Overexpression of peptide deformylase in breast, colon, and lung cancers
Human mitochondrial peptide deformylase (PDF) has been proposed as a novel cancer therapeutic target. However, very little is known about its expression and regulation in human tissues. The purpose of this study was to characterize the expression pattern of PDF in cancerous tissues and to identify m...
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| Veröffentlicht in: | BMC cancer 2013-07, Vol.13 (1), p.321-321, Article 321 |
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| description | Human mitochondrial peptide deformylase (PDF) has been proposed as a novel cancer therapeutic target. However, very little is known about its expression and regulation in human tissues. The purpose of this study was to characterize the expression pattern of PDF in cancerous tissues and to identify mechanisms that regulate its expression.
The mRNA expression levels of PDF and methionine aminopeptidase 1D (MAP1D), an enzyme involved in a related pathway with PDF, were determined using tissue panels containing cDNA from patients with various types of cancer (breast, colon, kidney, liver, lung, ovarian, prostate, or thyroid) and human cell lines. Protein levels of PDF were also determined in 2 colon cancer patients via western blotting. Colon cancer cells were treated with inhibitors of ERK, Akt, and mTOR signaling pathways and the resulting effects on PDF and MAP1D mRNA levels were determined by qPCR for colon and lung cancer cell lines. Finally, the effects of a PDF inhibitor, actinonin, on the proliferation of breast, colon, and prostate cell lines were determined using the CyQUANT assay.
PDF and MAP1D mRNA levels were elevated in cancer cell lines compared to non-cancer lines. PDF mRNA levels were significantly increased in breast, colon, and lung cancer samples while MAP1D mRNA levels were increased in just colon cancers. The expression of PDF and MAP1D varied with stage in these cancers. Further, PDF protein expression was elevated in colon cancer tissue samples. Inhibition of the MEK/ERK, but not PI3K or mTOR, pathway reduced the expression of PDF and MAP1D in both colon and lung cancer cell lines. Further, inhibition of PDF with actinonin resulted in greater reduction of breast, colon, and prostate cancer cell proliferation than non-cancer cell lines.
This is the first report showing that PDF is over-expressed in breast, colon, and lung cancers, and the first evidence that the MEK/ERK pathway plays a role in regulating the expression of PDF and MAP1D. The over-expression of PDF in several cancers and the inhibition of cancer cell growth by a PDF inhibitor suggest this enzyme may act as an oncogene to promote cancer cell proliferation. |
| doi_str_mv | 10.1186/1471-2407-13-321 |
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The mRNA expression levels of PDF and methionine aminopeptidase 1D (MAP1D), an enzyme involved in a related pathway with PDF, were determined using tissue panels containing cDNA from patients with various types of cancer (breast, colon, kidney, liver, lung, ovarian, prostate, or thyroid) and human cell lines. Protein levels of PDF were also determined in 2 colon cancer patients via western blotting. Colon cancer cells were treated with inhibitors of ERK, Akt, and mTOR signaling pathways and the resulting effects on PDF and MAP1D mRNA levels were determined by qPCR for colon and lung cancer cell lines. Finally, the effects of a PDF inhibitor, actinonin, on the proliferation of breast, colon, and prostate cell lines were determined using the CyQUANT assay.
PDF and MAP1D mRNA levels were elevated in cancer cell lines compared to non-cancer lines. PDF mRNA levels were significantly increased in breast, colon, and lung cancer samples while MAP1D mRNA levels were increased in just colon cancers. The expression of PDF and MAP1D varied with stage in these cancers. Further, PDF protein expression was elevated in colon cancer tissue samples. Inhibition of the MEK/ERK, but not PI3K or mTOR, pathway reduced the expression of PDF and MAP1D in both colon and lung cancer cell lines. Further, inhibition of PDF with actinonin resulted in greater reduction of breast, colon, and prostate cancer cell proliferation than non-cancer cell lines.
This is the first report showing that PDF is over-expressed in breast, colon, and lung cancers, and the first evidence that the MEK/ERK pathway plays a role in regulating the expression of PDF and MAP1D. The over-expression of PDF in several cancers and the inhibition of cancer cell growth by a PDF inhibitor suggest this enzyme may act as an oncogene to promote cancer cell proliferation.</description><identifier>ISSN: 1471-2407</identifier><identifier>EISSN: 1471-2407</identifier><identifier>DOI: 10.1186/1471-2407-13-321</identifier><identifier>PMID: 23815882</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Amidohydrolases - analysis ; Amidohydrolases - biosynthesis ; Aminopeptidases - analysis ; Aminopeptidases - biosynthesis ; Biomarkers, Tumor - analysis ; Biotechnology industry ; Blotting, Western ; Breast cancer ; Breast Neoplasms - metabolism ; Cancer ; Colon ; Colon cancer ; Colonic Neoplasms - metabolism ; Colorectal cancer ; Development and progression ; Enzymes ; Female ; Humans ; Kinases ; Lung Neoplasms - metabolism ; Male ; Medical research ; Mitochondrial DNA ; Physiological aspects ; Prevention ; Prostate cancer ; Proteins ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction - physiology ; Tissue Array Analysis</subject><ispartof>BMC cancer, 2013-07, Vol.13 (1), p.321-321, Article 321</ispartof><rights>COPYRIGHT 2013 BioMed Central Ltd.</rights><rights>2013 Randhawa et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2013 Randhawa et al.; licensee BioMed Central Ltd. 2013 Randhawa et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b682t-4c41b1bc1274aeda6fc6c7861034cfbf11c76c420c5562e5d2672a344a70410c3</citedby><cites>FETCH-LOGICAL-b682t-4c41b1bc1274aeda6fc6c7861034cfbf11c76c420c5562e5d2672a344a70410c3</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/PMC3722014/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3722014/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23815882$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Randhawa, Harsharan</creatorcontrib><creatorcontrib>Chikara, Shireen</creatorcontrib><creatorcontrib>Gehring, Drew</creatorcontrib><creatorcontrib>Yildirim, Tuba</creatorcontrib><creatorcontrib>Menon, Jyotsana</creatorcontrib><creatorcontrib>Reindl, Katie M</creatorcontrib><title>Overexpression of peptide deformylase in breast, colon, and lung cancers</title><title>BMC cancer</title><addtitle>BMC Cancer</addtitle><description>Human mitochondrial peptide deformylase (PDF) has been proposed as a novel cancer therapeutic target. However, very little is known about its expression and regulation in human tissues. The purpose of this study was to characterize the expression pattern of PDF in cancerous tissues and to identify mechanisms that regulate its expression.
The mRNA expression levels of PDF and methionine aminopeptidase 1D (MAP1D), an enzyme involved in a related pathway with PDF, were determined using tissue panels containing cDNA from patients with various types of cancer (breast, colon, kidney, liver, lung, ovarian, prostate, or thyroid) and human cell lines. Protein levels of PDF were also determined in 2 colon cancer patients via western blotting. