Therapeutic strategies targeting cancer stem cells
Increasing studies have demonstrated a small proportion of cancer stem cells (CSCs) exist in the cancer cell population. CSCs have powerful self-renewal capacity and tumor-initiating ability and are resistant to chemotherapy and radiation. Conventional anticancer therapies kill the rapidly prolifera...
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Veröffentlicht in: | Cancer biology & therapy 2013-04, Vol.14 (4), p.295-303 |
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description | Increasing studies have demonstrated a small proportion of cancer stem cells (CSCs) exist in the cancer cell population. CSCs have powerful self-renewal capacity and tumor-initiating ability and are resistant to chemotherapy and radiation. Conventional anticancer therapies kill the rapidly proliferating bulk cancer cells but spare the relatively quiescent CSCs, which cause cancer recurrence. So it is necessary to develop therapeutic strategies acting specifically on CSCs. In recent years, studies have shown that therapeutic agents such as metformin, salinomycin, DECA-14, rapamycin, oncostatin M (OSM), some natural compounds, oncolytic viruses, microRNAs, cell signaling pathway inhibitors, TNF-related apoptosis inducing ligand (TRAIL), interferon (IFN), telomerase inhibitors, all-trans retinoic acid (ATRA) and monoclonal antibodies can suppress the self-renewal of CSCs in vitro and in vivo. A combination of these agents and conventional chemotherapy drugs can significantly inhibit tumor growth, metastasis and recurrence. These strategies targeting CSCs may bring new hopes to cancer therapy. |
doi_str_mv | 10.4161/cbt.23622 |
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CSCs have powerful self-renewal capacity and tumor-initiating ability and are resistant to chemotherapy and radiation. Conventional anticancer therapies kill the rapidly proliferating bulk cancer cells but spare the relatively quiescent CSCs, which cause cancer recurrence. So it is necessary to develop therapeutic strategies acting specifically on CSCs. In recent years, studies have shown that therapeutic agents such as metformin, salinomycin, DECA-14, rapamycin, oncostatin M (OSM), some natural compounds, oncolytic viruses, microRNAs, cell signaling pathway inhibitors, TNF-related apoptosis inducing ligand (TRAIL), interferon (IFN), telomerase inhibitors, all-trans retinoic acid (ATRA) and monoclonal antibodies can suppress the self-renewal of CSCs in vitro and in vivo. A combination of these agents and conventional chemotherapy drugs can significantly inhibit tumor growth, metastasis and recurrence. These strategies targeting CSCs may bring new hopes to cancer therapy.</description><identifier>ISSN: 1538-4047</identifier><identifier>EISSN: 1555-8576</identifier><identifier>DOI: 10.4161/cbt.23622</identifier><identifier>PMID: 23358473</identifier><language>eng</language><publisher>United States: Taylor & Francis</publisher><subject>Animals ; cancer stem cell ; Humans ; Neoplasms - drug therapy ; Neoplasms - pathology ; Neoplasms - therapy ; Neoplastic Stem Cells - drug effects ; Neoplastic Stem Cells - pathology ; Neoplastic Stem Cells - physiology ; Neoplastic Stem Cells - virology ; Review ; Signal Transduction ; target ; therapy</subject><ispartof>Cancer biology & therapy, 2013-04, Vol.14 (4), p.295-303</ispartof><rights>Copyright © 2013 Landes Bioscience 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c486t-bc694a02b58f2d48bbbe735cd4add1cc00f8f495e01eb19a63307b1facb2bc6f3</citedby><cites>FETCH-LOGICAL-c486t-bc694a02b58f2d48bbbe735cd4add1cc00f8f495e01eb19a63307b1facb2bc6f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3667868/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3667868/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23358473$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ning, Xiaoyan</creatorcontrib><creatorcontrib>Shu, Jianchang</creatorcontrib><creatorcontrib>Du, Yiqi</creatorcontrib><creatorcontrib>Ben, Qiwen</creatorcontrib><creatorcontrib>Li, Zhaoshen</creatorcontrib><title>Therapeutic strategies targeting cancer stem cells</title><title>Cancer biology & therapy</title><addtitle>Cancer Biol Ther</addtitle><description>Increasing studies have demonstrated a small proportion of cancer stem cells (CSCs) exist in the cancer cell population. CSCs have powerful self-renewal capacity and tumor-initiating ability and are resistant to chemotherapy and radiation. Conventional anticancer therapies kill the rapidly proliferating bulk cancer cells but spare the relatively quiescent CSCs, which cause cancer recurrence. So it is necessary to develop therapeutic strategies acting specifically on CSCs. In recent years, studies have shown that therapeutic agents such as metformin, salinomycin, DECA-14, rapamycin, oncostatin M (OSM), some natural compounds, oncolytic viruses, microRNAs, cell signaling pathway inhibitors, TNF-related apoptosis inducing ligand (TRAIL), interferon (IFN), telomerase inhibitors, all-trans retinoic acid (ATRA) and monoclonal antibodies can suppress the self-renewal of CSCs in vitro and in vivo. A combination of these agents and conventional chemotherapy drugs can significantly inhibit tumor growth, metastasis and recurrence. These strategies targeting CSCs may bring new hopes to cancer therapy.