3,5-Dimethyl-H-furo[3,2-g]chromen-7-one as a potential anticancer drug by inducing p53-dependent apoptosis in human hepatoma HepG2 cells
Coumarins are natural compounds found in many plants that possess medical value by itself and its modified derivatives. Six novel coumarin derivatives were synthesized and examined for their potential anticancer cytotoxicity. Among the 6 derivatives, 3,5-dimethyl-(7)H-furo[3,2-g]chromen-7-one (DMFC)...
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| Veröffentlicht in: | Chemotherapy (Basel) 2011-04, Vol.57 (2), p.162-172 |
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| creator | Sun, Jian-guo Chen, Chao-yue Luo, Ke-wang Yeung, Chi-lam Au Tsang, Tsun-yee Huang, Zhi-zhen Wu, Ping Fung, Kwok-pui Kwok, Tim-tak Liu, Fei-yan |
| description | Coumarins are natural compounds found in many plants that possess medical value by itself and its modified derivatives.
Six novel coumarin derivatives were synthesized and examined for their potential anticancer cytotoxicity.
Among the 6 derivatives, 3,5-dimethyl-(7)H-furo[3,2-g]chromen-7-one (DMFC) presented the strongest cytotoxicity against human hepatoma HepG2 cells in vitro with an IC(50) value of 8.46 ± 0.28 μM in a 48-hour treatment. Further experiments revealed that DMFC induced apoptosis in HepG2 cells through both extrinsic and intrinsic apoptotic pathways in a p53-dependent manner. Mechanistically, DMFC activated caspases 3, 8 and 9, depolarized mitochondrial membrane potential and induced cytochrome c and apoptosis-inducing factor release. DMFC-induced apoptosis was also characterized by DNA fragmentation, phosphatidylserine externalization and sub-G1 peak in DNA histograms. Moreover, both caspase 8 and 9 inhibitors suppressed the apoptosis induced by DMFC. Western blot analyses revealed that DMFC also significantly increased the expression levels of p53, Fas death receptor, Fas-associated death domain protein and proapoptotic Bcl-2 family members such as Bax, Bad and tBid, as well as decreased the levels of pro-survival members such as Bcl-2 and Bcl-xl.
DMFC is potentially an effective therapeutic agent in liver cancer therapy. |
| doi_str_mv | 10.1159/000326915 |
| format | Article |
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Six novel coumarin derivatives were synthesized and examined for their potential anticancer cytotoxicity.
Among the 6 derivatives, 3,5-dimethyl-(7)H-furo[3,2-g]chromen-7-one (DMFC) presented the strongest cytotoxicity against human hepatoma HepG2 cells in vitro with an IC(50) value of 8.46 ± 0.28 μM in a 48-hour treatment. Further experiments revealed that DMFC induced apoptosis in HepG2 cells through both extrinsic and intrinsic apoptotic pathways in a p53-dependent manner. Mechanistically, DMFC activated caspases 3, 8 and 9, depolarized mitochondrial membrane potential and induced cytochrome c and apoptosis-inducing factor release. DMFC-induced apoptosis was also characterized by DNA fragmentation, phosphatidylserine externalization and sub-G1 peak in DNA histograms. Moreover, both caspase 8 and 9 inhibitors suppressed the apoptosis induced by DMFC. Western blot analyses revealed that DMFC also significantly increased the expression levels of p53, Fas death receptor, Fas-associated death domain protein and proapoptotic Bcl-2 family members such as Bax, Bad and tBid, as well as decreased the levels of pro-survival members such as Bcl-2 and Bcl-xl.
