Limits...
Specific Inhibition of β-Catenin in Jeko-1 Mantle Cell Lymphoma Cell Line Decreases Proliferation and Induces Apoptosis.

He J, Huang Y, Weng J, Xiao L, Weng K, Ma X - Med. Sci. Monit. (2015)

Bottom Line: In vitro studies indicated that β-catenin knockdown significantly inhibited cell proliferation and induced apoptosis in Jeko-1 cells.Both inhibitory agents increased Bax and caspase 3 proteins, and decreased Bcl-2, c-Myc, and Cyclin D1 proteins.The specific inhibition of β-catenin induces apoptosis and growth arrest, making it a potential therapeutic target against MCL.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, Zhangzhou Hospital Affiliated to Fujian Medical University, Zhangzhou, Fujian, China (mainland).

ABSTRACT

Background: The canonical Wnt signaling pathway has been considered as a potent oncogenic signaling in the initiation and progression of hematological malignancies. As a key regulator of the Wnt signaling pathway, the role of β-catenin in mantle cell lymphoma (MCL) pathogenesis and progression was investigated in this study.

Material and methods: A total of 30 MCL samples were collected from patients and were examined for the expression of β-catenin and p-GSK3β using immunohistochemical (IHC) staining. Further in vitro studies employed MTT and Western blot assays detecting proliferation and apoptosis-related proteins in MCL cell line Jeko-1, which were transfected with β-catenin shRNA or specific inhibitor XAV939.

Results: Expression of β-catenin and phosphorylated glycogen synthase kinase-3 beta (p-GSK3β) in MCL was significantly higher than those in controlled samples. In vitro studies indicated that β-catenin knockdown significantly inhibited cell proliferation and induced apoptosis in Jeko-1 cells. Furthermore, XAV939 induced apoptosis and growth arrest in Jeko-1 cells. Both inhibitory agents increased Bax and caspase 3 proteins, and decreased Bcl-2, c-Myc, and Cyclin D1 proteins.

Conclusions: The specific inhibition of β-catenin induces apoptosis and growth arrest, making it a potential therapeutic target against MCL.

No MeSH data available.


Related in: MedlinePlus

Immunohistochemical (IHC) images of β-catenin p-GSK3β in MCL and control samples (×200). A and B show representative images of β-catenin in control and MCL tissues; C and D show representative staining images of p-GSK3β in control and MCL tissues. Higher expression level of β-catenin and p-GSK3β existed in MCL tissues (B, D) when compared to control samples (A, C).
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4554364&req=5

f1-medscimonit-21-2218: Immunohistochemical (IHC) images of β-catenin p-GSK3β in MCL and control samples (×200). A and B show representative images of β-catenin in control and MCL tissues; C and D show representative staining images of p-GSK3β in control and MCL tissues. Higher expression level of β-catenin and p-GSK3β existed in MCL tissues (B, D) when compared to control samples (A, C).

Mentions: We measured the expression level of β-catenin and p-GSK3β protein in 30 MCL samples using IHC staining. β-catenin protein was found to be expressed in both nucleus and cytoplasm of MCL cells. In controlled samples, however, it was located only on the membrane s (Figure 1A, 1B). In total, we found 73.33% (22/30) β-catenin positive expression in MCL samples but only 6.67% (2/30) positive rates in controlled ones (chi-squared test, P<0.05). p-GSK3β protein was expressed in the nucleus (Figure 1C, 1D). About 66.67% (20/30) of MCL samples showed p-GSK3β-positive expression, while only 16.67% (5/30) of controlled samples showed p-GSK3β signals (P<0.05). Our results collectively indicate that the expression of β-catenin and p-GSK3β is up-regulated in MCL.


Specific Inhibition of β-Catenin in Jeko-1 Mantle Cell Lymphoma Cell Line Decreases Proliferation and Induces Apoptosis.

He J, Huang Y, Weng J, Xiao L, Weng K, Ma X - Med. Sci. Monit. (2015)

Immunohistochemical (IHC) images of β-catenin p-GSK3β in MCL and control samples (×200). A and B show representative images of β-catenin in control and MCL tissues; C and D show representative staining images of p-GSK3β in control and MCL tissues. Higher expression level of β-catenin and p-GSK3β existed in MCL tissues (B, D) when compared to control samples (A, C).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4554364&req=5

f1-medscimonit-21-2218: Immunohistochemical (IHC) images of β-catenin p-GSK3β in MCL and control samples (×200). A and B show representative images of β-catenin in control and MCL tissues; C and D show representative staining images of p-GSK3β in control and MCL tissues. Higher expression level of β-catenin and p-GSK3β existed in MCL tissues (B, D) when compared to control samples (A, C).
Mentions: We measured the expression level of β-catenin and p-GSK3β protein in 30 MCL samples using IHC staining. β-catenin protein was found to be expressed in both nucleus and cytoplasm of MCL cells. In controlled samples, however, it was located only on the membrane s (Figure 1A, 1B). In total, we found 73.33% (22/30) β-catenin positive expression in MCL samples but only 6.67% (2/30) positive rates in controlled ones (chi-squared test, P<0.05). p-GSK3β protein was expressed in the nucleus (Figure 1C, 1D). About 66.67% (20/30) of MCL samples showed p-GSK3β-positive expression, while only 16.67% (5/30) of controlled samples showed p-GSK3β signals (P<0.05). Our results collectively indicate that the expression of β-catenin and p-GSK3β is up-regulated in MCL.

Bottom Line: In vitro studies indicated that β-catenin knockdown significantly inhibited cell proliferation and induced apoptosis in Jeko-1 cells.Both inhibitory agents increased Bax and caspase 3 proteins, and decreased Bcl-2, c-Myc, and Cyclin D1 proteins.The specific inhibition of β-catenin induces apoptosis and growth arrest, making it a potential therapeutic target against MCL.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, Zhangzhou Hospital Affiliated to Fujian Medical University, Zhangzhou, Fujian, China (mainland).

ABSTRACT

Background: The canonical Wnt signaling pathway has been considered as a potent oncogenic signaling in the initiation and progression of hematological malignancies. As a key regulator of the Wnt signaling pathway, the role of β-catenin in mantle cell lymphoma (MCL) pathogenesis and progression was investigated in this study.

Material and methods: A total of 30 MCL samples were collected from patients and were examined for the expression of β-catenin and p-GSK3β using immunohistochemical (IHC) staining. Further in vitro studies employed MTT and Western blot assays detecting proliferation and apoptosis-related proteins in MCL cell line Jeko-1, which were transfected with β-catenin shRNA or specific inhibitor XAV939.

Results: Expression of β-catenin and phosphorylated glycogen synthase kinase-3 beta (p-GSK3β) in MCL was significantly higher than those in controlled samples. In vitro studies indicated that β-catenin knockdown significantly inhibited cell proliferation and induced apoptosis in Jeko-1 cells. Furthermore, XAV939 induced apoptosis and growth arrest in Jeko-1 cells. Both inhibitory agents increased Bax and caspase 3 proteins, and decreased Bcl-2, c-Myc, and Cyclin D1 proteins.

Conclusions: The specific inhibition of β-catenin induces apoptosis and growth arrest, making it a potential therapeutic target against MCL.

No MeSH data available.


Related in: MedlinePlus