FNC, a Novel Nucleoside Analogue, Blocks Invasion of Aggressive Non-Hodgkin Lymphoma Cell Lines Via Inhibition of the Wnt/β-Catenin Signaling Pathway

Zhang, Yan; Wang, Chenping; Ding, Xi-Xi; Wang, Ning; Ma, Fang; Jiang, Jinhua; Wang, Qingduan; Chang, Junbiao

doi:10.7314/apjcp.2014.15.16.6829

Cited by 17 publications

(12 citation statements)

References 27 publications

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“…Invasion and metastasis are important biological characteristics of malignant tumors. The processes are quite complicated and involve multiple molecular mechanisms, including the adhesion, migration and invasion . Cadherins are a family of transmembrane glycoproteins that play an indispensable role in intercellular adhesion.…”

Section: Discussionmentioning

confidence: 99%

Bone morphogenetic protein‐2 promotes osteosarcoma growth by promoting epithelial‐mesenchymal transition (EMT) through the Wnt/β‐catenin signaling pathway

Tian

Zhou

Chen

et al. 2019

Journal Orthopaedic Research

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The correlation between BMP-2 and osteosarcoma growth has gained increased interest in the recent years, however, there is still no consensus. In this study, we tested the effects of BMP-2 on osteosarcoma cells through both in vitro and in vivo experiments. The effect of BMP-2 on the proliferation, migration and invasion of osteosarcoma cells was tested in vitro. Subcutaneous and intratibial tumor models were used for the in vivo experiments in nude mice. The effects of BMP-2 on EMT of osteosarcoma cells and the Wnt/b-catenin signaling pathway were also tested using a variety of biochemical methods. In vitro tests did not show a significant effect of BMP-2 on tumor cell proliferation. However, BMP-2 increased the mobility of tumor cells and the invasion assay demonstrated that BMP-2 promoted invasion of osteosarcoma cells in vitro. In vivo animal study showed that BMP-2 dramatically enhanced tumor growth. We also found that BMP-2 induced EMT of osteosarcoma cells. The expression levels of Axin2 and Dkk-1 were both down regulated by BMP-2 treatment, while b-catenin, c-myc and Cyclin-D1 were all upregulated. The expression of Wnt3a and p-GSK-3b were also significantly upregulated indicating that the Wnt/b-catenin signaling pathway was activated during the EMT of osteosarcoma driven by BMP-2. From this study, we can conclude that BMP-2 significantly promotes growth of osteosarcoma cells (143B, MG63), and enhances mobility and invasiveness of tumor cells as demonstrated in vitro. The underlying mechanism might be that BMP-2 promotes EMT of osteosarcoma through the Wnt/b-catenin signaling pathway. ß

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Section: Discussionmentioning

confidence: 99%

Bone morphogenetic protein‐2 promotes osteosarcoma growth by promoting epithelial‐mesenchymal transition (EMT) through the Wnt/β‐catenin signaling pathway

Tian

Zhou

Chen

et al. 2019

Journal Orthopaedic Research

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“…Similar effects were also seen in various human cancer cell lines, such as lung adenocarcinoma and acute myeloid leukemia[15]. Furthermore, FNC could remarkably inhibit the adhesion, migration and invasion of Raji and JeKo-1 cell lines[16]. Based on our previous work, the mantle cell lymphoma cell line JeKo-1 was chosen to further study the effects of FNC on the proliferation of MCL and its molecular mechanism, providing an experimental basis for the early clinical application of FNC.…”

Section: Introductionmentioning

confidence: 65%

FNC efficiently inhibits mantle cell lymphoma growth

Zhang

Ding

et al. 2017

PLoS ONE

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FNC, 2'-deoxy-2'-β-fluoro-4'-azidocytidine, is a novel cytidine analogue, that has shown strong antiproliferative activity in human lymphoma, lung adenocarcinoma and acute myeloid leukemia. In this study, we investigated the effects of FNC on mantle cell lymphoma (MCL) and the underlying mechanisms. In in vitro experiments, cell viability was detected by the CCK8 assay, and cell cycle progression and apoptosis were assessed by flow cytometry, and the expression of relative apoptosis proteins were detected by Western Blot. The in vivo antitumor effect of FNC was investigated in a SCID xenograft model. Finally, the mechanisms of action of FNC were assessed using a whole human genome expression profile chip. The data showed that FNC inhibited cell growth in a dose- and time-dependent manner, and FNC could induce apoptosis by the death recepter pathways in JeKo-1 cells and arrest the cell cycle in the G1/S or G2/M phase. Notably, FNC showed in vivo efficacy in mice bearing JeKo-1 xenograft tumors. Gene expression profile analysis revealed that the differentially expressed genes were mainly focused on the immune system process, cellular process and death. These findings implied that FNC may be a valuable therapeutic in mantle cell lymphoma and provided an experimental basis for the early clinical application of FNC.

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“…They transduce cell proliferation and transformation signals through the phosphorylation and activation of PI3K/AKT, thereby inhibiting apoptosis. Zhang et al (2014) found when studying the non-hodgkin lymphoma that the activation of Wnt/β-catenin signal pathway could induce the downregulation of β-catenin and high expression of E-cadherin thus reducing the expressions of cytoadherence and tumor invasion-related proteins, which finally could inhibit the growth of tumors.We found that E-cadherin and β-catenin gene expression and protein translation were at lower levels in the experimental group than in the control group. However, the expression of caspase-3 was increased in the experimental group compared to the control group.…”

Section: Discussionmentioning

confidence: 99%

Correlation between E-Cadherin-Regulated Cell Adhesion and Human Osteosarcoma MG-63 Cell Anoikis

Lin

Cai²,

Ding³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Purpose: The aim of this study was to investigate the relationship between cell adhesion and anoikis evasion among human osteosarcoma cells (MG-63), and to further study the molecular mechanisms. Materials and Methods: Human osteosarcoma cells (MG-63) were assessed for apoptosis, and caspase-3, E-cadherin and β-catenin expression in EDTA and control non-EDTA groups. Results: MG-63 cells were predominantly aggregated when in suspension, and the suspended cells were more dispersed in the EDTA group. Following culture in suspension for 24 h, 48 h, or 72 h, the rates of apoptosis were 34.88%±3.64%, 59.3%±7.22% and 78.5%±5.21% in the experimental group and 7.34%±2.13%, 14.7%±3.69%, and 21.4%±3.60% in the control group, respectively. Caspase-3 expression progressively increased and E-cadherin and β-catenin were decreased in the experimental group, whereas there was no change in the control group. Conclusions: MG-63 cells could avoid anoikis through cell adhesion, and E-cadherin might play a role in this process.

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FNC, a Novel Nucleoside Analogue, Blocks Invasion of Aggressive Non-Hodgkin Lymphoma Cell Lines Via Inhibition of the Wnt/β-Catenin Signaling Pathway

Cited by 17 publications

References 27 publications

Bone morphogenetic protein‐2 promotes osteosarcoma growth by promoting epithelial‐mesenchymal transition (EMT) through the Wnt/β‐catenin signaling pathway

Bone morphogenetic protein‐2 promotes osteosarcoma growth by promoting epithelial‐mesenchymal transition (EMT) through the Wnt/β‐catenin signaling pathway

FNC efficiently inhibits mantle cell lymphoma growth

Correlation between E-Cadherin-Regulated Cell Adhesion and Human Osteosarcoma MG-63 Cell Anoikis

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