scholarly journals Factors Affecting the Recurrence of Giant Cell Tumor of Bone After Surgery: A Clinicopathological Study of 80 Cases from a Single Center

2015 ◽  
Vol 36 (5) ◽  
pp. 1961-1970 ◽  
Author(s):  
Dong-dong Cheng ◽  
Tu Hu ◽  
Hui-zhen Zhang ◽  
Jin Huang ◽  
Qing-cheng Yang
Keyword(s):  
Giant Cell Tumor ◽  
Pathological Fracture ◽  
Cell Tumor ◽  
Migration And Invasion ◽  
Ki 67 ◽  
Factors Affecting ◽  
Surgical Method ◽  
Kaplan Meier ◽  
Cd147 Expression

Background/Aims: This aim of the present study was to identify specific markers determining the recurrence of the giant cell tumor of bone (GCTB). Methods: This study involved the clinicopathological analysis of 80 cases. All of the clinical features, pathological fracture, Campanacci grade, histological features and surgical methods were reviewed. Immunohistochemistry was used to detect the expression of Ki-67, CD147, mutant p53 and p63 in GCTB. Comparisons between different groups were performed using the Chi-square test. The risk factors affecting recurrence were analyzed using a binary logistic model. Kaplan-Meier analysis was employed for the survival analysis between the groups. Cell proliferation assays, migration and invasion assays were used to detect the function of CD147 on GCTB in vitro. Results: The univariate analysis showed that Ki-67 and CD147 expression, pathological fracture, Campanacci grade and surgical method were associated with recurrence. The multivariate analysis revealed that CD147 expression, Campanacci grade and surgical method were the factors affecting GCTB recurrence. In addition, the Kaplan-Meier analysis revealed that these factors affected tumor-free survival time. In vitro study revealed that the CD147 knockdown by small interfering RNA (siRNA) technique dramatically reduced the proliferation, migration and invasion of GCTB. Conclusion: Our results suggest that CD147 may serve as an adequate marker for GCTB recurrence. Campanacci grade is a risk factor for GCTB recurrence, which is also affected by the surgical method used.

scholarly journals Overexpressed P75CUX1 promotes EMT in glioma infiltration by activating β-catenin

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Anqi Xu ◽  
Xizhao Wang ◽  
Jie Luo ◽  
Mingfeng Zhou ◽  
Renhui Yi ◽  
...  
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Tumor Grade ◽  
Prognostic Indicator ◽  
Migration And Invasion ◽  
Poor Overall Survival ◽  
Mesenchymal Transition ◽  
Kaplan Meier ◽  
Homeobox Protein

AbstractThe homeobox protein cut-like 1 (CUX1) comprises three isoforms and has been shown to be involved in the development of various types of malignancies. However, the expression and role of the CUX1 isoforms in glioma remain unclear. Herein, we first identified that P75CUX1 isoform exhibited consistent expression among three isoforms in glioma with specifically designed antibodies to identify all CUX1 isoforms. Moreover, a significantly higher expression of P75CUX1 was found in glioma compared with non-tumor brain (NB) tissues, analyzed with western blot and immunohistochemistry, and the expression level of P75CUX1 was positively associated with tumor grade. In addition, Kaplan–Meier survival analysis indicated that P75CUX1 could serve as an independent prognostic indicator to identify glioma patients with poor overall survival. Furthermore, CUX1 knockdown suppressed migration and invasion of glioma cells both in vitro and in vivo. Mechanistically, this study found that P75CUX1 regulated epithelial–mesenchymal transition (EMT) process mediated via β-catenin, and CUX1/β-catenin/EMT is a novel signaling cascade mediating the infiltration of glioma. Besides, CUX1 was verified to promote the progression of glioma via multiple other signaling pathways, such as Hippo and PI3K/AKT. In conclusion, we suggested that P75CUX1 could serve as a potential prognostic indicator as well as a novel treatment target in malignant glioma.

Giant Cell Tumor of Bone: A Model for the in Vitro Human Osteoclast Characterization

1989 ◽  
Vol 75 (4) ◽  
pp. 389-395 ◽  
Author(s):  
Mario Campanacci ◽  
Gian Paolo Bagnara ◽  
Massimo Serra ◽  
Marco Giovannini ◽  
Paolo Tornasi ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Giant Cell Tumor ◽  
Giant Cell ◽  
Giant Cells ◽  
Cell Tumor ◽  
Cell Populations ◽  
In Vitro Growth ◽  
Human Osteoclast ◽  
High Doses

The in vitro growth pattern of cells obtained from bioptic material of ten patients with giant cell tumor of bone (GCT) was investigated. Cytochemical reactions and monoclonal antibodies raised against macrophage markers were tested on the two histologically identifiable GCT cell populations. Only monoclonal antibody EBM/11 stained both mononuclear and giant cells. EBM/11 positivity and resistance of acid phosphatase to high doses of tartrate strongly suggest that both mononuclear and giant cells belong to the same lineage.

