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Title:
CDK5RAP3 suppresses Wnt/β-catenin signaling by inhibiting AKT phosphorylation in gastric cancer | Journal of Experimental & Clinical Cancer Research
Description:
Background CDK5RAP3 was initially isolated as a binding protein of the CDK5 activator p35. Although CDK5RAP3 has been shown to negatively regulate the Wnt/β-catenin signaling pathway in gastric cancer by repressing GSK-3β phosphorylation, its in-depth mechanism has not been determined. Methods Following CDK5RAP3 overexpression or knock down, CDK5RAP3 signaling pathways were investigated in gastric cancer cells by Western Blotting. Cell growth, invasion and migration were also evaluated in gastric cancer cell lines. We analyzed CDK5RAP3, AKT, p-AKT (Ser473), GSK-3β and p-GSK-3β (Ser9) expression in gastric tumor samples and adjacent non-tumor tissues from 295 patients using immunohistochemistry and Western Blotting. The prognostic significance of CDK5RAP3 and p-AKT (Ser473) was confirmed by a Log-rank test. Results Our study demonstrated that the expression of p-AKT (Ser473) and p-GSK-3β (Ser9) was negatively correlated with CDK5RAP3 in stable gastric cancer cell lines. CDK5RAP3 repressed AKT phosphorylation, which promoted GSK-3β phosphorylation, thereby suppressing β-catenin protein expression and, consequently, gastric cancer. The protein level of CDK5RAP3 was markedly decreased in most gastric tumor tissues compared with adjacent non-tumor tissues, and the levels of p-AKT (Ser473) and p-GSK-3β (Ser9) were also negatively correlated with those of CDK5RAP3. The prognostic value of CDK5RAP3 for overall survival was found to be dependent on AKT phosphorylation. Conclusion Our results demonstrated that CDK5RAP3 negatively regulates the Wnt/β-catenin signaling pathway by repressing AKT phosphorylation, which leads to better survival of patients with gastric cancer.
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Keywords {🔍}
cdkrap, cancer, akt, gastric, expression, ser, protein, gskβ, cell, article, phosphorylation, tumor, pubmed, signaling, pakt, google, scholar, fig, tissues, patients, cas, kinase, lin, cells, low, βcatenin, survival, fujian, high, invasion, pgskβ, wang, study, levels, human, samples, prognostic, proliferation, ihc, wntβcatenin, shown, migration, results, significantly, data, research, zhang, chen, western, blotting,
Topics {✒️}
wnt/β-catenin signaling pathway suppressed wnt/β-catenin signaling inhibit wnt/β-catenin signaling akt/gsk-3β/β-catenin signaling cdk5rap3-induced epithelial–mesenchymal transition chang-ming huang inhibit β-catenin signaling lenti-shc53-treated ags cells article download pdf samples exhibiting p-gsk-3β regulate β-catenin activity wnt signaling pathway including cellular responses regulating gsk-3β phosphorylation wnt/β-catenin [18 physically isolate gsk-3β p21-induced protein kinase4 hrp-conjugated secondary antibody selectively inhibits nf-kappab β-catenin signaling gsk-3β binding sites reduced phosphorylated gsk-3β promoted gsk-3β phosphorylation blocking gsk-3β phosphorylation kaplan-meier survival curve phosphatidylinositol-3 kinase-activated signaling regulate gsk-3β phosphorylation repressing gsk-3β phosphorylation gastrointestinal cancer glycogen synthase kinase-3beta activated akt induces kaplan-meier survival curves beta-catenin signaling cdk5rap3-overexpressing ags cells inhibiting β-catenin human prostate cancer samples exhibiting p-akt affect gsk-3β phosphorylation akt signaling pathway β-catenin levels free β-catenin [20] fujian medical university putative tumor suppressor β-catenin expression gastric cancer tissues gastric cancer cells gastric cancer samples cell signaling technology full access fujian province innovation
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headline:CDK5RAP3 suppresses Wnt/β-catenin signaling by inhibiting AKT phosphorylation in gastric cancer
description:CDK5RAP3 was initially isolated as a binding protein of the CDK5 activator p35. Although CDK5RAP3 has been shown to negatively regulate the Wnt/β-catenin signaling pathway in gastric cancer by repressing GSK-3β phosphorylation, its in-depth mechanism has not been determined. Following CDK5RAP3 overexpression or knock down, CDK5RAP3 signaling pathways were investigated in gastric cancer cells by Western Blotting. Cell growth, invasion and migration were also evaluated in gastric cancer cell lines. We analyzed CDK5RAP3, AKT, p-AKT (Ser473), GSK-3β and p-GSK-3β (Ser9) expression in gastric tumor samples and adjacent non-tumor tissues from 295 patients using immunohistochemistry and Western Blotting. The prognostic significance of CDK5RAP3 and p-AKT (Ser473) was confirmed by a Log-rank test. Our study demonstrated that the expression of p-AKT (Ser473) and p-GSK-3β (Ser9) was negatively correlated with CDK5RAP3 in stable gastric cancer cell lines. CDK5RAP3 repressed AKT phosphorylation, which promoted GSK-3β phosphorylation, thereby suppressing β-catenin protein expression and, consequently, gastric cancer. The protein level of CDK5RAP3 was markedly decreased in most gastric tumor tissues compared with adjacent non-tumor tissues, and the levels of p-AKT (Ser473) and p-GSK-3β (Ser9) were also negatively correlated with those of CDK5RAP3. The prognostic value of CDK5RAP3 for overall survival was found to be dependent on AKT phosphorylation. Our results demonstrated that CDK5RAP3 negatively regulates the Wnt/β-catenin signaling pathway by repressing AKT phosphorylation, which leads to better survival of patients with gastric cancer.
datePublished:2018-03-14T00:00:00Z
dateModified:2018-03-14T00:00:00Z
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keywords:
CDK5RAP3
AKT
GSK-3β
Gastric cancer
Survival
Cancer Research
Immunology
Apoptosis
Oncology
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headline:CDK5RAP3 suppresses Wnt/β-catenin signaling by inhibiting AKT phosphorylation in gastric cancer
description:CDK5RAP3 was initially isolated as a binding protein of the CDK5 activator p35. Although CDK5RAP3 has been shown to negatively regulate the Wnt/β-catenin signaling pathway in gastric cancer by repressing GSK-3β phosphorylation, its in-depth mechanism has not been determined. Following CDK5RAP3 overexpression or knock down, CDK5RAP3 signaling pathways were investigated in gastric cancer cells by Western Blotting. Cell growth, invasion and migration were also evaluated in gastric cancer cell lines. We analyzed CDK5RAP3, AKT, p-AKT (Ser473), GSK-3β and p-GSK-3β (Ser9) expression in gastric tumor samples and adjacent non-tumor tissues from 295 patients using immunohistochemistry and Western Blotting. The prognostic significance of CDK5RAP3 and p-AKT (Ser473) was confirmed by a Log-rank test. Our study demonstrated that the expression of p-AKT (Ser473) and p-GSK-3β (Ser9) was negatively correlated with CDK5RAP3 in stable gastric cancer cell lines. CDK5RAP3 repressed AKT phosphorylation, which promoted GSK-3β phosphorylation, thereby suppressing β-catenin protein expression and, consequently, gastric cancer. The protein level of CDK5RAP3 was markedly decreased in most gastric tumor tissues compared with adjacent non-tumor tissues, and the levels of p-AKT (Ser473) and p-GSK-3β (Ser9) were also negatively correlated with those of CDK5RAP3. The prognostic value of CDK5RAP3 for overall survival was found to be dependent on AKT phosphorylation. Our results demonstrated that CDK5RAP3 negatively regulates the Wnt/β-catenin signaling pathway by repressing AKT phosphorylation, which leads to better survival of patients with gastric cancer.
datePublished:2018-03-14T00:00:00Z
dateModified:2018-03-14T00:00:00Z
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keywords:
CDK5RAP3
AKT
GSK-3β
Gastric cancer
Survival
Cancer Research
Immunology
Apoptosis
Oncology
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