Apoptosis Induced by Tanshinone IIA and Cryptotanshinone Is Mediated by Distinct JAK/STAT3/5 and SHP1/2 Signaling in Chronic Myeloid Leukemia K562 Cells
Though tanshinone IIA and cryptotanshinone possess a variety of biological effects such as anti-inflammatory, antioxidative, antimetabolic, and anticancer effects, the precise molecular targets or pathways responsible for anticancer activities of tanshinone IIA and cryptotanshinone in chronic myeloi...
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| Veröffentlicht in: | Evidence-based complementary and alternative medicine 2013-01, Vol.2013 (2013), p.1-10 |
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| creator | Jung, Ji Hoon Kwon, Tae-Rin Jeong, Soo-Jin Kim, Eun-Ok Sohn, Eun Jung Yun, Miyong Kim, Sung-Hoon |
| description | Though tanshinone IIA and cryptotanshinone possess a variety of biological effects such as anti-inflammatory, antioxidative, antimetabolic, and anticancer effects, the precise molecular targets or pathways responsible for anticancer activities of tanshinone IIA and cryptotanshinone in chronic myeloid leukemia (CML) still remain unclear. In the present study, we investigated the effect of tanshinone IIA and cryptotanshinone on the Janus activated kinase (JAK)/signal transducer and activator of transcription (STAT) signaling during apoptotic process. We found that both tanshinone IIA and cryptotanshinone induced apoptosis by activation of caspase-9/3 and Sub-G1 accumulation in K562 cells. However, they have the distinct JAK/STAT pathway, in which tanshinone IIA inhibits JAK2/STAT5 signaling, whereas cryptotanshinone targets the JAK2/STAT3. In addition, tanshinone IIA enhanced the expression of both SHP-1 and -2, while cryptotanshinone regulated the expression of only SHP-1. Both tanshinone IIA and cryptotanshinone attenuated the expression of bcl-xL, survivin, and cyclin D1. Furthermore, tanshinone IIA augmented synergy with imatinib, a CML chemotherapeutic drug, better than cryptotanshinone in K562 cells. Overall, our findings suggest that the anticancer activity of tanshinone IIA and cryptotanshinone is mediated by the distinct the JAK/STAT3/5 and SHP1/2 signaling, and tanshinone IIA has the potential for combination therapy with imatinib in K562 CML cells. |
| doi_str_mv | 10.1155/2013/805639 |
| format | Article |
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In the present study, we investigated the effect of tanshinone IIA and cryptotanshinone on the Janus activated kinase (JAK)/signal transducer and activator of transcription (STAT) signaling during apoptotic process. We found that both tanshinone IIA and cryptotanshinone induced apoptosis by activation of caspase-9/3 and Sub-G1 accumulation in K562 cells. However, they have the distinct JAK/STAT pathway, in which tanshinone IIA inhibits JAK2/STAT5 signaling, whereas cryptotanshinone targets the JAK2/STAT3. In addition, tanshinone IIA enhanced the expression of both SHP-1 and -2, while cryptotanshinone regulated the expression of only SHP-1. Both tanshinone IIA and cryptotanshinone attenuated the expression of bcl-xL, survivin, and cyclin D1. Furthermore, tanshinone IIA augmented synergy with imatinib, a CML chemotherapeutic drug, better than cryptotanshinone in K562 cells. Overall, our findings suggest that the anticancer activity of tanshinone IIA and cryptotanshinone is mediated by the distinct the JAK/STAT3/5 and SHP1/2 signaling, and tanshinone IIA has the potential for combination therapy with imatinib in K562 CML cells.</description><identifier>ISSN: 1741-427X</identifier><identifier>EISSN: 1741-4288</identifier><identifier>DOI: 10.1155/2013/805639</identifier><identifier>PMID: 23878608</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Puplishing Corporation</publisher><subject>Antitumor activity ; Apoptosis ; Bcl-x protein ; Biological effects ; Cancer ; Caspase ; Caspase-9 ; Cell cycle ; Chronic myeloid leukemia ; Cryptotanshinone ; Cyclin D1 ; Cytokines ; Cytotoxicity ; Deoxyribonucleic acid ; DNA ; Imatinib ; Inflammation ; Janus kinase 2 ; Kinases ; Leukemia ; Medical research ; Myeloid leukemia ; Proteins ; SHP-1 protein ; Signal transduction ; Stat3 protein ; Stat5 protein ; Survivin ; Transcription</subject><ispartof>Evidence-based complementary and alternative medicine, 2013-01, Vol.2013 (2013), p.1-10</ispartof><rights>Copyright © 2013 Ji Hoon Jung et al.