scholarly journals Overexpression of CLEC18B Associates With the Proliferation, Migration, and Prognosis of Glioblastoma

ASN NEURO ◽  
2018 ◽  
Vol 10 ◽  
pp. 175909141878194 ◽  
Author(s):  
Rui-Ming Guo ◽  
Cheng-Bin Zhao ◽  
Peng Li ◽  
Liang Zhang ◽  
Su-Hua Zang ◽  
...  
Keyword(s):  
Inverse Correlation ◽  
The Cancer Genome Atlas ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Loss Of Function ◽  
Lectin Domain ◽  
Kaplan Meier ◽  
Cancer Genome Atlas ◽  
Interfering Rna

C-type lectin domain family 18 member B (CLEC18B), encoding a superfamily of CLEC, has been found to be expressed in some of cancer cells, which possibly indicates it associated with cancer. However, the defined functional characterizations of CLEC18B in glioblastoma multiforme (GBM) progression still remain unclear. To this end, clinical relevance of CLEC18B expression with GBM patients’ prognosis was analyzed both in The Cancer Genome Atlas dataset of 174 tissues and 40 GBM tumor tissues collected from our hospital by using the Kaplan–Meier survival and the Cox proportional hazard model. The role of CLEC18B in GBM was determined by loss-of-function assay using small interfering RNA approach in vitro. Functional and signaling analyses were also performed to understand how CLEC18B facilitated the aggressiveness of GBM at molecular and cellular levels using Cell Counting Kit-8 assay, wound-healing, transwell, and Western blot analyses. Results from our analyses showed that CLEC18B was markedly elevated in both GBM tissues and cells, and exhibited strong inverse correlation with overall survival in GBM patients. Moreover, CLEC18B was identified as an independent predictor of patient survival. Functionally, knockdown of CLEC18B inhibited the growth, migration, and invasion of GBM cells. Mechanistic studies revealed that silencing of CLEC18B resulted in downregulation of Wnt/β-catenin signaling activity. Collectively, our findings provide clinical, molecular, and cellular evidence of CLEC18B as a promising prognostic biomarker and therapeutic target for GBM.

scholarly journals Diamond Nanoparticles Downregulate Expression of CycD and CycE in Glioma Cells

Molecules ◽  
2019 ◽  
Vol 24 (8) ◽  
pp. 1549 ◽  
Author(s):  
Marta Grodzik ◽  
Jaroslaw Szczepaniak ◽  
Barbara Strojny-Cieslak ◽  
Anna Hotowy ◽  
Mateusz Wierzbicki ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Glioma Cells ◽  
Migration And Invasion ◽  
Control Group ◽  
Ki 67 ◽  
Normal Cells ◽  
Diamond Nanoparticles ◽  
Dividing Cells

Our previous studies have shown that diamond nanoparticles (NDs) exhibited antiangiogenic and proapoptotic properties in vitro in glioblastoma multiforme (GBM) cells and in tumors in vivo. Moreover, NDs inhibited adhesion, leading to the suppression of migration and invasion of GBM. In the present study, we hypothesized that the NDs might also inhibit proliferation and cell cycle in glioma cells. Experiments were performed in vitro with the U87 and U118 lines of GBM cells, and for comparison, the Hs5 line of stromal cells (normal cells) after 24 h and 72 h of treatment. The analyses included cell morphology, cell death, viability, and cell cycle analysis, double timing assay, and gene expression (Rb, E2F1, CycA, CycB, CycD, CycE, PTEN, Ki-67). After 72 h of ND treatment, the expression level of Rb, CycD, and CycE in the U118 cells, and E2F1, CycD, and CycE in the U87 cells were significantly lower in comparison to those in the control group. We observed that decreased expression of cyclins inhibited the G1/S phase transition, arresting the cell cycle in the G0/G1 phase in glioma cells. The NDs did not affect the cell cycle as well as PTEN and Ki-67 expression in normal cells (Hs5), although it can be assumed that the NDs reduced proliferation and altered the cell cycle in fast dividing cells.

scholarly journals The Role of TWIST in Angiogenesis and Cell Migration in Giant Cell Tumor of Bone

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Shalini Singh ◽  
Isabella W. Y. Mak ◽  
Divya Handa ◽  
Michelle Ghert
Keyword(s):  
Cell Migration ◽  
Giant Cell Tumor ◽  
Giant Cell ◽  
Stromal Cells ◽  
Epithelial Mesenchymal Transition ◽  
Cell Tumor ◽  
Stable Cell Line ◽  
Mesenchymal Transition

