJournal of Cancer Research and Therapeutics
dc.rightsOPEN
dc.subjectPterocarpans
dc.subjectSquamous Cell Carcinoma of Head and Neck
dc.subjectmedicarpin
dc.subjectPTEN Phosphohydrolase
dc.subjectHead and neck squamous cell carcinoma
dc.subjectin vitro
dc.subjectApoptosis
dc.subjectSativa
dc.subjectPhosphatidylinositol 3-Kinases
dc.subject<p>PTEN/AKT signal pathway</p>
dc.subjectHEK293 Cells
dc.subjectHead and Neck Neoplasms
dc.subjectCell Line, Tumor
dc.subjectHumans
dc.subjectProspective Studies
dc.subjectProto-Oncogene Proteins c-akt
dc.subjectCell Proliferation
dc.subjectSignal Transduction
dc.subject.sdg3. Good health
dc.titleThe effect of medicarpin on PTEN/AKT signal pathway in head and neck squamous cell carcinoma
dc.typeArticle
dspace.entity.typePublication
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It was found that <jats:italic toggle=\"yes\">PTEN</jats:italic> and <jats:italic toggle=\"yes\">AKT</jats:italic> gene expressions increased after the medicarpin administration while <jats:italic toggle=\"yes\">PDK1</jats:italic> gene expression was decreased in SCCL-MT1 cells (<jats:italic toggle=\"yes\">P</jats:italic> = 0.0002, <jats:italic toggle=\"yes\">P</jats:italic> = 0.0003, and <jats:italic toggle=\"yes\">P</jats:italic> = 0.05, respectively). Protein expression results showed that medicarpin-treated cells significantly increased in pAKT (<jats:italic toggle=\"yes\">P</jats:italic> = 0.024), pPTEN (<jats:italic toggle=\"yes\">P</jats:italic> = 0.032), and decreased pPDK1 (<jats:italic toggle=\"yes\">P</jats:italic> = 0.059) in SCCL-MT1.</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions:</jats:title> <jats:p>Our data show that medicarpin modulates HNSCC cells by increasing the <jats:italic toggle=\"yes\">PTEN</jats:italic> and decreasing <jats:italic toggle=\"yes\">PDK1</jats:italic> expressions. <jats:italic toggle=\"yes\">PDK1</jats:italic> gene expression effects mTOR pathway which may increase <jats:italic toggle=\"yes\">AKT</jats:italic> gene. Our study suggests that both medicarpin extracts combination with the HNSCC drug may be more effective in cancer treatment. Future prospective studies that integrate molecular and pharmacogenetic studies are crucial for revealing the mechanism and preventive medical efforts.</jats:p> </jats:sec>"],"publicationDate":"2022-01-01","publisher":"Ovid Technologies (Wolters Kluwer Health)","embargoEndDate":null,"sources":["Crossref"],"formats":["application/pdf"],"contributors":["İstanbul University Cerrahpaşa Institutional Repository"],"coverages":null,"bestAccessRight":{"code":"c_abf2","label":"OPEN","scheme":"http://vocabularies.coar-repositories.org/documentation/access_rights/"},"container":{"name":"Journal of Cancer Research and Therapeutics","issnPrinted":"0973-1482","issnOnline":"1998-4138","issnLinking":null,"ep":"184","iss":null,"sp":"180","vol":"18","edition":null,"conferencePlace":null,"conferenceDate":null},"documentationUrls":null,"codeRepositoryUrl":null,"programmingLanguage":null,"contactPeople":null,"contactGroups":null,"tools":null,"size":null,"version":null,"geoLocations":null,"id":"doi_dedup___::e4b6800c5b04cc5ab20c7bb4f42e654a","originalIds":["10.4103/jcrt.jcrt_641_21","50|doiboost____|e4b6800c5b04cc5ab20c7bb4f42e654a","35381781","oai:acikerisim.iuc.edu.tr:20.500.12831/8686","50|od_____10033::b79c4fff1d75f4796a04bbe4b4814a57"],"pids":[{"scheme":"doi","value":"10.4103/jcrt.jcrt_641_21"},{"scheme":"pmid","value":"35381781"},{"scheme":"handle","value":"20.500.12831/8686"}],"dateOfCollection":null,"lastUpdateTimeStamp":null,"indicators":{"citationImpact":{"citationCount":3,"influence":2.6298592e-9,"popularity":4.226676e-9,"impulse":3,"citationClass":"C5","influenceClass":"C5","impulseClass":"C5","popularityClass":"C4"}},"instances":[{"pids":[{"scheme":"doi","value":"10.4103/jcrt.jcrt_641_21"}],"type":"Article","urls":["https://doi.org/10.4103/jcrt.jcrt_641_21"],"publicationDate":"2022-01-01","refereed":"peerReviewed"},{"pids":[{"scheme":"doi","value":"10.4103/jcrt.jcrt_641_21"}],"type":"Article","urls":["https://doi.org/10.4103/jcrt.jcrt_641_21"],"refereed":"nonPeerReviewed"},{"pids":[{"scheme":"pmid","value":"35381781"}],"alternateIdentifiers":[{"scheme":"doi","value":"10.4103/jcrt.jcrt_641_21"}],"type":"Article","urls":["https://pubmed.ncbi.nlm.nih.gov/35381781"],"publicationDate":"2022-04-07","refereed":"nonPeerReviewed"},{"pids":[{"scheme":"handle","value":"20.500.12831/8686"}],"alternateIdentifiers":[{"scheme":"doi","value":"10.4103/jcrt.jcrt_641_21"}],"type":"Article","urls":["https://hdl.handle.net/20.500.12831/8686","https://doi.org/10.4103/jcrt.jcrt_641_21"],"publicationDate":"2022-01-01","refereed":"nonPeerReviewed"}],"isGreen":true,"isInDiamondJournal":false}
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