Oncogenic mutation or overexpression of oncogenic KRAS or BRAF is not sufficient to confer oncogene addiction
Oncogene addiction is a cellular property by which cancer cells become highly dependent on the expression of oncogenes for their survival. Oncogene addiction can be exploited to design molecularly targeted drugs that kill only cancer cells by inhibiting the specific oncogenes. Genes and cell lines e...
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| Veröffentlicht in: | PloS one 2021-04, Vol.16 (4), p.e0249388-e0249388 |
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| creator | Ito, Reina E Oneyama, Chitose Aoki, Kazuhiro |
| description | Oncogene addiction is a cellular property by which cancer cells become highly dependent on the expression of oncogenes for their survival. Oncogene addiction can be exploited to design molecularly targeted drugs that kill only cancer cells by inhibiting the specific oncogenes. Genes and cell lines exhibiting oncogene addiction, as well as the mechanisms by which cell death is induced when addicted oncogenes are suppressed, have been extensively studied. However, it is still not fully understood how oncogene addiction is acquired in cancer cells. Here, we take a synthetic biology approach to investigate whether oncogenic mutation or oncogene expression suffices to confer the property of oncogene addiction to cancer cells. We employed human mammary epithelium-derived MCF-10A cells expressing the oncogenic KRAS or BRAF. MCF-10A cells harboring an oncogenic mutation in a single-allele of KRAS or BRAF showed weak transformation activity, but no characteristics of oncogene addiction. MCF-10A cells overexpressing oncogenic KRAS demonstrated the transformation activity, but MCF-10A cells overexpressing oncogenic BRAF did not. Neither cell line exhibited any oncogene addiction properties. These results indicate that the introduction of oncogenic mutation or the overexpression of oncogenes is not sufficient for cells to acquire oncogene addiction, and that oncogene addiction is not associated with transformation activity. |
| doi_str_mv | 10.1371/journal.pone.0249388 |
| format | Article |
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Oncogene addiction can be exploited to design molecularly targeted drugs that kill only cancer cells by inhibiting the specific oncogenes. Genes and cell lines exhibiting oncogene addiction, as well as the mechanisms by which cell death is induced when addicted oncogenes are suppressed, have been extensively studied. However, it is still not fully understood how oncogene addiction is acquired in cancer cells. Here, we take a synthetic biology approach to investigate whether oncogenic mutation or oncogene expression suffices to confer the property of oncogene addiction to cancer cells. We employed human mammary epithelium-derived MCF-10A cells expressing the oncogenic KRAS or BRAF. MCF-10A cells harboring an oncogenic mutation in a single-allele of KRAS or BRAF showed weak transformation activity, but no characteristics of oncogene addiction. MCF-10A cells overexpressing oncogenic KRAS demonstrated the transformation activity, but MCF-10A cells overexpressing oncogenic BRAF did not. Neither cell line exhibited any oncogene addiction properties. These results indicate that the introduction of oncogenic mutation or the overexpression of oncogenes is not sufficient for cells to acquire oncogene addiction, and that oncogene addiction is not associated with transformation activity.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0249388</identifier><identifier>PMID: 33793658</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Addiction ; Addictions ; Angiogenesis ; Biology and Life Sciences ; Cancer ; Cancer cells ; Cell proliferation ; Cell survival ; Control ; Doxycycline ; Gene mutations ; Growth rate ; Health aspects ; Inactivation ; K-Ras protein ; Kinases ; Medicine and Health Sciences ; Mutation ; Oncogenes ; Physiological aspects ; Plasmids ; Properties (attributes) ; Proto-oncogenes ; Research and Analysis Methods ; Social Sciences ; Survival ; Transcription activation ; Tumor suppressor genes ; Tumorigenesis ; Tumors</subject><ispartof>PloS one, 2021-04, Vol.16 (4), p.e0249388-e0249388</ispartof><rights>COPYRIGHT 2021 Public Library of Science</rights><rights>2021 Ito et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 Ito et al 2021 Ito et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-d7f3693d555b1031971cd709454a37b1c4b8dde1ec1d697243666acf6d61c4613</citedby><cites>FETCH-LOGICAL-c692t-d7f3693d555b1031971cd709454a37b1c4b8dde1ec1d697243666acf6d61c4613</cites><orcidid>0000-0001-7263-1555</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/PMC8016361/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8016361/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2100,2926,23864,27922,27923,53789,53791,79370,79371</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33793658$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Gupta, Romi</contributor><creatorcontrib>Ito, Reina E</creatorcontrib><creatorcontrib>Oneyama, Chitose</creatorcontrib><creatorcontrib>Aoki, Kazuhiro</creatorcontrib><title>Oncogenic