Giant cell tumor of bone (GCT) is a bone tumor consisting of numerous multinucleated osteoclastic giant cells involved in bone resorption and neoplastic osteoblast-like stromal cells responsible for tumor growth. The tumor occasionally metastasizes to the lung; however, factors leading to metastasis in this tumor are unknown. The TWIST-1 protein (also referred to as TWIST) has been suggested to be involved in epithelial-mesenchymal transition (EMT) and tumor progression in some cancers. In this study we investigated the functional role of TWIST in GCT cell angiogenesis and migration. Overexpression of TWIST in neoplastic GCT stromal cells significantly increased mRNA and protein expression of VEGF and VEGFR1 in vitro, whereas knockdown of TWIST resulted in decreased VEGF and VEGFR1 expression. A stable cell line with TWIST overexpression resulted in features of EMT including increased cell migration and downregulation of E-cadherin. The results of our study indicate that TWIST may play an important role in angiogenesis and cell migration in GCT.

scholarly journals Elevated FOXC2 Expression Promotes Invasion of HCC Cell Lines and is Associated with Poor Prognosis in Hepatocellular Carcinoma

2017 ◽  
Vol 44 (1) ◽  
pp. 99-109 ◽  
Author(s):  
Fang Yang ◽  
Lizhi Lv ◽  
Kun Zhang ◽  
Qiucheng Cai ◽  
Jianyong Liu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Flow Cytometric Analysis ◽  
Vital Role ◽  
Migration And Invasion ◽  
Flow Cytometric ◽  
Kaplan Meier ◽  
Proliferation Assays ◽  
The Relationship

Background/Aims: Increasing evidence has indicated that Forkhead box protein C2 (FOXC2) plays an important role in carcinogenesis. However, the expression and the role of FOXC2 in hepatocellular carcinoma (HCC) have not been extensively studied. Methods: FOXC2 expression was analyzed by quantitative real-time polymerase chain reaction, Western blot analysis and immunohistochemistry in HCC tissue and cells. The relationship between FOXC2 expression and patient clinical significance and survival were assessed by Pearson’s correlation and Kaplan-Meier analysis, respectively. Cell proliferation assays, colony formation assays, flow cytometric analysis and Transwell assays were employed to measure the effects of FOXC2 on HCC cells in vitro. Results: The expression of FOXC2 was increased in HCC tissue, and high FOXC2 expression was associated with worse patient survival. Knockdown of FOXC2 inhibited HCC cell growth, migration, and invasion in vitro, as well as tumor growth. Furthermore, we found that activation of AKT-mediated MMP-2 and MMP-9 was involved in FOXC2 promoting an aggressive phenotype. Conclusions: Taken together, these findings demonstrate that FOXC2 is upregulated in HCC tissue and is associated with tumor size, vascular invasion and advanced TNM stage. Further investigation suggested that FOXC2 may play a vital role in promoting proliferation and invasion in HCC and serves as a novel therapeutic target in HCC.

Metachronous multicentric giant-cell tumor of the bone in the lower limb. Case report and Ki-67 immunohistochemistry study

2003 ◽  
Vol -1 (1) ◽  
pp. 1-1
Author(s):  
Marc-Antoine Rousseau ◽  
Adriana Handra-Luca ◽  
Jean-Yves Lazennec ◽  
Yves Catonn� ◽  
G�rard Saillant
Keyword(s):  
Case Report ◽  
Giant Cell Tumor ◽  
Giant Cell ◽  
Lower Limb ◽  
Cell Tumor ◽  
Ki 67

scholarly journals Combination of Melatonin and Zoledronic Acid Suppressed the Giant Cell Tumor of Bone in vitro and in vivo

2021 ◽  
Vol 9 ◽  
Author(s):  
Xudong Wang ◽  
Peiqiang Su ◽  
Yan Kang ◽  
Caixia Xu ◽  
Jincheng Qiu ◽  
...  
Keyword(s):  
Zoledronic Acid ◽  
Osteogenic Differentiation ◽  
Giant Cell Tumor ◽  
Giant Cell ◽  
Therapeutic Effect ◽  
Antitumor Effect ◽  
Cell Tumor ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Antitumor Effects

Melatonin (Mlt) confers potential antitumor effects in various types of cancer. However, to the best of our knowledge, the role of Mlt in the giant cell tumor of bone (GCTB) remains unknown. Moreover, further research is required to assess whether Mlt can enhance the therapeutic effect of zoledronic acid (Zol), a commonly used anti-GCTB drug. In this research, we investigated the effects of Mlt, Zol, and the combination of these two drugs on GCTB cells’ characteristics, including cell proliferation, apoptosis, osteogenic differentiation, migration, and invasion. The cell counting kit-8 (CCK-8) assay, colony formation assay, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay (TUNEL), alkaline phosphatase (ALP) staining, alizarin red staining (ARS), scratch wound healing assay, and transwell experiment were performed, respectively. Our results showed that Mlt could effectively inhibit the proliferation, migration, and invasion of GCTB cells, as well as promote the apoptosis and osteogenic differentiation of tumor cells. Of note, a stronger antitumor effect was observed when Mlt was combined with Zol treatment. This therapeutic effect might be achieved by inhibiting the activation of both the Hippo and NF-κB pathways. In conclusion, our study suggests that Mlt can be a new treatment for GCTB, which could further enhance the antitumor effect of Zol.

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