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

Han, Xin; Wang, Da-zhong; Yuan, Meng; Bai, Weiliang

doi:10.1080/21655979.2021.1999375

Cited by 2 publications

(2 citation statements)

References 42 publications

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“…Phosphorylation of GSK‐3β by the membrane androgen receptor mAR can promote the development of colon cancer (Gu et al, 2014). GSK‐3β phosphorylation is inhibited after LMTK2 knockdown, resulting in the inhibition of gastric cancer growth (Han et al, 2022). Thus, GSK‐3β phosphorylation is crucial for tumor growth.…”

Section: Discussionmentioning

confidence: 99%

AQP8 may affect glioma proliferation and growth by regulating GSK‐3β phosphorylation and nuclear transport of β‐catenin

Cai

Shen

Zhao³

et al. 2023

Intl J of Devlp Neuroscience

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Purpose The purpose of this work is to examine the impact of AQP8 on the proliferation and development of human glioma cell lines A172 and U251 and to determine if aquaporin 8 (AQP8) is associated with GSK‐3β phosphorylation and nuclear transport of β‐catenin in the Wnt signaling pathway. Methods AQP8 knockdown cell lines were constructed using a CRISPR/Cas9 double vector lentivirus infection. SAM/dCas9 was used to construct AQP8 overexpression cell lines and the CV084 lentivirus vector was used to construct AQP8 rescue cell lines. AQP8 and its mRNA, and phosphorylated GSK‐3β, β‐catenin, and other related proteins, were detected using western blot and qRT‐PCR. Glioma cell apoptosis was detected using Hoechst 33342 dye. The migration of glioma cells was discovered using a wound healing assay. β‐catenin localization in cells was detected using immunofluorescence staining. Results The proliferative and migratory capacities of A172 and U251 cells were significantly enhanced after AQP8 overexpression. The Wnt signaling pathways appeared to have higher levels of phosphorylated GSK‐3β and β‐catenin, and a rise in the fluorescence intensity ratio of β‐catenin in the nucleus and cytoplasm, which suggests that β‐catenin translocated into the nucleus, while AQP8 knockdown produced the opposite effect. Further, overexpression of AQP8 in AQP8 knockdown cell lines rescued the reduction of related protein levels caused by AQP8 knockdown. Conclusion High AQP8 expression promotes proliferation and growth of glioma cells, a process associated with phosphorylation of GSK‐3β and nuclear translocation of β‐catenin.

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Section: Discussionmentioning

confidence: 99%

AQP8 may affect glioma proliferation and growth by regulating GSK‐3β phosphorylation and nuclear transport of β‐catenin

Cai

Shen

Zhao³

et al. 2023

Intl J of Devlp Neuroscience

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“…Moreover, DACT1 could induce β-catenin accumulation in the cytoplasm by inhibiting glycogen synthase kinase beta (GSK3-β) activity and interacting directly with β-catenin [ 14 ]. Nuclear β-catenin is an important transcriptional effector of the canonical Wnt signaling pathway, and cytoplasmic β-catenin is a crucial regulator of the cytoskeleton, and signal transduction [ 15 , 16 ]. Thus, the effect of DACT1 on β-catenin is closely related to its location.…”

Section: Discussionmentioning

confidence: 99%

Disheveled binding antagonist of β-catenin 1 interacted with β-catenin and connexin 43 in human-induced pluripotent stem cells-derived cardiomyocytes

et al. 2022

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Previously, we demonstrated that the disheveled binding antagonist of β-catenin 1 (DACT1) was involved in atrial fibrillation by regulating the reorganization of connexin 43 and β-catenin in cardiomyocytes. Little is known, however, about DACT1 in human normal myocardial cells. Therefore, we used cardiomyocytes (CMs) derived from human embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs) to investigate the role of DACT1 and its connection with β-catenin and connexin 43. While the ESC-CMs and iPSC-CMs were differentiated using commercial differentiation kits, the cardiac-specific markers were detected by immunofluorescence. The expression level of DACT1 was detected using western blotting, whereas the interaction of DACT1 and connexin 43 or β-catenin was detected by immunofluorescence and co-immunoprecipitation (co-IP) assays. Both H1-CMs and SF-CMs were immunostained for cardiac-specific markers, including Troponin I, Troponin T, α-actinin, NKX2.5, and GATA6. While DACT1 was not expressed in both H1 ESCs and SF-iPSCs, it was, however, highly expressed in differentiated CMs, being also localized in the cytoplasm and the nucleus of differentiated CMs. Interestingly, the DACT1 expression in different nuclei was different in the same multinucleated cell. Moreover, DACT1 colocalized with β-catenin in both the cytoplasm and nucleus of differentiated CMs, and it also colocalized with connexin 43 in the perinuclear region and the gap junctions of differentiated CMs. Co-IP results showed that DACT1 could directly bind to β-catenin and connexin 43. Taken together, DACT1 interacted with β-catenin and connexin 43 in human-induced pluripotent stem cells-derived cardiomyocytes.

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

Cited by 2 publications

References 42 publications

AQP8 may affect glioma proliferation and growth by regulating GSK‐3β phosphorylation and nuclear transport of β‐catenin

AQP8 may affect glioma proliferation and growth by regulating GSK‐3β phosphorylation and nuclear transport of β‐catenin

Disheveled binding antagonist of β-catenin 1 interacted with β-catenin and connexin 43 in human-induced pluripotent stem cells-derived cardiomyocytes

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