Mechanisms of Curcumin-Induced Apoptosis of Ehrlich's Ascites Carcinoma Cells
Curcumin, the active ingredient from the spice turmeric (Curcuma longa Linn), is a potent antioxidant and anti-inflammatory agent. It has been recently demonstrated to possess discrete chemopreventive activities. However, the molecular mechanisms underlying such anticancer properties of curcumin sti...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2001-11, Vol.288 (3), p.658-665 |
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| container_title | Biochemical and biophysical research communications |
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| creator | Pal, Suman Choudhuri, Tathagata Chattopadhyay, Sreya Bhattacharya, Arindam Datta, Goutam K. Das, Tanya Sa, Gaurisankar |
| description | Curcumin, the active ingredient from the spice turmeric (Curcuma longa Linn), is a potent antioxidant and anti-inflammatory agent. It has been recently demonstrated to possess discrete chemopreventive activities. However, the molecular mechanisms underlying such anticancer properties of curcumin still remain unrealized, although it has been postulated that induction of apoptosis in cancer cells might be a probable explanation. In the current study, curcumin was found to decrease the Ehrlich's ascites carcinoma (EAC) cell number by the induction of apoptosis in the tumor cells as evident from flow-cytometric analysis of cell cycle phase distribution of nuclear DNA and oligonucleosomal fragmentation. Probing further into the molecular signals leading to apoptosis of EAC cells, we observed that curcumin is causing tumor cell death by the up-regulation of the proto-oncoprotein Bax, release of cytochrome c from the mitochondria, and activation of caspase-3. The status of Bcl-2 remains unchanged in EAC, which would signify that curcumin is bypassing the Bcl-2 checkpoint and overriding its protective effect on apoptosis. |
| doi_str_mv | 10.1006/bbrc.2001.5823 |
| format | Article |
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It has been recently demonstrated to possess discrete chemopreventive activities. However, the molecular mechanisms underlying such anticancer properties of curcumin still remain unrealized, although it has been postulated that induction of apoptosis in cancer cells might be a probable explanation. In the current study, curcumin was found to decrease the Ehrlich's ascites carcinoma (EAC) cell number by the induction of apoptosis in the tumor cells as evident from flow-cytometric analysis of cell cycle phase distribution of nuclear DNA and oligonucleosomal fragmentation. Probing further into the molecular signals leading to apoptosis of EAC cells, we observed that curcumin is causing tumor cell death by the up-regulation of the proto-oncoprotein Bax, release of cytochrome c from the mitochondria, and activation of caspase-3. The status of Bcl-2 remains unchanged in EAC, which would signify that curcumin is bypassing the Bcl-2 checkpoint and overriding its protective effect on apoptosis.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1006/bbrc.2001.5823</identifier><identifier>PMID: 11676493</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Antineoplastic Agents - pharmacology ; Apoptosis ; apoptosis, curcumin, tumor, oncoprotein ; Bax protein ; Bcl-2 protein ; bcl-2-Associated X Protein ; Carcinoma, Ehrlich Tumor - metabolism ; Carcinoma, Ehrlich Tumor - pathology ; Caspase 3 ; Caspases - metabolism ; Cell Count ; Cell Cycle - drug effects ; Curcumin - pharmacology ; cytochrome c ; Cytochrome c Group - metabolism ; Cytosol - enzymology ; DNA Fragmentation - drug effects ; DNA, Neoplasm - drug effects ; DNA, Neoplasm - metabolism ; Flow Cytometry ; Male ; Mice ; Proto-Oncogene Proteins - metabolism ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Tumor Cells, Cultured</subject><ispartof>Biochemical and biophysical research communications, 2001-11, Vol.288 (3), p.658-665</ispartof><rights>2001 Academic Press</rights><rights>Copyright 2001 Academic Press.