Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chondrosarcoma is a highly malignant cartilage-forming bone tumor that has the capacity to invade locally and cause distant metastasis. Moreover, chondrosarcoma is intrinsically resistant to conventional chemotherapy or radiotherapy. The novel benzofuran derivative, BL-038 (2-amino-3-(2,6-dichlorophenyl)-6-(4-methoxyphenyl)benzofuran-4-yl acetate), has been evaluated for its anticancer effects in human chondrosarcoma cells. BL-038 caused cell apoptosis in two human chondrosarcoma cell lines, JJ012 and SW1353, but not in primary chondrocytes. Treatment of chondrosarcoma with BL-038 also induced reactive oxygen species (ROS) production. Furthermore, BL-038 decreased mitochondrial membrane potential (MMP) and changed mitochondrial-related apoptosis, by downregulating the anti-apoptotic activity members (Bcl-2, Bcl-xL) and upregulating pro-apoptotic members (Bax, Bak) of the B-cell lymphoma 2 (Bcl-2) family of proteins, key regulators of the apoptotic machinery in cells. These results demonstrate that in human chondrosarcoma cells, the apoptotic and cytotoxic effects of BL-038 are mediated by the intrinsic mitochondria-mediated apoptotic pathway, which in turn causes the release of cytochrome c, the activation of caspase-9 and caspase-3, and the cleavage of poly (ADP-ribose) polymerase (PARP), to elicit apoptosis response. Our results show that the benzofuran derivative BL-038 induces apoptosis in chondrosarcoma cells.
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PMID:BL-038, a Benzofuran Derivative, Induces Cell Apoptosis in Human Chondrosarcoma Cells through Reactive Oxygen Species/Mitochondrial Dysfunction and the Caspases Dependent Pathway. 2761 7

Chondrosarcoma is one of the bone tumor with high mortality in respond to poor radiation and chemotherapy treatment. Here, we analyze the antitumor activity of a novel benzofuran derivative, 2-amino-3-(2-chlorophenyl)-6-(4-dimethylaminophenyl)benzofuran-4-yl acetate (ACDB), in human chondrosarcoma cells. ACDB increased the cell apoptosis of human chondrosarcomas without harm in chondrocytes. ACDB also enhanced endoplasmic reticulum (ER) stress, which was characterized by varieties in the cytosolic calcium levels and induced the expression of glucose-regulated protein (GRP) and calpain. Furthermore, the ACDB-induced chondrosarcoma apoptosis was associated with the upregulation of the B cell lymphoma-2 (Bcl-2) family members including pro- and anti-apoptotic proteins, downregulation of dysfunctional mitochondria that released cytochrome C, and subsequent activation of caspases-3. In addition, the ACDB-mediated cellular apoptosis was suppressed by transfecting cells with glucose-regulated protein (GRP) and calpain siRNA or treating cells with ER stress chelators and caspase inhibitors. Interestingly, animal experiments illustrated a reduction in the tumor volume following ACDB treatment. Together, these results suggest that ACDB may be a novel tumor suppressor of chondrosarcoma, and this study demonstrates that the novel antitumor agent, ACDB, induced apoptosis by mitochondrial dysfunction and ER stress in human chondrosarcoma cells in vitro and in vivo.
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PMID:A novel benzofuran derivative, ACDB, induces apoptosis of human chondrosarcoma cells through mitochondrial dysfunction and endoplasmic reticulum stress. 2783 79

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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PMID:Puerarin induces cell apoptosis in human chondrosarcoma cell line SW1353 via inhibition of the PI3K/Akt signaling pathway. 2911 86