{"title":"抗坏血酸对体外骨癌细胞的影响","authors":"G. Fernandes, Andrew W. Barone, R. Dziak","doi":"10.1080/23312025.2017.1288335","DOIUrl":null,"url":null,"abstract":"Abstract Ascorbic acid (Vitamin C) has long been known for its anti-cancer properties and in the present study the effects of ascorbic acid (AsA) on osteogenic differentiation, apoptosis, and signaling pathways of the human G29 osteosarcoma cell line were studied. The expression of Runt-related transcription factor-2 (RUNX2) and osteocalcin genes were evaluated by real-time polymerase chain reaction (PCR). Osteoblastic maturation was assessed with alkaline phosphatase activity and mineralization with alizarin red deposition, and apoptosis with a caspase-2 apoptotic assay as well as the cell viability via the cytotoxicity assay. The possible role of the MAP kinase pathway (p44/42, p38, and p-JNK signaling pathway) was also studied. Our results showed that RUNX2 and osteocalcin gene expression, mineralization, cell viability, and metabolic activity levels were increased in cells treated with low concentrations of AsA with respect to untreated cells. At higher concentrations, AsA resulted in decreases in these parameters and induced apoptosis of the G292 osteosarcoma cells via downregulation of the MAPK pathway. The findings presented here support the ability of AsA to modulate the viability and differentiation of the G292 type of bone cancer cell with increases or decreases depending on the AsA concentration suggesting a need for further evaluation of the possible use of this vitamin in the regulation of bone cell cancer growth.","PeriodicalId":10412,"journal":{"name":"Cogent Biology","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23312025.2017.1288335","citationCount":"18","resultStr":"{\"title\":\"The effect of ascorbic acid on bone cancer cells in vitro\",\"authors\":\"G. Fernandes, Andrew W. Barone, R. Dziak\",\"doi\":\"10.1080/23312025.2017.1288335\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Abstract Ascorbic acid (Vitamin C) has long been known for its anti-cancer properties and in the present study the effects of ascorbic acid (AsA) on osteogenic differentiation, apoptosis, and signaling pathways of the human G29 osteosarcoma cell line were studied. The expression of Runt-related transcription factor-2 (RUNX2) and osteocalcin genes were evaluated by real-time polymerase chain reaction (PCR). Osteoblastic maturation was assessed with alkaline phosphatase activity and mineralization with alizarin red deposition, and apoptosis with a caspase-2 apoptotic assay as well as the cell viability via the cytotoxicity assay. The possible role of the MAP kinase pathway (p44/42, p38, and p-JNK signaling pathway) was also studied. Our results showed that RUNX2 and osteocalcin gene expression, mineralization, cell viability, and metabolic activity levels were increased in cells treated with low concentrations of AsA with respect to untreated cells. At higher concentrations, AsA resulted in decreases in these parameters and induced apoptosis of the G292 osteosarcoma cells via downregulation of the MAPK pathway. The findings presented here support the ability of AsA to modulate the viability and differentiation of the G292 type of bone cancer cell with increases or decreases depending on the AsA concentration suggesting a need for further evaluation of the possible use of this vitamin in the regulation of bone cell cancer growth.\",\"PeriodicalId\":10412,\"journal\":{\"name\":\"Cogent Biology\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2017-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1080/23312025.2017.1288335\",\"citationCount\":\"18\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cogent Biology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1080/23312025.2017.1288335\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cogent Biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/23312025.2017.1288335","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
The effect of ascorbic acid on bone cancer cells in vitro
Abstract Ascorbic acid (Vitamin C) has long been known for its anti-cancer properties and in the present study the effects of ascorbic acid (AsA) on osteogenic differentiation, apoptosis, and signaling pathways of the human G29 osteosarcoma cell line were studied. The expression of Runt-related transcription factor-2 (RUNX2) and osteocalcin genes were evaluated by real-time polymerase chain reaction (PCR). Osteoblastic maturation was assessed with alkaline phosphatase activity and mineralization with alizarin red deposition, and apoptosis with a caspase-2 apoptotic assay as well as the cell viability via the cytotoxicity assay. The possible role of the MAP kinase pathway (p44/42, p38, and p-JNK signaling pathway) was also studied. Our results showed that RUNX2 and osteocalcin gene expression, mineralization, cell viability, and metabolic activity levels were increased in cells treated with low concentrations of AsA with respect to untreated cells. At higher concentrations, AsA resulted in decreases in these parameters and induced apoptosis of the G292 osteosarcoma cells via downregulation of the MAPK pathway. The findings presented here support the ability of AsA to modulate the viability and differentiation of the G292 type of bone cancer cell with increases or decreases depending on the AsA concentration suggesting a need for further evaluation of the possible use of this vitamin in the regulation of bone cell cancer growth.