Methyl jasmonate decreases membrane fluidity and induces apoptosis via tumor necrosis factor receptor 1 in breast cancer cells
In recent years, studies with plant compounds have shown both chemotherapeutic and chemopreventive properties. The current study with plant stress hormones (jasmonates) showed growth inhibitory effects in breast cancer cells. Cis-jasmone (CJ) and methyl jasmonate (MJ) inhibited the long-term prolife...
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Veröffentlicht in: | Anti-cancer drugs 2008-09, Vol.19 (8), p.766-776 |
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creator | Yeruva, Laxmi Elegbede, J. Abiodun Carper, Stephen W. |
description | In recent years, studies with plant compounds have shown both chemotherapeutic and chemopreventive properties. The current study with plant stress hormones (jasmonates) showed growth inhibitory effects in breast cancer cells. Cis-jasmone (CJ) and methyl jasmonate (MJ) inhibited the long-term proliferation of MDA-MB-435 and MCF-7 cells. Cell cycle analysis showed G0/G1 and S-phase arrest with increasing apoptotic population. Cellular signaling studies with MJ showed decreased membrane fluidity and activation of extrinsic and intrinsic apoptotic pathways. Specifically in extrinsic apoptotic pathway increased expression of TNFR1, activation of MAPK and caspase-8 was observed. MJ also decreased the mitochondrial membrane potential and activated caspase-3 in breast cancer cells. In conclusion our results revealed novel signaling mechanism of MJ in breast cancer cells, indicating that MJ could have potential applications for chemotherapeutic purposes. |
doi_str_mv | 10.1097/CAD.0b013e32830b5894 |
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Abiodun ; Carper, Stephen W.</creator><creatorcontrib>Yeruva, Laxmi ; Elegbede, J. Abiodun ; Carper, Stephen W.</creatorcontrib><description>In recent years, studies with plant compounds have shown both chemotherapeutic and chemopreventive properties. The current study with plant stress hormones (jasmonates) showed growth inhibitory effects in breast cancer cells. Cis-jasmone (CJ) and methyl jasmonate (MJ) inhibited the long-term proliferation of MDA-MB-435 and MCF-7 cells. Cell cycle analysis showed G0/G1 and S-phase arrest with increasing apoptotic population. Cellular signaling studies with MJ showed decreased membrane fluidity and activation of extrinsic and intrinsic apoptotic pathways. Specifically in extrinsic apoptotic pathway increased expression of TNFR1, activation of MAPK and caspase-8 was observed. MJ also decreased the mitochondrial membrane potential and activated caspase-3 in breast cancer cells. In conclusion our results revealed novel signaling mechanism of MJ in breast cancer cells, indicating that MJ could have potential applications for chemotherapeutic purposes.</description><identifier>ISSN: 0959-4973</identifier><identifier>EISSN: 1473-5741</identifier><identifier>DOI: 10.1097/CAD.0b013e32830b5894</identifier><identifier>PMID: 18690087</identifier><language>eng</language><ispartof>Anti-cancer drugs, 2008-09, Vol.19 (8), p.766-776</ispartof><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>230,314,780,784,885,27924,27925</link.rule.ids></links><search><creatorcontrib>Yeruva, Laxmi</creatorcontrib><creatorcontrib>Elegbede, J. 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The current study with plant stress hormones (jasmonates) showed growth inhibitory effects in breast cancer cells. Cis-jasmone (CJ) and methyl jasmonate (MJ) inhibited the long-term proliferation of MDA-MB-435 and MCF-7 cells. Cell cycle analysis showed G0/G1 and S-phase arrest with increasing apoptotic population. Cellular signaling studies with MJ showed decreased membrane fluidity and activation of extrinsic and intrinsic apoptotic pathways. Specifically in extrinsic apoptotic pathway increased expression of TNFR1, activation of MAPK and caspase-8 was observed. MJ also decreased the mitochondrial membrane potential and activated caspase-3 in breast cancer cells. In conclusion our results revealed novel signaling mechanism of MJ in breast cancer cells, indicating that MJ could have potential applications for chemotherapeutic purposes.</abstract><pmid>18690087</pmid><doi>10.1097/CAD.0b013e32830b5894</doi></addata></record> |
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title | Methyl jasmonate decreases membrane fluidity and induces apoptosis via tumor necrosis factor receptor 1 in breast cancer cells |
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