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c406t-92001c83293c3a03a7ffe24631a34190fab93093e98b6c0711dfcaa0d4ca88443</citedby><cites>FETCH-LOGICAL-c406t-92001c83293c3a03a7ffe24631a34190fab93093e98b6c0711dfcaa0d4ca88443</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1006/bbrc.2001.5823$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27928,27929,45999</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11676493$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pal, Suman</creatorcontrib><creatorcontrib>Choudhuri, Tathagata</creatorcontrib><creatorcontrib>Chattopadhyay, Sreya</creatorcontrib><creatorcontrib>Bhattacharya, Arindam</creatorcontrib><creatorcontrib>Datta, Goutam K.</creatorcontrib><creatorcontrib>Das, Tanya</creatorcontrib><creatorcontrib>Sa, Gaurisankar</creatorcontrib><title>Mechanisms of Curcumin-Induced Apoptosis of Ehrlich's Ascites Carcinoma Cells</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Curcumin, the active ingredient from the spice turmeric (Curcuma longa Linn), is a potent antioxidant and anti-inflammatory agent. It has been recently demonstrated to possess discrete chemopreventive activities. However, the molecular mechanisms underlying such anticancer properties of curcumin still remain unrealized, although it has been postulated that induction of apoptosis in cancer cells might be a probable explanation. In the current study, curcumin was found to decrease the Ehrlich's ascites carcinoma (EAC) cell number by the induction of apoptosis in the tumor cells as evident from flow-cytometric analysis of cell cycle phase distribution of nuclear DNA and oligonucleosomal fragmentation. Probing further into the molecular signals leading to apoptosis of EAC cells, we observed that curcumin is causing tumor cell death by the up-regulation of the proto-oncoprotein Bax, release of cytochrome c from the mitochondria, and activation of caspase-3. The status of Bcl-2 remains unchanged in EAC, which would signify that curcumin is bypassing the Bcl-2 checkpoint and overriding its protective effect on apoptosis.</description><subject>Animals</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>apoptosis, curcumin, tumor, oncoprotein</subject><subject>Bax protein</subject><subject>Bcl-2 protein</subject><subject>bcl-2-Associated X Protein</subject><subject>Carcinoma, Ehrlich Tumor - metabolism</subject><subject>Carcinoma, Ehrlich Tumor - pathology</subject><subject>Caspase 3</subject><subject>Caspases - metabolism</subject><subject>Cell Count</subject><subject>Cell Cycle - drug effects</subject><subject>Curcumin - pharmacology</subject><subject>cytochrome c</subject><subject>Cytochrome c Group - metabolism</subject><subject>Cytosol - enzymology</subject><subject>DNA Fragmentation - drug effects</subject><subject>DNA, Neoplasm - drug effects</subject><subject>DNA, Neoplasm - metabolism</subject><subject>Flow Cytometry</subject><subject>Male</subject><subject>Mice</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Tumor Cells, Cultured</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kD1PwzAQhi0EoqWwMqJMMCWcY-PGYxUVqNSKBSQ2y7k4qlG-sBMk_j0OrcTEdMM99-q9h5BrCgkFEPdF4TBJAWjykKXshMwpSIhTCvyUzCEQcSrp-4xceP8RKMqFPCczSsVScMnmZLczuNet9Y2PuirKR4djY9t405YjmjJa9V0_dN7-btd7V1vc3_lo5dEOxke5dmjbrtFRburaX5KzStfeXB3ngrw9rl_z53j78rTJV9sYOYghllNhzFgqGTINTC-ryqRcMKoZpxIqXUgGkhmZFQJhSWlZodZQctRZxjlbkNtDbu-6z9H4QTXWY2igW9ONXtEsfCg4C2ByANF13jtTqd7ZRrtvRUFNAtUkUE191CQwHNwck8eiMeUffjQWgOwAmPDflzVOBRWmDa6sMziosrP_Zf8Avad-Pw</recordid><startdate>20011102</startdate><enddate>20011102</enddate><creator>Pal, Suman</creator><creator>Choudhuri, Tathagata</creator><creator>Chattopadhyay, Sreya</creator><creator>Bhattacharya, Arindam</creator><creator>Datta, Goutam K.