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dc.contributor.authorLi, H
dc.contributor.authorWang, C
dc.contributor.authorLan, L
dc.contributor.authorBehrens, A
dc.contributor.authorTomaschko, M
dc.contributor.authorRuiz, J
dc.contributor.authorSu, Q
dc.contributor.authorZhao, G
dc.contributor.authorYuan, C
dc.contributor.authorXiao, X
dc.contributor.authorLi, B
dc.contributor.authorYan, L
dc.contributor.authorWu, W
dc.contributor.authorLi, W
dc.contributor.authorChen, J
dc.contributor.authorHe, Y
dc.contributor.authorZhang, C
dc.date.accessioned2021-09-02T08:47:28Z
dc.date.available2021-09-02T08:47:28Z
dc.identifier.citationAging, 2021, 13 (4), pp. 5197 - 5225
dc.identifier.issn1945-4589
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/4787
dc.identifier.eissn1945-4589
dc.identifier.doi10.18632/aging.202440
dc.description.abstractIn the process of epithelial-mesenchymal transition (EMT), epithelial cancer cells transdifferentiate into mesenchymal-like cells with high motility and aggressiveness, resulting in the spread of tumor cells. Immune cells and inflammation in the tumor microenvironment are the driving factors of EMT, but few studies have explored the core targets of the interaction between EMT and tumor immune cells. We analyzed thousands of cases of gastric cancer and gastric tissue specimens of TCGA, CPTAC, GTEx and analyzing QPCR and IHC data of 56 gastric cancer patients in SYSU Gastric Cancer Research Center. It was known that EMT has an important connection with the infiltration of NK cells, and that the expression of vinculin may be the target of the phenomenon. The increased expression of vinculin is closely related to the aggressiveness and distant metastasis of cancer, which affects the survival prognosis of the patient. Moreover, through <i>in vitro</i> experiments under 3D conditions, we found that vinculin, cell invasion and metastasis are clearly linked. VCL can affect EMT and tumor immunity by regulating EPCAM gene expression. The role and mechanism of action of vinculin have been controversial, but this molecule may downregulate EpCAM (epithelial cellular adhesion molecule) and its own role in gastric cancer through DNA methylation, causing NK cells to enrich into tumor cells and kill tumor cells. At the same time, it promotes the occurrence of EMT, which in turn causes tumor metastasis and thus poorer prognosis.
dc.formatPrint-Electronic
dc.format.extent5197 - 5225
dc.languageeng
dc.language.isoeng
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.subjectKiller Cells, Natural
dc.subjectLymphocytes, Tumor-Infiltrating
dc.subjectHumans
dc.subjectAdenocarcinoma
dc.subjectStomach Neoplasms
dc.subjectNeoplasm Invasiveness
dc.subjectNeoplasm Metastasis
dc.subjectVinculin
dc.subjectPrognosis
dc.subjectAged
dc.subjectMiddle Aged
dc.subjectFemale
dc.subjectMale
dc.subjectEpithelial-Mesenchymal Transition
dc.subjectEpithelial Cell Adhesion Molecule
dc.titleHigh expression of vinculin predicts poor prognosis and distant metastasis and associates with influencing tumor-associated NK cell infiltration and epithelial-mesenchymal transition in gastric cancer.
dc.typeJournal Article
dcterms.dateAccepted2020-10-27
rioxxterms.versionVoR
rioxxterms.versionofrecord10.18632/aging.202440
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfAging
pubs.issue4
pubs.notesNot known
pubs.organisational-group/ICR
pubs.organisational-group/ICR
pubs.publication-statusPublished
pubs.volume13en_US
pubs.embargo.termsNot known
dc.contributor.icrauthorBehrens, Axelen


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