Lemur tyrosine kinase 2 silencing inhibits the proliferation of gastric cancer cells by regulating GSK-3β phosphorylation and β-catenin nuclear translocation

Previous studies on the mechanism of proliferation and cell cycle progression of gastric cancer cells have shown promising perspectives for the prevention and treatment of gastric cancer. The aim of the present study was to investigate the role of lemur tyrosine kinase 2 (LMTK2) in gastric cancer ce...

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Autores principales: Xin Han, Da-zhong Wang, Meng Yuan, Wei-jun Bai
Formato: article
Lenguaje:EN
Publicado: Taylor & Francis Group 2021
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Acceso en línea:https://doaj.org/article/8a2d5a9e6a294da88c0b14475ff9a8f1
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spelling oai:doaj.org-article:8a2d5a9e6a294da88c0b14475ff9a8f12021-11-04T15:51:54ZLemur tyrosine kinase 2 silencing inhibits the proliferation of gastric cancer cells by regulating GSK-3β phosphorylation and β-catenin nuclear translocation2165-59792165-598710.1080/21655979.2021.1999375https://doaj.org/article/8a2d5a9e6a294da88c0b14475ff9a8f12021-10-01T00:00:00Zhttp://dx.doi.org/10.1080/21655979.2021.1999375https://doaj.org/toc/2165-5979https://doaj.org/toc/2165-5987Previous studies on the mechanism of proliferation and cell cycle progression of gastric cancer cells have shown promising perspectives for the prevention and treatment of gastric cancer. The aim of the present study was to investigate the role of lemur tyrosine kinase 2 (LMTK2) in gastric cancer cell proliferation and cell cycle progression, as well as in tumor-bearing nude mouse models. The expression levels of LMTK2 were determined in gastric cancer cell lines. In addition, the effects of LMTK2 silencing or overexpression on cell proliferation were measured using Cell Counting Kit-8, BrdU and colony formation assays. Cell cycle progression was analyzed using flow cytometry and western blotting. The expression levels of proteins associated with the β-catenin pathway were assessed using western blot analysis. A tumor-bearing nude mouse model was established by injecting gastric cancer cells, and the effect of LMTK2 knockdown or overexpression on tumor growth was examined. The expression levels of LMTK2 were found to be upregulated in all gastric cancer cell lines. Moreover, LMTK2 knockdown inhibited cell proliferation, colony formation and cell cycle progression. LMTK2 knockdown also inhibited the activation of GSK-3β/β-catenin signaling, as evidenced by reduced GSK-3β phosphorylation and nuclear β-catenin levels. LMTK2 knockdown also suppressed tumor growth, whereas overexpression accelerated this process. In conclusion, LMTK2 silencing can inhibit the proliferation of gastric cancer cells in vitro and tumor growth in vivo by regulating GSK-3β phosphorylation and β-catenin nuclear translocation.Xin HanDa-zhong WangMeng YuanWei-jun BaiTaylor & Francis Grouparticlegastric cancerlemur tyrosine kinase 2proliferationgsk-3ββ-cateninBiotechnologyTP248.13-248.65ENBioengineered, Vol 0, Iss 0 (2021)
institution DOAJ
collection DOAJ
language EN
topic gastric cancer
lemur tyrosine kinase 2
proliferation
gsk-3β
β-catenin
Biotechnology
TP248.13-248.65
spellingShingle gastric cancer
lemur tyrosine kinase 2
proliferation
gsk-3β
β-catenin
Biotechnology
TP248.13-248.65
Xin Han
Da-zhong Wang
Meng Yuan
Wei-jun Bai
Lemur tyrosine kinase 2 silencing inhibits the proliferation of gastric cancer cells by regulating GSK-3β phosphorylation and β-catenin nuclear translocation
description Previous studies on the mechanism of proliferation and cell cycle progression of gastric cancer cells have shown promising perspectives for the prevention and treatment of gastric cancer. The aim of the present study was to investigate the role of lemur tyrosine kinase 2 (LMTK2) in gastric cancer cell proliferation and cell cycle progression, as well as in tumor-bearing nude mouse models. The expression levels of LMTK2 were determined in gastric cancer cell lines. In addition, the effects of LMTK2 silencing or overexpression on cell proliferation were measured using Cell Counting Kit-8, BrdU and colony formation assays. Cell cycle progression was analyzed using flow cytometry and western blotting. The expression levels of proteins associated with the β-catenin pathway were assessed using western blot analysis. A tumor-bearing nude mouse model was established by injecting gastric cancer cells, and the effect of LMTK2 knockdown or overexpression on tumor growth was examined. The expression levels of LMTK2 were found to be upregulated in all gastric cancer cell lines. Moreover, LMTK2 knockdown inhibited cell proliferation, colony formation and cell cycle progression. LMTK2 knockdown also inhibited the activation of GSK-3β/β-catenin signaling, as evidenced by reduced GSK-3β phosphorylation and nuclear β-catenin levels. LMTK2 knockdown also suppressed tumor growth, whereas overexpression accelerated this process. In conclusion, LMTK2 silencing can inhibit the proliferation of gastric cancer cells in vitro and tumor growth in vivo by regulating GSK-3β phosphorylation and β-catenin nuclear translocation.
format article
author Xin Han
Da-zhong Wang
Meng Yuan
Wei-jun Bai
author_facet Xin Han
Da-zhong Wang
Meng Yuan
Wei-jun Bai
author_sort Xin Han
title Lemur tyrosine kinase 2 silencing inhibits the proliferation of gastric cancer cells by regulating GSK-3β phosphorylation and β-catenin nuclear translocation
title_short Lemur tyrosine kinase 2 silencing inhibits the proliferation of gastric cancer cells by regulating GSK-3β phosphorylation and β-catenin nuclear translocation
title_full Lemur tyrosine kinase 2 silencing inhibits the proliferation of gastric cancer cells by regulating GSK-3β phosphorylation and β-catenin nuclear translocation
title_fullStr Lemur tyrosine kinase 2 silencing inhibits the proliferation of gastric cancer cells by regulating GSK-3β phosphorylation and β-catenin nuclear translocation
title_full_unstemmed Lemur tyrosine kinase 2 silencing inhibits the proliferation of gastric cancer cells by regulating GSK-3β phosphorylation and β-catenin nuclear translocation
title_sort lemur tyrosine kinase 2 silencing inhibits the proliferation of gastric cancer cells by regulating gsk-3β phosphorylation and β-catenin nuclear translocation
publisher Taylor & Francis Group
publishDate 2021
url https://doaj.org/article/8a2d5a9e6a294da88c0b14475ff9a8f1
work_keys_str_mv AT xinhan lemurtyrosinekinase2silencinginhibitstheproliferationofgastriccancercellsbyregulatinggsk3bphosphorylationandbcateninnucleartranslocation
AT dazhongwang lemurtyrosinekinase2silencinginhibitstheproliferationofgastriccancercellsbyregulatinggsk3bphosphorylationandbcateninnucleartranslocation
AT mengyuan lemurtyrosinekinase2silencinginhibitstheproliferationofgastriccancercellsbyregulatinggsk3bphosphorylationandbcateninnucleartranslocation
AT weijunbai lemurtyrosinekinase2silencinginhibitstheproliferationofgastriccancercellsbyregulatinggsk3bphosphorylationandbcateninnucleartranslocation
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