Human calcitonin has the same inhibitory effect on osteoclastic bone resorption by human giant cell tumor cells as salmon calcitonin

1996 ◽  
Vol 59 (2) ◽  
pp. 100-104 ◽  
Author(s):  
S. Lida ◽  
S. Kakudo ◽  
Y. Mori ◽  
M. Matsui ◽  
K. Magota ◽  
...  
1993 ◽  
Vol &NA; (296) ◽  
pp. 229???241 ◽  
Author(s):  
RICHARD O. C. OREFFO ◽  
G. JUNE MARSHALL ◽  
MARY KIRCHEN ◽  
CARLOS GARCIA ◽  
WOLF E. GALLWITZ ◽  
...  

2010 ◽  
Vol 41 (9) ◽  
pp. 1320-1329 ◽  
Author(s):  
Isabella W.Y. Mak ◽  
Eric P. Seidlitz ◽  
Robert W. Cowan ◽  
Robert E. Turcotte ◽  
Snezana Popovic ◽  
...  

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Baohui Su ◽  
Yanguang Yuan ◽  
Junshan Zhang ◽  
Yuezhong Li ◽  
Qihui Zhang

Objective. To explore the therapeutic effects and mechanism of fluorescent mitoxantrone hydrochloride nanoparticles on giant cell tumor of bone. Methods. The adsorption capacity of nanoparticles to hydroxyapatite (HA), cell adsorption capacity, encapsulation rate, particle size, and potential of the nanoparticles were determined by HPLC and Zetasizer Nano ZS nanomicelle potentiometer. MTT assay was used to determine the toxicity of nanoparticles to cells. The fluorescent intensity of the nanoparticles and their location in the cells were observed under a fluorescence microscope. RT-qPCR and Western blotting were then used to measure the expression levels of miRNA, mRNA, and proteins in cells. Transwell and Annexin V-FITC/PI staining tests were used to study the cell invasion and apoptotic rate, respectively. The dual-luciferase reporter gene experiment was then carried out to verify the binding relationship between miR-125b and its predicted target. Results. ALN-FOL-MTO-NLC nanoparticles showed a stronger adsorption capacity for HA and stronger toxicity to GCTB28 cells. Compared to normal tissues, the expression level of miR-125b in giant bone tumor tissue and cells was significantly downregulated, and the expression level of miR-125b was upregulated to some extent after treatment. Overexpression of miR-125b or treatment of ALN-FOL-MTO-NLC nanoparticles can inhibit the malignant behavior of GCTB28 cells, whereas the inhibition of the expression of miR-125b can promote the malignant behavior of GCTB28 cells. The result showed that parathyroid hormone receptor 1 (PTH1R) was a downstream target gene for miR-125b. Rescue experiment showed that the treatment of GCTB28 with ALN-FOL-MTO-NLC nanoparticles while inhibiting miR-125b expression can reduce the inhibitory effect of miR-125b on the malignant behavior of GCTB28 cells, whereas upregulating the expression levels of miR-125b and PTH1R in GCTB28 cells had no significant effect on the malignant behavior of GCTB28 cells. Conclusion. ALN-FOL-MTO-NLC nanoparticles have a certain inhibitory effect on the malignant behavior of giant cell tumor of bone through the miR-125b/PTH1R molecular axis.


2018 ◽  
Vol 1 (Supplement) ◽  
pp. 44
Author(s):  
A.M. Bratu ◽  
I.A. Sălcianu ◽  
A.I. Nicula ◽  
C. Zaharia ◽  
A.N. Marinescu

Abstract Giant cell tumor of soft tissue (GCTST) is usually of synovial origin. It affects synovial membrane, serous bursae, and tendinous tunnels. The most common localizations are in the hands and forearms. Anatomopathological, GCTST is considered as being composed of a cellular fibroblastic stroma in which the tumor cells are distributed. This type of tumor is composed of a mononuclear complex and osteoclast-like giant multinucleated cells, similar to those found in the giant cell tumor at the bone level. Histologically, some authors consider that GCTST is a strictly benign tumor, consisting of welldefined multinucleated histiocytes admixed with eosinophils, lymphocytes and scattered spindleshaped cells, or hemosiderin deposits in its structure, and tumor cells do not have mitosis or atypia. Other authors consider that GCTST is a type of low-grade sarcoma; this entity was named “malignant fibrous histiocytoma, giant cell type” due to the histological similarity with malignant fibrous histiocytoma. The case of a female patient, suspected of giant cell tumor of the brachioradialis tendon sheath was presented. The MRI aspect of this tumor is not the typical one. The MRI examination consisted of a series of sequences, with T1 and T2 weighted images, fat suppression sequence, performed in all three planes, axial, sagittal, and coronal. Also, the examination was performed native, after the administration of intravenous contrast substance, when the 3D multiplanar sequences were performed. The final diagnosis was the post-operative anatomopathological examination, which confirmed that it was a giant cell tumor. We present this case for its less frequent localization - forearm, and the interest it might have in surgical treatment.


2004 ◽  
Vol 75 (1) ◽  
pp. 71-77 ◽  
Author(s):  
Y. Y. Cheng ◽  
L. Huang ◽  
K. M. Lee ◽  
J. K. Xu ◽  
M. H. Zheng ◽  
...  

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Shang Sang ◽  
Zhichang Zhang ◽  
Shu Qin ◽  
Changwei Li ◽  
Yang Dong

Giant cell tumor (GCT) of bone is an aggressive skeletal tumor characterized by localized bone resorption. MicroRNA-16-5p (miR-16-5p) has been reported to be downregulated in lesions of patients with GCT, but little is known about its role in GCT. To explore the underlying function of miR-16-5p in GCT, we first detected its expression in patients with GCT. The results showed that osteoclast formation increased, whereas miR-16-5p expression considerably decreased with the severity of bone destruction. Furthermore, we found that miR-16-5p expression considerably decreased with the progression of receptor activator of nuclear factor-κB ligand- (RANKL-) induced osteoclastogenesis. Functionally, miR-16-5p mimics significantly reduced RANKL-induced osteoclast formation. However, treatment with an inhibitor of miR-16-5p significantly promoted osteoclastogenesis. These findings reveal that miR-16-5p inhibits osteoclastogenesis and that it may represent a therapeutic target for giant cell tumor of bone.


2016 ◽  
Vol 36 (6) ◽  
pp. 3181-3187
Author(s):  
Joseph Chi-Ching Tsui ◽  
Carol Po-Ying Lau ◽  
Alex Chun Cheung ◽  
Kwok-Chuen Wong ◽  
Lin Huang ◽  
...  

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