Lemur tyrosine kinase 2 silencing inhibits the proliferation of gastric cancer cells by regulating GSK-3β phosphorylation and β-catenin nuclear translocation
| العنوان: | Lemur tyrosine kinase 2 silencing inhibits the proliferation of gastric cancer cells by regulating GSK-3β phosphorylation and β-catenin nuclear translocation |
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| المؤلفون: | Wei-jun Bai, Da-zhong Wang, Xin Han, Meng Yuan |
| المصدر: | Bioengineered, Vol 0, Iss 0 (2021) |
| بيانات النشر: | Taylor & Francis Group, 2021. |
| سنة النشر: | 2021 |
| مصطلحات موضوعية: | proliferation, Bioengineering, Protein Serine-Threonine Kinases, Applied Microbiology and Biotechnology, LMTK2, Mice, Nude mouse, Stomach Neoplasms, Cell Line, Tumor, gsk-3β, medicine, Animals, Phosphorylation, beta Catenin, Cell Proliferation, TYK2 Kinase, Gene knockdown, Glycogen Synthase Kinase 3 beta, biology, Lemur, Chemistry, Cell growth, gastric cancer, Cancer, General Medicine, lemur tyrosine kinase 2, β-catenin, medicine.disease, biology.organism_classification, Catenin, Cancer cell, Cancer research, TP248.13-248.65, Biotechnology |
| الوصف: | 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. |
| اللغة: | English |
| تدمد: | 2165-5987 2165-5979 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8cb2ae53633f5daad3840be7ae0a58b2Test https://doaj.org/article/8a2d5a9e6a294da88c0b14475ff9a8f1Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....8cb2ae53633f5daad3840be7ae0a58b2 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 21655987 21655979 |
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