Paclitaxel Induce Apoptosis of Giant Cells Tumor of Bone <i>via</i> TP53INP1 Signaling

Xiao, Weiyuan; Zong, Zhen; Qiu, Manle; Chen, Xiuyuan; Shen, Hongxing; Lao, Li

doi:10.1111/os.12414

Cited by 8 publications

(5 citation statements)

References 32 publications

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“…The RT-PCR analysis further confirmed that CXCL8 was downregulated significantly upon the Siglec-15 knockdown ( Figure 8 E). Many studies have indicated that the CXCL family plays critical roles in the regulation of cancer development [ 29 , 30 , 31 ]. To identify the downstream genes linked to CXCL8, we found the nine highest-linked candidate genes (CXCL2, CXCL3, CXCL5, CXCL10, CXCL11, ADORA1, BDKRB1, C5AR1, and NMU) in module 2 ( Figure 8 D).…”

Section: Resultsmentioning

confidence: 99%

“…The human GCTB stromal cells (Hs737. T) were purchased from the American Type Culture Collection (ATCC) and were then cultured in a high-glucose DMEM, containing 15% FBS and 1% penicillin/streptomycin, at 37 °C in a humidified 5% CO 2 atmosphere [ 29 ]. When the GCTB stromal cell confluence reached 80–90%, the cells were digested by 0.25% trypsin-EDTA.…”

Section: Methodsmentioning

confidence: 99%

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Siglec-15 as a New Perspective Therapy Target in Human Giant Cell Tumor of Bone

et al. 2022

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The main features of a giant cell tumor of bone (GCTB) are frequent recurrence and aggressive osteolysis, which leads to a poor prognosis in patients. Although the treatment methods for a GCTB, such as scraping and resection, effectively inhibit the disease, the tendency toward malignant transformation remains. Therefore, it is important to identify new treatment methods for a GCTB. In this study, we first found high Siglec-15 expression in GCTB tissues, which was significantly associated with Campanacci staging and tumor recurrence. In Spearman’s analysis, Siglec-15 expression was significantly correlated with Ki-67 levels in tumor tissues. In vitro, the mRNA and protein levels of Siglec-15 were high in GCTB stromal cells (Hs737. T), and Siglec-15 knockdown inhibited the biological characteristics of GCTB stromal cells. The RNA sequencing results enabled a prediction of the downstream genes by using the Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Ontology (GO), and MCODE analyses, and the findings showed that CXCL8 was significantly regulated by Siglec-15 and might be a promising downstream target gene of Siglec-15. Therefore, Siglec-15 may be a potential immunotherapy target for a GCTB.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Siglec-15 as a New Perspective Therapy Target in Human Giant Cell Tumor of Bone

et al. 2022

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“…Our study found that miR-205-5p and TP53INP1 were involved in curcumin-mediated effects on the biological functions of C6661-IR, and the former directly targeted the latter. TP53INP1 is located on the human chromosome 8q22 and plays a vital role in the apoptotic network [41]. It can be activated by p53, p73, and E2F, leading to apoptosis and cell cycle arrest [42].…”

Section: Discussionmentioning

confidence: 99%

Curcumin Increases Radiosensitivity of Radioresistant Nasopharyngeal Cancer

Wang¹,

Jun²,

Wang³

et al. 2023

Discovery Medicine

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Objectives: To study the effects of curcumin on the proliferation, invasion, apoptosis, and radiosensitivity of the radioresistant nasopharyngeal carcinoma (NPC) C6661-IR strain as well as the potential radiosensitization mechanism. Methods: NPC cells were continuously irradiated with different intensities of radiation to induce radiation-resistant cell lines. A plate clone formation assay was used to evaluate the effect of curcumin on the radiosensitivity of NPC cells. 3-(4,5-Dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide thiazolyl blue (MTT) assay was conducted to detect changes in cell viability. Flow cytometry was employed to analyze apoptosis percentage as well as Transwell® assay and immunofluorescence assay to observe cell invasion. Western blotting was applied to detect the expression levels of Bax, Bcl-2, and pro/cleaved-caspase 3. MiR-205-5p mimics and si-TP53INP1 were synthesized and transfected into C6661-IR cells, and the cells were then incubated with 10 µm/L curcumin. Real-time quantitative reverse transcription PCR (RT-qPCR) was used to measure miR-205-5p levels and western blotting was conducted to detect the expression of TP53INP1. Results: The optimal radiation dose of X-ray was 6 Gy, and this dose was used in all subsequent experiments. Curcumin treatment significantly inhibited the proliferation and invasion of C6661-IR cells, promoted apoptosis and enhanced radiosensitivity. Compared to the 0 Gy+Cur group and the 6 Gy+Cur group, the miR-205-5p levels were higher in the C6661-IR cells of the 0 Gy and 6 Gy groups. Moreover, miR-204-5p was found to directly target TP53INP1. Curcumin downregulated miR-205-5p levels and upregulated TP53INP1 expression (p < 0.05). Thus, modulation of miR-205-5p or TP53INP1 expression attenuates the biological effects of curcumin on C6661-IR cells. Conclusions: Curcumin inhibited the proliferation and invasion of C6661-IR, promoted apoptosis, and enhanced its radiosensitivity to X-rays by mediating miR-205-5p/TP53INP1 expression.

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“…Apoptosis is widely accepted as a process of programmed cell death. Studies have shown that PTX and its agent can induce apoptosis of tumor cells, such as giant cells, sarcoma cells, lung cancer cells, breast cancer cells, and liver cancer cells ( Ren et al, 2018 ; Xiao et al, 2019 ; Li et al, 2020 ; Xiaomeng et al, 2020 ). Therefore, we investigated whether PTX induces FLS apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Paclitaxel Inhibits Synoviocyte Migration and Inflammatory Mediator Production in Rheumatoid Arthritis

et al. 2021

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Activated fibroblast-like synoviocytes (FLSs) play a crucial role in the pathogenesis and progression of rheumatoid arthritis (RA). It is urgent to develop new drugs that can effectively inhibit the abnormal activation of RA-FLS. In our study, the RA-FLS cell line, MH7A, and mice with collagen-induced arthritis (CIA) were used to evaluate the effect of paclitaxel (PTX). Based on the results, PTX inhibited the migration of RA-FLS in a dose-dependent manner and significantly reduced the spontaneous expression of IL-6, IL-8, and RANKL mRNA and TNF-α-induced transcription of the IL-1β, IL-8, MMP-8, and MMP-9 genes. However, PTX had no significant effect on apoptosis in RA-FLS. Mechanistic studies revealed that PTX significantly inhibited the TNF-α-induced phosphorylation of ERK1/2 and JNK in the mitogen-activated protein kinase (MAPK) pathway and suppressed the TNF-α-induced activation of AKT, p70S6K, 4EBP1, and HIF-1α in the AKT/mTOR pathway. Moreover, PTX alleviated synovitis and bone destruction in CIA mice. In conclusion, PTX inhibits the migration and inflammatory mediator production of RA-FLS by targeting the MAPK and AKT/mTOR signaling pathways, which provides an experimental basis for the potential application in the treatment of RA.

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

Cited by 8 publications

References 32 publications

Siglec-15 as a New Perspective Therapy Target in Human Giant Cell Tumor of Bone

Siglec-15 as a New Perspective Therapy Target in Human Giant Cell Tumor of Bone

Curcumin Increases Radiosensitivity of Radioresistant Nasopharyngeal Cancer

Paclitaxel Inhibits Synoviocyte Migration and Inflammatory Mediator Production in Rheumatoid Arthritis

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