JAK/STAT pathway interacts with intercellular cell adhesion molecule (ICAM) and vascular cell adhesion molecule (VCAM) while prostate cancer stem cells form tumor spheroids

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dc.contributor.authorDuzagac F.
dc.contributor.authorInan S.
dc.contributor.authorSimsek F.E.
dc.contributor.authorAcikgoz E.
dc.contributor.authorGuven U.
dc.contributor.authorKhan S.A.
dc.contributor.authorRouhrazi H.
dc.contributor.authorOltulu F.
dc.contributor.authorAktug H.
dc.contributor.authorErol A.
dc.contributor.authorOktem G.
dc.date.accessioned2024-07-22T08:12:59Z
dc.date.available2024-07-22T08:12:59Z
dc.date.issued2015
dc.description.abstractPurpose: JAK/STAT is an evolutionarily conserved pathway and very important for second messenger system. This pathway is important in malignant transformation and accumulated evidence indicates that this pathway is involved in tumorigenesis and progression of several cancers. It was possible to assume that activation of JAK/STAT pathway is associated with increase in the expressions of ICAM-1 and VCAM-1. In this study we hypothesized that when cells were maintained as spheroids or monolayers, the structure of cancer stem cells (CSCs) could show differentiation when compared with non-CSCs. Methods: DU-145 human prostate cancer cells were cultured using the Ege University molecular embryology laboratory medium supplemented with 10% fetal bovine serum. Clusters of differentiation 133 (CD133)(+high)/CD44(+high) prostate CSCs were isolated from the DU145 cell line by using BD FACSAria. CD133+/CD44+ CSCs were cultured until confluent with 3% noble agar. The expression of these proteins in CSCs and non-CSCs was analyzed by immunohistochemistry. Results: Different expression profiles were observed in the conventional two-dimensional (2D) and three-dimensional (3D) experimental model system when CSCs and non-CSCs were compared. Human prostate CSCs exhibited intense ICAM-1 and VCAM-1 immunoreaction when compared with non-CSCs. These findings were supported by the fact that VCAM-1 on the surface of cancer cells binds to its counterreceptor, the a4fil integrin (also known as very-late antigen, VLA-4), on metastasis-associated macrophages, triggering VCAM-1-mediated activation of the phosphoinositide 3-kinase growth and survival pathway in cancer cells. Conclusions: The results of this study showed that changes in JAK/STAT pathway are related with adhesion molecules and could affect cancer progression.
dc.identifier.issn11070625
dc.identifier.urihttp://akademikarsiv.cbu.edu.tr:4000/handle/123456789/16250
dc.language.isoEnglish
dc.publisherZerbinis Publications
dc.subjectCell Line, Tumor
dc.subjectHumans
dc.subjectImmunohistochemistry
dc.subjectIntercellular Adhesion Molecule-1
dc.subjectJanus Kinases
dc.subjectMale
dc.subjectNeoplastic Stem Cells
dc.subjectProstatic Neoplasms
dc.subjectSignal Transduction
dc.subjectSpheroids, Cellular
dc.subjectSTAT Transcription Factors
dc.subjectVascular Cell Adhesion Molecule-1
dc.subjectCD133 antigen
dc.subjectHermes antigen
dc.subjectintercellular adhesion molecule 1
dc.subjectJanus kinase
dc.subjectJanus kinase 2
dc.subjectphosphatidylinositol 3 kinase
dc.subjectSTAT protein
dc.subjectSTAT2 protein
dc.subjectSTAT5 protein
dc.subjectvascular cell adhesion molecule 1
dc.subjectvery late activation antigen 4
dc.subjectintercellular adhesion molecule 1
dc.subjectJanus kinase
dc.subjectSTAT protein
dc.subjectvascular cell adhesion molecule 1
dc.subjectArticle
dc.subjectcancer growth
dc.subjectcancer stem cell
dc.subjectcell differentiation
dc.subjectcontrolled study
dc.subjecthuman
dc.subjecthuman cell
dc.subjecthuman tissue
dc.subjectimmunohistochemistry
dc.subjectmacrophage
dc.subjectmetastasis
dc.subjectmolecular interaction
dc.subjectprostate cancer
dc.subjectprotein expression
dc.subjecttumor spheroid
dc.subjectcancer stem cell
dc.subjectmale
dc.subjectmulticellular spheroid
dc.subjectpathology
dc.subjectphysiology
dc.subjectprostate tumor
dc.subjectsignal transduction
dc.subjecttumor cell line
dc.titleJAK/STAT pathway interacts with intercellular cell adhesion molecule (ICAM) and vascular cell adhesion molecule (VCAM) while prostate cancer stem cells form tumor spheroids
dc.typeArticle

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