DMFC is potentially an effective therapeutic agent in liver cancer therapy.</description><identifier>ISSN: 0009-3157</identifier><identifier>EISSN: 1421-9794</identifier><identifier>DOI: 10.1159/000326915</identifier><identifier>PMID: 21454974</identifier><language>eng</language><publisher>Switzerland: S. Karger AG</publisher><subject>Antineoplastic Agents - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Apoptosis Inducing Factor - metabolism ; bcl-X Protein - biosynthesis ; bcl-X Protein - genetics ; Benzofurans - pharmacology ; Carcinoma, Hepatocellular - drug therapy ; Carcinoma, Hepatocellular - genetics ; Carcinoma, Hepatocellular - metabolism ; Carcinoma, Hepatocellular - pathology ; Caspases - metabolism ; Cellular biology ; Chemotherapy ; Coumarins - pharmacology ; Cytochromes c - metabolism ; DNA Fragmentation - drug effects ; fas Receptor - biosynthesis ; fas Receptor - genetics ; Hep G2 Cells ; Humans ; Liver cancer ; Liver Neoplasms - drug therapy ; Liver Neoplasms - genetics ; Liver Neoplasms - metabolism ; Liver Neoplasms - pathology ; Membrane Potential, Mitochondrial - drug effects ; Pharmacology ; Phosphatidylserines - metabolism ; Proto-Oncogene Proteins c-bcl-2 - biosynthesis ; Proto-Oncogene Proteins c-bcl-2 - genetics ; Tumor Suppressor Protein p53 - biosynthesis ; Tumor Suppressor Protein p53 - genetics ; Tumor Suppressor Protein p53 - metabolism</subject><ispartof>Chemotherapy (Basel), 2011-04, Vol.57 (2), p.162-172</ispartof><rights>Copyright © 2011 S. Karger AG, Basel.</rights><rights>Copyright (c) 2011 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21454974$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sun, Jian-guo</creatorcontrib><creatorcontrib>Chen, Chao-yue</creatorcontrib><creatorcontrib>Luo, Ke-wang</creatorcontrib><creatorcontrib>Yeung, Chi-lam Au</creatorcontrib><creatorcontrib>Tsang, Tsun-yee</creatorcontrib><creatorcontrib>Huang, Zhi-zhen</creatorcontrib><creatorcontrib>Wu, Ping</creatorcontrib><creatorcontrib>Fung, Kwok-pui</creatorcontrib><creatorcontrib>Kwok, Tim-tak</creatorcontrib><creatorcontrib>Liu, Fei-yan</creatorcontrib><title>3,5-Dimethyl-H-furo[3,2-g]chromen-7-one as a potential anticancer drug by inducing p53-dependent apoptosis in human hepatoma HepG2 cells</title><title>Chemotherapy (Basel)</title><addtitle>Chemotherapy</addtitle><description>Coumarins are natural compounds found in many plants that possess medical value by itself and its modified derivatives.
Six novel coumarin derivatives were synthesized and examined for their potential anticancer cytotoxicity.
Among the 6 derivatives, 3,5-dimethyl-(7)H-furo[3,2-g]chromen-7-one (DMFC) presented the strongest cytotoxicity against human hepatoma HepG2 cells in vitro with an IC(50) value of 8.46 ± 0.28 μM in a 48-hour treatment. Further experiments revealed that DMFC induced apoptosis in HepG2 cells through both extrinsic and intrinsic apoptotic pathways in a p53-dependent manner. Mechanistically, DMFC activated caspases 3, 8 and 9, depolarized mitochondrial membrane potential and induced cytochrome c and apoptosis-inducing factor release. DMFC-induced apoptosis was also characterized by DNA fragmentation, phosphatidylserine externalization and sub-G1 peak in DNA histograms. Moreover, both caspase 8 and 9 inhibitors suppressed the apoptosis induced by DMFC. Western blot analyses revealed that DMFC also significantly increased the expression levels of p53, Fas death receptor, Fas-associated death domain protein and proapoptotic Bcl-2 family members such as Bax, Bad and tBid, as well as decreased the levels of pro-survival members such as Bcl-2 and Bcl-xl.
