CCR5 blockage by maraviroc induces cytotoxic and apoptotic effects in colorectal cancer cells
Alterations in the expression of C–C chemokine receptor type 5 ( CCR5 or CD195 ) have been correlated with disease progression in different cancers. Recently, a few investigations have reported the blockage of this receptor by an antagonist (maraviroc) and its antineoplastic effects on tumor cell gr...
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| Veröffentlicht in: | Medical oncology (Northwood, London, England) London, England), 2015-05, Vol.32 (5), p.158, Article 158 |
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| creator | Pervaiz, Asim Ansari, Shariq Berger, Martin R. Adwan, Hassan |
| description | Alterations in the expression of C–C chemokine receptor type 5 (
CCR5
or
CD195
) have been correlated with disease progression in different cancers. Recently, a few investigations have reported the blockage of this receptor by an antagonist (maraviroc) and its antineoplastic effects on tumor cell growth. However, little is known about the mechanistic reasons behind these antineoplastic effects of
CCR5
blockage by maraviroc. In this study, we blocked the
CCR5
receptor by maraviroc in SW480 and SW620 colorectal cancer cells to study the resulting changes in biological properties and related pathways. This blockage induced significantly reduced proliferation and a profound arrest in G1 phase of the cell cycle. Concomitantly, maraviroc caused significant signs of apoptosis at morphological level. Significant modulation of multiple apoptosis-relevant genes was also noticed at mRNA levels. In addition, we found remarkable increases in cleaved caspases at protein level. These modulations led us to propose a signaling pathway for the observed apoptotic effects. In conclusion, blocking the
CCR5
by maraviroc induces significant cytotoxic and apoptotic effects in colorectal cancer cells. Thus, maraviroc can be considered a model compound, which may foster the development of further
CCR5
antagonists to be used for the treatment of colorectal cancer. |
| doi_str_mv | 10.1007/s12032-015-0607-x |
| format | Article |
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CCR5
or
CD195
) have been correlated with disease progression in different cancers. Recently, a few investigations have reported the blockage of this receptor by an antagonist (maraviroc) and its antineoplastic effects on tumor cell growth. However, little is known about the mechanistic reasons behind these antineoplastic effects of
CCR5
blockage by maraviroc. In this study, we blocked the
CCR5
receptor by maraviroc in SW480 and SW620 colorectal cancer cells to study the resulting changes in biological properties and related pathways. This blockage induced significantly reduced proliferation and a profound arrest in G1 phase of the cell cycle. Concomitantly, maraviroc caused significant signs of apoptosis at morphological level. Significant modulation of multiple apoptosis-relevant genes was also noticed at mRNA levels. In addition, we found remarkable increases in cleaved caspases at protein level. These modulations led us to propose a signaling pathway for the observed apoptotic effects. In conclusion, blocking the
CCR5
by maraviroc induces significant cytotoxic and apoptotic effects in colorectal cancer cells. Thus, maraviroc can be considered a model compound, which may foster the development of further
CCR5
antagonists to be used for the treatment of colorectal cancer.</description><identifier>ISSN: 1357-0560</identifier><identifier>EISSN: 1559-131X</identifier><identifier>DOI: 10.1007/s12032-015-0607-x</identifier><identifier>PMID: 25840792</identifier><identifier>CODEN: MONCEZ</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Antineoplastic Agents - pharmacology ; Apoptosis - drug effects ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Colorectal cancer ; Colorectal Neoplasms - drug therapy ; Colorectal Neoplasms - metabolism ; Cyclohexanes - pharmacology ; G1 Phase ; Hematology ; Humans ; Internal Medicine ; Medicine ; Medicine & Public Health ; Oncology ; Original Paper ; Pathology ; Receptors, CCR5 - metabolism ; RNA, Messenger - genetics ; Signal Transduction - drug effects ; Triazoles - pharmacology</subject><ispartof>Medical oncology (Northwood, London, England), 2015-05, Vol.32 (5), p.158, Article 158</ispartof><rights>Springer Science+Business Media New York 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c512t-9c6ab75be9c753da631e9616a1833d99d9d25c4ca8bc8ae0a63fbcca1c8d229c3</citedby><cites>FETCH-LOGICAL-c512t-9c6ab75be9c753da631e9616a1833d99d9d25c4ca8bc8ae0a63fbcca1c8d229c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12032-015-0607-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12032-015-0607-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25840792$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pervaiz, Asim</creatorcontrib><creatorcontrib>Ansari, Shariq</creatorcontrib><creatorcontrib>Berger, Martin R.</creatorcontrib><creatorcontrib>Adwan, Hassan</creatorcontrib><title>CCR5 blockage by maraviroc induces cytotoxic and apoptotic effects in colorectal cancer cells</title><title>Medical oncology (Northwood, London, England)</title><addtitle>Med Oncol</addtitle><addtitle>Med Oncol</addtitle><description>Alterations in the expression of C–C chemokine receptor type 5 (
CCR5
or
CD195
) have been correlated with disease progression in different cancers. Recently, a few investigations have reported the blockage of this receptor by an antagonist (maraviroc) and its antineoplastic effects on tumor cell growth. However, little is known about the mechanistic reasons behind these antineoplastic effects of
CCR5
blockage by maraviroc. In this study, we blocked the
CCR5
receptor by maraviroc in SW480 and SW620 colorectal cancer cells to study the resulting changes in biological properties and related pathways. This blockage induced significantly reduced proliferation and a profound arrest in G1 phase of the cell cycle. Concomitantly, maraviroc caused significant signs of apoptosis at morphological level. Significant modulation of multiple apoptosis-relevant genes was also noticed at mRNA levels. In addition, we found remarkable increases in cleaved caspases at protein level. These modulations led us to propose a signaling pathway for the observed apoptotic effects. In conclusion, blocking the
CCR5
by maraviroc induces significant cytotoxic and apoptotic effects in colorectal cancer cells. Thus, maraviroc can be considered a model compound, which may foster the development of further
CCR5
antagonists to be used for the treatment of colorectal cancer.</description><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis - drug effects</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Colorectal cancer</subject><subject>Colorectal Neoplasms - drug therapy</subject><subject>Colorectal Neoplasms - metabolism</subject><subject>Cyclohexanes - pharmacology</subject><subject>G1 Phase</subject><subject>Hematology</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Oncology</subject><subject>Original Paper</subject><subject>Pathology</subject><subject>Receptors, CCR5 - metabolism</subject><subject>RNA, Messenger - genetics</subject><subject>Signal Transduction - drug effects</subject><subject>Triazoles - pharmacology</subject><issn>1357-0560</issn><issn>1559-131X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kF1LwzAUhoMobk5_gDcS8Dqaj6VtLqX4BQNBFLyRkJ6mo7NratLK9u_N6BRvvEpe8pz3kAehc0avGKXpdWCcCk4ok4QmNCWbAzRlUirCBHs7jHchU0JlQifoJIQVpZxJro7RhMtsTlPFp-g9z58lLhoHH2ZpcbHFa-PNV-0d4LotB7ABw7Z3vdvUgE1bYtO5LuaYbFVZ6EPkMLjG-RhMg8G0YD0G2zThFB1Vpgn2bH_O0Ovd7Uv-QBZP94_5zYKAZLwnChJTpLKwClIpSpMIZlXCEsMyIUqlSlVyCXMwWQGZsTQCVQFgGGQl5wrEDF2OvZ13n4MNvV65wbdxpWaJUjQTcp5Fio0UeBeCt5XufB2_u9WM6p1QPQrVUajeCdWbOHOxbx6KtS1_J34MRoCPQIhP7dL6P6v_bf0GqfeCRw</recordid><startdate>20150501</startdate><enddate>20150501</enddate><creator>Pervaiz, Asim</creator><creator>Ansari, Shariq</creator><creator>Berger, Martin R.