mutation or overexpression of oncogenic KRAS or BRAF is not sufficient to confer oncogene addiction</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Oncogene addiction is a cellular property by which cancer cells become highly dependent on the expression of oncogenes for their survival. Oncogene addiction can be exploited to design molecularly targeted drugs that kill only cancer cells by inhibiting the specific oncogenes. Genes and cell lines exhibiting oncogene addiction, as well as the mechanisms by which cell death is induced when addicted oncogenes are suppressed, have been extensively studied. However, it is still not fully understood how oncogene addiction is acquired in cancer cells. Here, we take a synthetic biology approach to investigate whether oncogenic mutation or oncogene expression suffices to confer the property of oncogene addiction to cancer cells. We employed human mammary epithelium-derived MCF-10A cells expressing the oncogenic KRAS or BRAF. MCF-10A cells harboring an oncogenic mutation in a single-allele of KRAS or BRAF showed weak transformation activity, but no characteristics of oncogene addiction. MCF-10A cells overexpressing oncogenic KRAS demonstrated the transformation activity, but MCF-10A cells overexpressing oncogenic BRAF did not. Neither cell line exhibited any oncogene addiction properties. These results indicate that the introduction of oncogenic mutation or the overexpression of oncogenes is not sufficient for cells to acquire oncogene addiction, and that oncogene addiction is not associated with transformation activity.</description><subject>Addiction</subject><subject>Addictions</subject><subject>Angiogenesis</subject><subject>Biology and Life Sciences</subject><subject>Cancer</subject><subject>Cancer cells</subject><subject>Cell proliferation</subject><subject>Cell survival</subject><subject>Control</subject><subject>Doxycycline</subject><subject>Gene mutations</subject><subject>Growth rate</subject><subject>Health aspects</subject><subject>Inactivation</subject><subject>K-Ras protein</subject><subject>Kinases</subject><subject>Medicine and Health Sciences</subject><subject>Mutation</subject><subject>Oncogenes</subject><subject>Physiological aspects</subject><subject>Plasmids</subject><subject>Properties 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Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ito, Reina E</au><au>Oneyama, Chitose</au><au>Aoki, Kazuhiro</au><au>Gupta, Romi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oncogenic mutation or overexpression of oncogenic KRAS or BRAF is not sufficient to confer oncogene addiction</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2021-04-01</date><risdate>2021</risdate><volume>16</volume><issue>4</issue><spage>e0249388</spage><epage>e0249388</epage><pages>e0249388-e0249388</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Oncogene addiction is a cellular property by which cancer cells become highly dependent on the expression of oncogenes for their survival. Oncogene addiction can be exploited to design molecularly targeted drugs that kill only cancer cells by inhibiting the specific oncogenes. Genes and cell lines exhibiting oncogene addiction, as well as the mechanisms by which cell death is induced when addicted oncogenes are suppressed, have been extensively studied. However, it is still not fully understood how oncogene addiction is acquired in cancer cells. Here, we take a synthetic biology approach to investigate whether oncogenic mutation or oncogene expression suffices to confer the property of oncogene addiction to cancer cells. We employed human mammary epithelium-derived MCF-10A cells expressing the oncogenic KRAS or BRAF. MCF-10A cells harboring an oncogenic mutation in a single-allele of KRAS or BRAF showed weak transformation activity, but no characteristics of oncogene addiction. MCF-10A cells overexpressing oncogenic KRAS demonstrated the transformation activity, but MCF-10A cells overexpressing oncogenic BRAF did not. Neither cell line exhibited any oncogene addiction properties. These results indicate that the introduction of oncogenic mutation or the overexpression of oncogenes is not sufficient for cells to acquire oncogene addiction, and that oncogene addiction is not associated with transformation activity.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>33793658</pmid><doi>10.1371/journal.pone.0249388</doi><tpages>e0249388</tpages><orcidid>https://orcid.org/0000-0001-7263-1555</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Addiction Addictions Angiogenesis Biology and Life Sciences Cancer Cancer cells Cell proliferation Cell survival Control Doxycycline Gene mutations Growth rate Health aspects Inactivation K-Ras protein Kinases Medicine and Health Sciences Mutation Oncogenes Physiological aspects Plasmids Properties (attributes) Proto-oncogenes Research and Analysis Methods Social Sciences Survival Transcription activation Tumor suppressor genes Tumorigenesis Tumors |
| title | Oncogenic mutation or overexpression of oncogenic KRAS or BRAF is not sufficient to confer oncogene addiction |
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