</rights><rights>Copyright © 2013 Ji Hoon Jung et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2013 Ji Hoon Jung et al. 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c565t-30bd216d8bbe53f1c8f52239bf58a7dbd8bc9482c0cdf9f03f162e99f670b8903</citedby><cites>FETCH-LOGICAL-c565t-30bd216d8bbe53f1c8f52239bf58a7dbd8bc9482c0cdf9f03f162e99f670b8903</cites><orcidid>0000-0001-6529-1767 ; 0000-0002-9892-7714</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3710643/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3710643/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23878608$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Rahman, Khalid</contributor><contributor>Khalid Rahman</contributor><creatorcontrib>Jung, Ji Hoon</creatorcontrib><creatorcontrib>Kwon, Tae-Rin</creatorcontrib><creatorcontrib>Jeong, Soo-Jin</creatorcontrib><creatorcontrib>Kim, Eun-Ok</creatorcontrib><creatorcontrib>Sohn, Eun Jung</creatorcontrib><creatorcontrib>Yun, Miyong</creatorcontrib><creatorcontrib>Kim, Sung-Hoon</creatorcontrib><title>Apoptosis Induced by Tanshinone IIA and Cryptotanshinone Is Mediated by Distinct JAK/STAT3/5 and SHP1/2 Signaling in Chronic Myeloid Leukemia K562 Cells</title><title>Evidence-based complementary and alternative medicine</title><addtitle>Evid Based Complement Alternat Med</addtitle><description>Though tanshinone IIA and cryptotanshinone possess a variety of biological effects such as anti-inflammatory, antioxidative, antimetabolic, and anticancer effects, the precise molecular targets or pathways responsible for anticancer activities of tanshinone IIA and cryptotanshinone in chronic myeloid leukemia (CML) still remain unclear. In the present study, we investigated the effect of tanshinone IIA and cryptotanshinone on the Janus activated kinase (JAK)/signal transducer and activator of transcription (STAT) signaling during apoptotic process. We found that both tanshinone IIA and cryptotanshinone induced apoptosis by activation of caspase-9/3 and Sub-G1 accumulation in K562 cells. However, they have the distinct JAK/STAT pathway, in which tanshinone IIA inhibits JAK2/STAT5 signaling, whereas cryptotanshinone targets the JAK2/STAT3. In addition, tanshinone IIA enhanced the expression of both SHP-1 and -2, while cryptotanshinone regulated the expression of only SHP-1. Both tanshinone IIA and cryptotanshinone attenuated the expression of bcl-xL, survivin, and cyclin D1. Furthermore, tanshinone IIA augmented synergy with imatinib, a CML chemotherapeutic drug, better than cryptotanshinone in K562 cells. Overall, our findings suggest that the anticancer activity of tanshinone IIA and cryptotanshinone is mediated by the distinct the JAK/STAT3/5 and SHP1/2 signaling, and tanshinone IIA has the potential for combination therapy with imatinib in K562 CML cells.</description><subject>Antitumor activity</subject><subject>Apoptosis</subject><subject>Bcl-x protein</subject><subject>Biological effects</subject><subject>Cancer</subject><subject>Caspase</subject><subject>Caspase-9</subject><subject>Cell cycle</subject><subject>Chronic myeloid leukemia</subject><subject>Cryptotanshinone</subject><subject>Cyclin D1</subject><subject>Cytokines</subject><subject>Cytotoxicity</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Imatinib</subject><subject>Inflammation</subject><subject>Janus kinase 2</subject><subject>Kinases</subject><subject>Leukemia</subject><subject>Medical research</subject><subject>Myeloid leukemia</subject><subject>Proteins</subject><subject>SHP-1 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Induced by Tanshinone IIA and Cryptotanshinone Is Mediated by Distinct JAK/STAT3/5 and SHP1/2 Signaling in Chronic Myeloid Leukemia K562 Cells</title><author>Jung, Ji Hoon ; Kwon, Tae-Rin ; Jeong, Soo-Jin ; Kim, Eun-Ok ; Sohn, Eun Jung ; Yun, Miyong ; Kim, Sung-Hoon</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c565t-30bd216d8bbe53f1c8f52239bf58a7dbd8bc9482c0cdf9f03f162e99f670b8903</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Antitumor