</creator><creator>Das, Tanya</creator><creator>Sa, Gaurisankar</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TM</scope></search><sort><creationdate>20011102</creationdate><title>Mechanisms of Curcumin-Induced Apoptosis of Ehrlich's Ascites Carcinoma Cells</title><author>Pal, Suman ; Choudhuri, Tathagata ; Chattopadhyay, Sreya ; Bhattacharya, Arindam ; Datta, Goutam K. ; Das, Tanya ; Sa, Gaurisankar</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c406t-92001c83293c3a03a7ffe24631a34190fab93093e98b6c0711dfcaa0d4ca88443</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Apoptosis</topic><topic>apoptosis, curcumin, tumor, oncoprotein</topic><topic>Bax protein</topic><topic>Bcl-2 protein</topic><topic>bcl-2-Associated X Protein</topic><topic>Carcinoma, Ehrlich Tumor - metabolism</topic><topic>Carcinoma, Ehrlich Tumor - pathology</topic><topic>Caspase 3</topic><topic>Caspases - metabolism</topic><topic>Cell Count</topic><topic>Cell Cycle - drug effects</topic><topic>Curcumin - pharmacology</topic><topic>cytochrome c</topic><topic>Cytochrome c Group - metabolism</topic><topic>Cytosol - enzymology</topic><topic>DNA Fragmentation - drug effects</topic><topic>DNA, Neoplasm - drug effects</topic><topic>DNA, Neoplasm - metabolism</topic><topic>Flow Cytometry</topic><topic>Male</topic><topic>Mice</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pal, Suman</creatorcontrib><creatorcontrib>Choudhuri, Tathagata</creatorcontrib><creatorcontrib>Chattopadhyay, Sreya</creatorcontrib><creatorcontrib>Bhattacharya, Arindam</creatorcontrib><creatorcontrib>Datta, Goutam K.</creatorcontrib><creatorcontrib>Das, Tanya</creatorcontrib><creatorcontrib>Sa, Gaurisankar</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pal, Suman</au><au>Choudhuri, Tathagata</au><au>Chattopadhyay, Sreya</au><au>Bhattacharya, Arindam</au><au>Datta, Goutam K.</au><au>Das, Tanya</au><au>Sa, Gaurisankar</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanisms of Curcumin-Induced Apoptosis of Ehrlich's Ascites Carcinoma Cells</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2001-11-02</date><risdate>2001</risdate><volume>288</volume><issue>3</issue><spage>658</spage><epage>665</epage><pages>658-665</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Curcumin, the active ingredient from the spice turmeric (Curcuma longa Linn), is a potent antioxidant and anti-inflammatory agent. It has been recently demonstrated to possess discrete chemopreventive activities. However, the molecular mechanisms underlying such anticancer properties of curcumin still remain unrealized, although it has been postulated that induction of apoptosis in cancer cells might be a probable explanation. In the current study, curcumin was found to decrease the Ehrlich's ascites carcinoma (EAC) cell number by the induction of apoptosis in the tumor cells as evident from flow-cytometric analysis of cell cycle phase distribution of nuclear DNA and oligonucleosomal fragmentation. Probing further into the molecular signals leading to apoptosis of EAC cells, we observed that curcumin is causing tumor cell death by the up-regulation of the proto-oncoprotein Bax, release of cytochrome c from the mitochondria, and activation of caspase-3. The status of Bcl-2 remains unchanged in EAC, which would signify that curcumin is bypassing the Bcl-2 checkpoint and overriding its protective effect on apoptosis.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>11676493</pmid><doi>10.1006/bbrc.2001.5823</doi><tpages>8</tpages></addata></record> |
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| subjects | Animals Antineoplastic Agents - pharmacology Apoptosis apoptosis, curcumin, tumor, oncoprotein Bax protein Bcl-2 protein bcl-2-Associated X Protein Carcinoma, Ehrlich Tumor - metabolism Carcinoma, Ehrlich Tumor - pathology Caspase 3 Caspases - metabolism Cell Count Cell Cycle - drug effects Curcumin - pharmacology cytochrome c Cytochrome c Group - metabolism Cytosol - enzymology DNA Fragmentation - drug effects DNA, Neoplasm - drug effects DNA, Neoplasm - metabolism Flow Cytometry Male Mice Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins c-bcl-2 - metabolism Tumor Cells, Cultured |
| title | Mechanisms of Curcumin-Induced Apoptosis of Ehrlich's Ascites Carcinoma Cells |
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