</creator><creator>Adwan, Hassan</creator><general>Springer US</general><general>Springer Nature B.V</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20150501</creationdate><title>CCR5 blockage by maraviroc induces cytotoxic and apoptotic effects in colorectal cancer cells</title><author>Pervaiz, Asim ; Ansari, Shariq ; Berger, Martin R. ; Adwan, Hassan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c512t-9c6ab75be9c753da631e9616a1833d99d9d25c4ca8bc8ae0a63fbcca1c8d229c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Antineoplastic Agents - pharmacology</topic><topic>Apoptosis - drug effects</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Colorectal cancer</topic><topic>Colorectal Neoplasms - drug therapy</topic><topic>Colorectal Neoplasms - metabolism</topic><topic>Cyclohexanes - pharmacology</topic><topic>G1 Phase</topic><topic>Hematology</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Oncology</topic><topic>Original Paper</topic><topic>Pathology</topic><topic>Receptors, CCR5 - metabolism</topic><topic>RNA, Messenger - genetics</topic><topic>Signal Transduction - drug effects</topic><topic>Triazoles - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pervaiz, Asim</creatorcontrib><creatorcontrib>Ansari, Shariq</creatorcontrib><creatorcontrib>Berger, Martin R.</creatorcontrib><creatorcontrib>Adwan, Hassan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Medical oncology (Northwood, London, England)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pervaiz, Asim</au><au>Ansari, Shariq</au><au>Berger, Martin R.</au><au>Adwan, Hassan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CCR5 blockage by maraviroc induces cytotoxic and apoptotic effects in colorectal cancer cells</atitle><jtitle>Medical oncology (Northwood, London, England)</jtitle><stitle>Med Oncol</stitle><addtitle>Med Oncol</addtitle><date>2015-05-01</date><risdate>2015</risdate><volume>32</volume><issue>5</issue><spage>158</spage><pages>158-</pages><artnum>158</artnum><issn>1357-0560</issn><eissn>1559-131X</eissn><coden>MONCEZ</coden><abstract>Alterations in the expression of C–C chemokine receptor type 5 (
CCR5
or
CD195
) have been correlated with disease progression in different cancers. Recently, a few investigations have reported the blockage of this receptor by an antagonist (maraviroc) and its antineoplastic effects on tumor cell growth. However, little is known about the mechanistic reasons behind these antineoplastic effects of
CCR5
blockage by maraviroc. In this study, we blocked the
CCR5
receptor by maraviroc in SW480 and SW620 colorectal cancer cells to study the resulting changes in biological properties and related pathways. This blockage induced significantly reduced proliferation and a profound arrest in G1 phase of the cell cycle. Concomitantly, maraviroc caused significant signs of apoptosis at morphological level. Significant modulation of multiple apoptosis-relevant genes was also noticed at mRNA levels. In addition, we found remarkable increases in cleaved caspases at protein level. These modulations led us to propose a signaling pathway for the observed apoptotic effects. In conclusion, blocking the
CCR5
by maraviroc induces significant cytotoxic and apoptotic effects in colorectal cancer cells. Thus, maraviroc can be considered a model compound, which may foster the development of further
CCR5
antagonists to be used for the treatment of colorectal cancer.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>25840792</pmid><doi>10.1007/s12032-015-0607-x</doi></addata></record> |
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| identifier | ISSN: 1357-0560 |
| ispartof | Medical oncology (Northwood, London, England), 2015-05, Vol.32 (5), p.158, Article 158 |
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| source | MEDLINE; SpringerLink Journals |
| subjects | Antineoplastic Agents - pharmacology Apoptosis - drug effects Cell Line, Tumor Cell Proliferation - drug effects Colorectal cancer Colorectal Neoplasms - drug therapy Colorectal Neoplasms - metabolism Cyclohexanes - pharmacology G1 Phase Hematology Humans Internal Medicine Medicine Medicine & Public Health Oncology Original Paper Pathology Receptors, CCR5 - metabolism RNA, Messenger - genetics Signal Transduction - drug effects Triazoles - pharmacology |
| title | CCR5 blockage by maraviroc induces cytotoxic and apoptotic effects in colorectal cancer cells |
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