Chondrosarcoma of Bone

Leddy, Lee R.; Holmes, R.

doi:10.1007/978-3-319-07323-1_6

Cited by 113 publications

(96 citation statements)

References 55 publications

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“…The advent of effective systemic chemotherapy has dramatically improved long-term survival in other primary malignant bone tumors, such as osteosarcoma and Ewing's sarcoma, chondrosarcoma continues to have a poor prognosis due to the limited effectiveness of adjuvant therapy [1]. Chondrosarcoma shows a predilection for metastasis to the lungs.…”

Section: Discussionmentioning

confidence: 99%

“…The higher the grade, the more likely the tumor is to metastasize to other areas of the body. Although high-grade tumors develop in approximately only 5–10% of chondrosarcoma patients, these aggressive tumors remain the major cause of death [1, 2]. Thus, metastasis is a major obstacle that must be overcome for the successful treatment of chondrosarcoma.…”

Section: Introductionmentioning

confidence: 99%

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Endothelin-1 promotes epithelial-mesenchymal transition in human chondrosarcoma cells by repressing miR-300

Huang

Hsieh

et al. 2016

Oncotarget

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Chondrosarcoma is a malignant tumor of mesenchymal origin predominantly composed of cartilage-producing cells. This type of bone cancer is extremely resistant to radiotherapy and chemotherapy. Surgical resection is the primary treatment, but is often difficult and not always practical for metastatic disease, so more effective treatments are needed. In particular, it would be helpful to identify molecular markers as targets for therapeutic intervention. Endothelin-1 (ET-1), a potent vasoconstrictor, has been shown to enhance chondrosarcoma angiogenesis and metastasis. We report that ET-1 promotes epithelial–mesenchymal transition (EMT) in human chondrosarcoma cells. EMT is a key pathological event in cancer progression, during which epithelial cells lose their junctions and apical-basal polarity and adopt an invasive phenotype. Our study verifies that ET-1 induces the EMT phenotype in chondrosarcoma cells via the AMP-activated protein kinase (AMPK) pathway. In addition, we show that ET-1 increases EMT by repressing miR-300, which plays an important role in EMT-enhanced tumor metastasis. We also show that miR-300 directly targets Twist, which in turn results in a negative regulation of EMT. We found a highly positive correlation between ET-1 and Twist expression levels as well as tumor stage in chondrosarcoma patient specimens. Therefore, ET-1 may represent a potential novel molecular therapeutic target in chondrosarcoma metastasis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Endothelin-1 promotes epithelial-mesenchymal transition in human chondrosarcoma cells by repressing miR-300

Huang

Hsieh

et al. 2016

Oncotarget

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show abstract

“…Chondrosarcoma is a malignant soft tissue sarcoma with poor prognosis, and it is the second most common primary bone tumor among all malignant bone tumors (1). At present, surgical resection remains the primary treatment option for chondrosarcoma (2).…”

Section: Introductionmentioning

confidence: 99%

Puerarin induces cell apoptosis in human chondrosarcoma cell line SW1353 via inhibition of the PI3K/Akt signaling pathway

Huang

Cao

et al. 2017

Oncol Lett

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Abstract. Chondrosarcoma is a malignant soft tissue sarcoma with poor prognosis. Puerarin has been demonstrated to possess anticancer properties; however, the effects of puerarin in human chondrosarcoma cells remain unknown. The present study aimed to investigate the anticancer effects of puerarin in SW1353 human chondrosarcoma cells. SW1353 cells were treated with increasing concentrations of puerarin for different durations. Cell viability was evaluated using MTT assays. Cell apoptosis rates were determined by flow cytometry. The activities of caspase-3 and caspase-9 were measured by enzymatic assay. The expression of RAC-alpha serine/threonine-protein kinase (Akt), phosphorylated-Akt, caspase-3 and apoptosis-associated proteins, including B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax) were detected by western blotting. Puerarin significantly decreased cell viability and significantly induced apoptosis of SW1353 cells. In addition, puerarin significantly increased the enzymatic activities of caspase-3 and caspase-9. Puerarin treatment suppressed the expression of p-Akt and Bcl-2 but promoted the expression of Bax and cleaved caspase-3 in SW1353 cells. Notably, the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 abrogated the decreased phosphorylation of Akt, suggesting that the PI3K/Akt signaling pathway is involved in mediating the anticancer effects of puerarin. The data from the present study indicated that puerarin exhibits anticancer effects in SW1353 cells and may be a potential therapeutic drug for patients with chondrosarcoma.

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“…Chondrosarcoma is a common malignant histological tumor; worldwide, the incidence of chondrosarcoma is second only to that of primary tumors of bone, and male-to-female ratio of the incidence of this disease is 1.5: 1[38]. Recently, the combination of curative surgery with chemotherapy has improved the five-year of patients with chondrosarcoma, but many of these patients either do not respond to chemotherapy or develop drug resistance to current chemotherapy regimens [39].…”

Section: Discussionmentioning

confidence: 99%

Inhibiting ROS-TFEB-Dependent Autophagy Enhances Salidroside-Induced Apoptosis in Human Chondrosarcoma Cells

Zeng

Xiao

Cai

et al. 2017

Cell Physiol Biochem

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Background/Aims: Autophagy modulation has been considered a potential therapeutic strategy for human chondrosarcoma, and a previous study indicated that salidroside exhibits significant anti-carcinogenic activity. However, the ability of salidroside to induce autophagy and its role in human chondrosarcoma cell death remains unclear. Methods: We exposed SW1353 cells to different concentrations of salidroside (0.5, 1 and 2 mM) for 24 h. RT-PCR, Western-blotting, Immunocytofluorescence, and Luciferase Reporter Assays were used to evaluate whether salidroside activated the TFEB-dependent autophagy. Results: We show that salidroside induced significant apoptosis in the human chondrosarcoma cell line SW1353. In addition, we demonstrate that salidroside-induced an autophagic response in SW1353 cells, as evidenced by the upregulation of LC3-II and downregulation of P62. Moreover, pharmacological or genetic blocking of autophagy enhanced salidroside -induced apoptosis, indicating the cytoprotective role of autophagy in salidroside-treated SW1353 cells. Salidroside also induced TFEB ^(Ser142) dephosphorylation, subsequently to activated TFEB nuclear translocation and increase of TFEB reporter activity, which contributed to lysosomal biogenesis and the expression of autophagy-related genes. Importantly, we found that salidroside triggered the generation of ROS in SW1353 cells. Furthermore, NAC, a ROS scavenger, abrogated the effects of salidroside on TFEB-dependent autophagy. Conclusions: These data demonstrate that salidroside increased TFEB-dependent autophagy by activating ROS signaling pathways in human chondrosarcoma cells. These data also suggest that blocking ROS-TFEB-dependent autophagy to enhance the activity of salidroside warrants further attention in treatment of human chondrosarcoma cells.

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Chondrosarcoma of Bone

Cited by 113 publications

References 55 publications

Endothelin-1 promotes epithelial-mesenchymal transition in human chondrosarcoma cells by repressing miR-300

Endothelin-1 promotes epithelial-mesenchymal transition in human chondrosarcoma cells by repressing miR-300

Puerarin induces cell apoptosis in human chondrosarcoma cell line SW1353 via inhibition of the PI3K/Akt signaling pathway

Inhibiting ROS-TFEB-Dependent Autophagy Enhances Salidroside-Induced Apoptosis in Human Chondrosarcoma Cells

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