Apoptosis in Giant Cell Tumors of Bone.

Kakizoe, Mitsuo

doi:10.2739/kurumemedj.47.125

Cited by 2 publications

(2 citation statements)

References 23 publications

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“…Alternatively p63 could regulate cell death or proliferation. p63 can induce expression of molecules such as CD95 and TRAIL which influence apoptosis, [25][26][27][28] or inhibit proliferation by blocking binding of the NF-Y transcription factor which is required for transcription of cyclin B and cdk1 genes involved in regulating the cell cycle. 29 Determination of the functional significance of p63 in giant cell tumor of bone requires further study.…”

Section: Discussionmentioning

confidence: 99%

Giant cell tumor of bone express p63

Dickson

Wunder

et al. 2008

Modern Pathology

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p63 contributes to skeletal development and tumor formation; however, little is known regarding its activity in the context of bone and soft tissue neoplasms. The purpose of this study was to investigate p63 expression in giant cell tumor of bone and to determine whether it can be used to discriminate between other giant cell-rich tumors. Seventeen cases of giant cell tumor of bone were examined to determine the cell type expressing p63 and identify the isoforms present. Total RNA or cell protein was extracted from mononuclear-or giant cellenriched fractions or intact giant cell tumor of bone and examined by RT-PCR or western blot, respectively. Immunohistochemistry was used to evaluate p63 expression in paraffin embedded sections of giant cell tumor of bone and in tumors containing multinucleated giant cells, including: giant cell tumor of tendon sheath, pigmented villonodular synovitis, aneurysmal bone cyst, chondroblastoma, and central giant cell granuloma. The mononuclear cell component in all cases of giant cell tumor of bone was found to express all forms of TAp63 (a, b, and c), whereas only low levels of the TAp63 a and b isoforms were detected in multinucleated cells; DNp63 was not detected in these tumors. Western blot analysis identified p63 protein as being predominately localized to mononuclear cells compared to giant cells. This was confirmed by immunohistochemical staining of paraffin-embedded tumor sections, with expression identified in all cases of giant cell tumor of bone. Only a proportion of cases of aneurysmal bone cyst and chondroblastoma showed p63 immunoreactivity whereas it was not detected in central giant cell granuloma, giant cell tumor of tendon sheath, or pigmented villonodular synovitis. The differential expression of p63 in giant cell tumor of bone and central giant cell granuloma suggest that these two tumors may have a different pathogenesis. Moreover, p63 may be a useful biomarker to differentiate giant cell tumor of bone from central giant cell granuloma and other giant cell-rich tumors, such as giant cell tumor of tendon sheath and pigmented villonodular synovitis.

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Section: Discussionmentioning

confidence: 99%

Giant cell tumor of bone express p63

Dickson

Wunder

et al. 2008

Modern Pathology

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“…It is well known that the transformation of cancer cells leads to an increasing trend of apoptosis. Therefore, apoptosis of multinucleated giant cells and stromal cells may increase in GCTB to regulate tumor regression. Our understanding of the anti‐proliferation and apoptosis mechanisms will enable us to put forward more rational methods of cancer treatment.…”

Section: Introductionmentioning

confidence: 99%

Paclitaxel Induce Apoptosis of Giant Cells Tumor of Bone via TP53INP1 Signaling

Xiao

Zong

Qiu

et al. 2018

Orthopaedic Surgery

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Objective To evaluate the antitumor capability and to investigate the underlying molecular mechanism of paclitaxel. Methods First, cck‐8 and apoptosis assays were used to determine survival and apoptotic effects of HS 737.T cells under treatment of paclitaxel. Next, RNA‐seq and bioinformatics were used to determine the differentially expressed genes and to analyze the pathway involved. Quantitative real‐time polymerase chain reaction was used to verify the accuracy of some differentially expressed genes (DEG). ClueGO was used to decode and visualize functionally grouped GO terms of differentially expressed genes, and to map the DEG protein–protein interactions (PPI) network. Western blotting was used to check the expression of target genes, the cleavage of Caspase‐3 and PARP1, and the phosphorylation level of p53. Finally, transcriptomics, bioinformatics, and RNAi were used to estimate the antitumor capability and to identify the underlying mechanisms of paclitaxel in GCTB. Results Our data revealed that paclitaxel had significant time‐dependent effects on the viability and induced apoptosis of HS 737.T cells. RNA‐seq and bioinformatics analysis showed that apoptosis, death receptor signaling pathway, TNF signaling pathway, and TP53 regulated transcription of cell death genes pathway were closely associated with paclitaxel in the treatment of GCTB. Western bolt results revealed that paclitaxel induced cleavage of Caspase‐3 and PARP1, and increased the phosphorylation level of p53 in HS 737.T cells. RNAi results showed that the expression level of TP53INP1 was significantly decreased in HS737.T cells (the decrease was more than 70%). In addition, we found that the inhibitory ratios of paclitaxel on HS737.T cells deficient in TP53INP1 were less than in HS737.T cells with empty vector (19.88 and 40.60%, respectively). Hence, our data revealed that TP53INP1 regulated paclitaxel‐driven apoptosis in HS737.T cells. Conclusion Paclitaxel can significantly repress cell proliferation and induce apoptosis of HS 737.T cells through activating Caspase‐3, PARP1, p53, and TP53INP1. Paclitaxel may be an effective drug in the management of GCTB.

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Apoptosis in Giant Cell Tumors of Bone.

Cited by 2 publications

References 23 publications

Giant cell tumor of bone express p63

Giant cell tumor of bone express p63

Paclitaxel Induce Apoptosis of Giant Cells Tumor of Bone via TP53INP1 Signaling

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