DMFC is potentially an effective therapeutic agent in liver cancer therapy.</description><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis Inducing Factor - metabolism</subject><subject>bcl-X Protein - biosynthesis</subject><subject>bcl-X Protein - genetics</subject><subject>Benzofurans - pharmacology</subject><subject>Carcinoma, Hepatocellular - drug therapy</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Caspases - metabolism</subject><subject>Cellular biology</subject><subject>Chemotherapy</subject><subject>Coumarins - pharmacology</subject><subject>Cytochromes c - metabolism</subject><subject>DNA Fragmentation - drug effects</subject><subject>fas Receptor - biosynthesis</subject><subject>fas Receptor - genetics</subject><subject>Hep G2 Cells</subject><subject>Humans</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - drug therapy</subject><subject>Liver Neoplasms - genetics</subject><subject>Liver Neoplasms - metabolism</subject><subject>Liver Neoplasms - pathology</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Pharmacology</subject><subject>Phosphatidylserines - metabolism</subject><subject>Proto-Oncogene Proteins c-bcl-2 - biosynthesis</subject><subject>Proto-Oncogene Proteins c-bcl-2 - genetics</subject><subject>Tumor Suppressor Protein p53 - biosynthesis</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><issn>0009-3157</issn><issn>1421-9794</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqF0b1uFDEQB3ALgciRUPACyKKhicH2-GNdohBySJHSQBWhk9c7e7fRrm3Wu8W9QR4bR0maNDTzl0Y_jWY0hHwQ_IsQ2n3lnIM0TuhXZCOUFMxZp16TTe07BkLbE_KulLsHZkC8JSdSKK2cVRtyD-eafR8mXA7HkW1Zv87pFs4l2_8JhzlNGJllKSL1hXqa04JxGfxIfY3gY8CZdvO6p-2RDrFbwxD3NGtgHWaMXcXU55SXVIZSAT2sk68Vs1_S5OkW85WkAcexnJE3vR8Lvn_KU_L7x-Wviy27vrn6efHtmmXRqIW10gTJOcreG5Bc2QCNg840EpzvguUmhF720GoupQYhUXtsPYjehl4pDafk8-PcPKe_K5ZlNw3lYQMfMa1l57gVRmjg_5WNASUlGFHlpxfyLq1zrGdUpBphFXcVfXxCaztht8vzMPn5uHv-BfwDbj-IKw</recordid><startdate>201104</startdate><enddate>201104</enddate><creator>Sun, Jian-guo</creator><creator>Chen, Chao-yue</creator><creator>Luo, Ke-wang</creator><creator>Yeung, Chi-lam Au</creator><creator>Tsang, Tsun-yee</creator><creator>Huang, Zhi-zhen</creator><creator>Wu, Ping</creator><creator>Fung, Kwok-pui</creator><creator>Kwok, Tim-tak</creator><creator>Liu, Fei-yan</creator><general>S. 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Six novel coumarin derivatives were synthesized and examined for their potential anticancer cytotoxicity.
Among the 6 derivatives, 3,5-dimethyl-(7)H-furo[3,2-g]chromen-7-one (DMFC) presented the strongest cytotoxicity against human hepatoma HepG2 cells in vitro with an IC(50) value of 8.46 ± 0.28 μM in a 48-hour treatment. Further experiments revealed that DMFC induced apoptosis in HepG2 cells through both extrinsic and intrinsic apoptotic pathways in a p53-dependent manner. Mechanistically, DMFC activated caspases 3, 8 and 9, depolarized mitochondrial membrane potential and induced cytochrome c and apoptosis-inducing factor release. DMFC-induced apoptosis was also characterized by DNA fragmentation, phosphatidylserine externalization and sub-G1 peak in DNA histograms. Moreover, both caspase 8 and 9 inhibitors suppressed the apoptosis induced by DMFC. Western blot analyses revealed that DMFC also significantly increased the expression levels of p53, Fas death receptor, Fas-associated death domain protein and proapoptotic Bcl-2 family members such as Bax, Bad and tBid, as well as decreased the levels of pro-survival members such as Bcl-2 and Bcl-xl.
DMFC is potentially an effective therapeutic agent in liver cancer therapy.</abstract><cop>Switzerland</cop><pub>S. Karger AG</pub><pmid>21454974</pmid><doi>10.1159/000326915</doi><tpages>11</tpages></addata></record> |
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| ispartof | Chemotherapy (Basel), 2011-04, Vol.57 (2), p.162-172 |
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| subjects | Antineoplastic Agents - pharmacology Apoptosis Apoptosis - drug effects Apoptosis Inducing Factor - metabolism bcl-X Protein - biosynthesis bcl-X Protein - genetics Benzofurans - pharmacology Carcinoma, Hepatocellular - drug therapy Carcinoma, Hepatocellular - genetics Carcinoma, Hepatocellular - metabolism Carcinoma, Hepatocellular - pathology Caspases - metabolism Cellular biology Chemotherapy Coumarins - pharmacology Cytochromes c - metabolism DNA Fragmentation - drug effects fas Receptor - biosynthesis fas Receptor - genetics Hep G2 Cells Humans Liver cancer Liver Neoplasms - drug therapy Liver Neoplasms - genetics Liver Neoplasms - metabolism Liver Neoplasms - pathology Membrane Potential, Mitochondrial - drug effects Pharmacology Phosphatidylserines - metabolism Proto-Oncogene Proteins c-bcl-2 - biosynthesis Proto-Oncogene Proteins c-bcl-2 - genetics Tumor Suppressor Protein p53 - biosynthesis Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism |
| title | 3,5-Dimethyl-H-furo[3,2-g]chromen-7-one as a potential anticancer drug by inducing p53-dependent apoptosis in human hepatoma HepG2 cells |
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