ArticleOrthopaedic surgery2019
Paclitaxel Induce Apoptosis of Giant Cells Tumor of Bone via TP53INP1 Signaling.
Article in Orthopaedic surgery, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Molecular and Antiangiogenic Effects of Paclitaxel-Loaded Nanoparticles: Influence of the Nanocarrier Type.Molecular pharmaceutics · 2026Article
- In Vitro Antitumor and Antimetastatic Activity of a New Lapachol Derivative against Metastatic Breast Carcinoma.Asian Pacific journal of cancer prevention : APJCP · 2024Article
- Siglec-15 as a New Perspective Therapy Target in Human Giant Cell Tumor of Bone.Current oncology (Toronto, Ont.) · 2022Article
- Study on the Mechanism of Action of Paclitaxel-Loaded Polylactic-co-glycolic Acid Nanoparticles in Non-Small-Cell Lung Carcinoma Cells.Computational and mathematical methods in medicine · 2022Article
- Paclitaxel Inhibits Synoviocyte Migration and Inflammatory Mediator Production in Rheumatoid Arthritis.Frontiers in pharmacology · 2021Article
- Wnt Signaling Protects against Paclitaxel-Induced Spiral Ganglion Neuron Damage in the Mouse CochleaBioMed research international · 2019Article
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Authors and funding
6 authors.
Funding
Abstract
objectiveTo evaluate the antitumor capability and to investigate the underlying molecular mechanism of paclitaxel.
methodsFirst, 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.
resultsOur 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.
conclusionPaclitaxel 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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