</description><subject>Animals</subject><subject>cancer stem cell</subject><subject>Humans</subject><subject>Neoplasms - drug therapy</subject><subject>Neoplasms - pathology</subject><subject>Neoplasms - therapy</subject><subject>Neoplastic Stem Cells - drug effects</subject><subject>Neoplastic Stem Cells - pathology</subject><subject>Neoplastic Stem Cells - physiology</subject><subject>Neoplastic Stem Cells - virology</subject><subject>Review</subject><subject>Signal Transduction</subject><subject>target</subject><subject>therapy</subject><issn>1538-4047</issn><issn>1555-8576</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNplkMlKBDEQhoMo7gdfQOaoh9ZsnaQvgogbCF7Gc0jSlZlIL2OSUXx7M46K4ikF9dWfqg-hI4LPOBHk3Nl8RpmgdAPtkrquK1VLsbmqmao45nIH7aX0jDGVVDTbaIcyVisu2S6i0zlEs4BlDm6ScjQZZgHSJJs4gxyG2cSZwUEsPegnDrouHaAtb7oEh1_vPnq6uZ5e3VUPj7f3V5cPleNK5Mo60XCDqa2Vpy1X1lqQrHYtN21LnMPYK8-bGjABSxojGMPSEm-cpWXWs310sc5dLG0PrYOhrNfpRQy9ie96NEH_7Qxhrmfjq2ZCSCVUCTj5CojjyxJS1n1IqxPMAOMyacIoo7KhkhT0dI26OKYUwf98Q7BeOdbFsf50XNjj33v9kN9SC8DXQBj8GHvzNsau1dm8d2P0segMSbP_uR-lYYtb</recordid><startdate>20130401</startdate><enddate>20130401</enddate><creator>Ning, Xiaoyan</creator><creator>Shu, Jianchang</creator><creator>Du, Yiqi</creator><creator>Ben, Qiwen</creator><creator>Li, Zhaoshen</creator><general>Taylor & Francis</general><general>Landes Bioscience</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20130401</creationdate><title>Therapeutic strategies targeting cancer stem cells</title><author>Ning, Xiaoyan ; Shu, Jianchang ; Du, Yiqi ; Ben, Qiwen ; Li, Zhaoshen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c486t-bc694a02b58f2d48bbbe735cd4add1cc00f8f495e01eb19a63307b1facb2bc6f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>cancer stem cell</topic><topic>Humans</topic><topic>Neoplasms - drug therapy</topic><topic>Neoplasms - pathology</topic><topic>Neoplasms - therapy</topic><topic>Neoplastic Stem Cells - drug effects</topic><topic>Neoplastic Stem Cells - pathology</topic><topic>Neoplastic Stem Cells - physiology</topic><topic>Neoplastic Stem Cells - virology</topic><topic>Review</topic><topic>Signal Transduction</topic><topic>target</topic><topic>therapy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ning, Xiaoyan</creatorcontrib><creatorcontrib>Shu, Jianchang</creatorcontrib><creatorcontrib>Du, Yiqi</creatorcontrib><creatorcontrib>Ben, Qiwen</creatorcontrib><creatorcontrib>Li, Zhaoshen</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer biology & therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ning, Xiaoyan</au><au>Shu, Jianchang</au><au>Du, Yiqi</au><au>Ben, Qiwen</au><au>Li, Zhaoshen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Therapeutic strategies targeting cancer stem cells</atitle><jtitle>Cancer biology & therapy</jtitle><addtitle>Cancer Biol Ther</addtitle><date>2013-04-01</date><risdate>2013</risdate><volume>14</volume><issue>4</issue><spage>295</spage><epage>303</epage><pages>295-303</pages><issn>1538-4047</issn><eissn>1555-8576</eissn><abstract>Increasing studies have demonstrated a small proportion of cancer stem cells (CSCs) exist in the cancer cell population. CSCs have powerful self-renewal capacity and tumor-initiating ability and are resistant to chemotherapy and radiation. Conventional anticancer therapies kill the rapidly proliferating bulk cancer cells but spare the relatively quiescent CSCs, which cause cancer recurrence. So it is necessary to develop therapeutic strategies acting specifically on CSCs. In recent years, studies have shown that therapeutic agents such as metformin, salinomycin, DECA-14, rapamycin, oncostatin M (OSM), some natural compounds, oncolytic viruses, microRNAs, cell signaling pathway inhibitors, TNF-related apoptosis inducing ligand (TRAIL), interferon (IFN), telomerase inhibitors, all-trans retinoic acid (ATRA) and monoclonal antibodies can suppress the self-renewal of CSCs in vitro and in vivo. A combination of these agents and conventional chemotherapy drugs can significantly inhibit tumor growth, metastasis and recurrence. These strategies targeting CSCs may bring new hopes to cancer therapy.</abstract><cop>United States</cop><pub>Taylor & Francis</pub><pmid>23358473</pmid><doi>10.4161/cbt.23622</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals cancer stem cell Humans Neoplasms - drug therapy Neoplasms - pathology Neoplasms - therapy Neoplastic Stem Cells - drug effects Neoplastic Stem Cells - pathology Neoplastic Stem Cells - physiology Neoplastic Stem Cells - virology Review Signal Transduction target therapy |
title | Therapeutic strategies targeting cancer stem cells |
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