activity</topic><topic>Apoptosis</topic><topic>Bcl-x protein</topic><topic>Biological effects</topic><topic>Cancer</topic><topic>Caspase</topic><topic>Caspase-9</topic><topic>Cell cycle</topic><topic>Chronic myeloid leukemia</topic><topic>Cryptotanshinone</topic><topic>Cyclin D1</topic><topic>Cytokines</topic><topic>Cytotoxicity</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Imatinib</topic><topic>Inflammation</topic><topic>Janus kinase 2</topic><topic>Kinases</topic><topic>Leukemia</topic><topic>Medical research</topic><topic>Myeloid leukemia</topic><topic>Proteins</topic><topic>SHP-1 protein</topic><topic>Signal transduction</topic><topic>Stat3 protein</topic><topic>Stat5 protein</topic><topic>Survivin</topic><topic>Transcription</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jung, Ji Hoon</creatorcontrib><creatorcontrib>Kwon, Tae-Rin</creatorcontrib><creatorcontrib>Jeong, Soo-Jin</creatorcontrib><creatorcontrib>Kim, Eun-Ok</creatorcontrib><creatorcontrib>Sohn, Eun Jung</creatorcontrib><creatorcontrib>Yun, Miyong</creatorcontrib><creatorcontrib>Kim, Sung-Hoon</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic 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JAK/STAT3/5 and SHP1/2 Signaling in Chronic Myeloid Leukemia K562 Cells</atitle><jtitle>Evidence-based complementary and alternative medicine</jtitle><addtitle>Evid Based Complement Alternat Med</addtitle><date>2013-01-01</date><risdate>2013</risdate><volume>2013</volume><issue>2013</issue><spage>1</spage><epage>10</epage><pages>1-10</pages><issn>1741-427X</issn><eissn>1741-4288</eissn><abstract>Though tanshinone IIA and cryptotanshinone possess a variety of biological effects such as anti-inflammatory, antioxidative, antimetabolic, and anticancer effects, the precise molecular targets or pathways responsible for anticancer activities of tanshinone IIA and cryptotanshinone in chronic myeloid leukemia (CML) still remain unclear. In the present study, we investigated the effect of tanshinone IIA and cryptotanshinone on the Janus activated kinase (JAK)/signal transducer and activator of transcription (STAT) signaling during apoptotic process. We found that both tanshinone IIA and cryptotanshinone induced apoptosis by activation of caspase-9/3 and Sub-G1 accumulation in K562 cells. However, they have the distinct JAK/STAT pathway, in which tanshinone IIA inhibits JAK2/STAT5 signaling, whereas cryptotanshinone targets the JAK2/STAT3. In addition, tanshinone IIA enhanced the expression of both SHP-1 and -2, while cryptotanshinone regulated the expression of only SHP-1. Both tanshinone IIA and cryptotanshinone attenuated the expression of bcl-xL, survivin, and cyclin D1. Furthermore, tanshinone IIA augmented synergy with imatinib, a CML chemotherapeutic drug, better than cryptotanshinone in K562 cells. Overall, our findings suggest that the anticancer activity of tanshinone IIA and cryptotanshinone is mediated by the distinct the JAK/STAT3/5 and SHP1/2 signaling, and tanshinone IIA has the potential for combination therapy with imatinib in K562 CML cells.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Puplishing Corporation</pub><pmid>23878608</pmid><doi>10.1155/2013/805639</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-6529-1767</orcidid><orcidid>https://orcid.org/0000-0002-9892-7714</orcidid><oa>free_for_read</oa></addata></record> |
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| issn | 1741-427X 1741-4288 |
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| source | Wiley Online Library Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection; PubMed Central Open Access |
| subjects | Antitumor activity Apoptosis Bcl-x protein Biological effects Cancer Caspase Caspase-9 Cell cycle Chronic myeloid leukemia Cryptotanshinone Cyclin D1 Cytokines Cytotoxicity Deoxyribonucleic acid DNA Imatinib Inflammation Janus kinase 2 Kinases Leukemia Medical research Myeloid leukemia Proteins SHP-1 protein Signal transduction Stat3 protein Stat5 protein Survivin Transcription |
| title | Apoptosis Induced by Tanshinone IIA and Cryptotanshinone Is Mediated by Distinct JAK/STAT3/5 and SHP1/2 Signaling in Chronic Myeloid Leukemia K562 Cells |
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