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TASK-3 gene knockdown dampens invasion and migration and promotes apoptosis in KATO III and MKN-45 human gastric adenocarcinoma cell lines

dc.contributor.authorCikutovíc-Molina R.
dc.contributor.authorHerrada A.A.
dc.contributor.authorGonzález W.
dc.contributor.authorBrown N.
dc.contributor.authorZúñiga L.
dc.date.accessioned2020-09-02T22:14:53Z
dc.date.available2020-09-02T22:14:53Z
dc.date.issued2019
dc.identifier10.3390/ijms20236077
dc.identifier.citation20, 23, -
dc.identifier.issn16616596
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4025
dc.descriptionIncidence and mortality of gastric cancer is increasing worldwide, in part, because of the lack of new therapeutic targets to treat this disease. Different types of ion channels participate in the hallmarks of cancer. In this context, ion channels are known to exert control over the cell cycle, mechanisms that support survival, angiogenesis, migration, and cell invasion. In particular, TASK-3 (KCNK9), a member of the K2P potassium channel family, has attracted much interest because of its oncogenic properties. However, despite multiple lines of evidence linking TASK-3 to tumorigenesis in various types of cancer, its relationship with gastric cancer has not been fully examined. Therefore, we set out to assess the effect of TASK-3 gene knockdown on KATO III and MKN-45 human gastric adenocarcinoma cell lines by using a short hairpin RNA (shRNA)-mediated knockdown. Our results demonstrate that knocking down TASK-3 reduces cell proliferation and viability because of an increase in apoptosis without an apparent effect on cell cycle checkpoints. In addition, cell migration and invasion are reduced after knocking down TASK-3 in these cell lines. The present study highlights TASK-3 as a key protein involved in migration and cell survival in gastric cancer and corroborates its potential as a therapeutic target for gastric cancer treatment. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.
dc.language.isoen
dc.publisherMDPI AG
dc.subjectApoptosis
dc.subjectCell proliferation
dc.subjectGastric cancer
dc.subjectInvasion
dc.subjectMigration
dc.subjectTASK-3
dc.subjectKCNK9 protein
dc.subjectpotassium channel
dc.subjectshort hairpin RNA
dc.subjectunclassified drug
dc.subjectKCNK9 protein, human
dc.subjecttandem pore domain potassium channel
dc.subjectapoptosis
dc.subjectArticle
dc.subjectcarcinogenesis
dc.subjectcell cycle checkpoint
dc.subjectcell proliferation
dc.subjectcell viability
dc.subjectcontrolled study
dc.subjectgene expression
dc.subjectgene knockdown
dc.subjectHEK293T cell line
dc.subjecthuman
dc.subjecthuman cell
dc.subjectKATO III cell line
dc.subjectmetastasis inhibition
dc.subjectMKN45 cell line
dc.subjectprotein depletion
dc.subjectstomach adenocarcinoma
dc.subjectTASK 3 gene
dc.subjectadenocarcinoma
dc.subjectapoptosis
dc.subjectcell motion
dc.subjectcell survival
dc.subjectgene expression regulation
dc.subjectgene knockdown
dc.subjectgenetics
dc.subjectneovascularization (pathology)
dc.subjectpathology
dc.subjectstomach tumor
dc.subjecttumor cell line
dc.subjecttumor invasion
dc.subjectAdenocarcinoma
dc.subjectApoptosis
dc.subjectCell Line, Tumor
dc.subjectCell Movement
dc.subjectCell Proliferation
dc.subjectCell Survival
dc.subjectGene Expression Regulation, Neoplastic
dc.subjectGene Knockdown Techniques
dc.subjectHumans
dc.subjectNeoplasm Invasiveness
dc.subjectNeovascularization, Pathologic
dc.subjectPotassium Channels, Tandem Pore Domain
dc.subjectStomach Neoplasms
dc.titleTASK-3 gene knockdown dampens invasion and migration and promotes apoptosis in KATO III and MKN-45 human gastric adenocarcinoma cell lines
dc.typeArticle


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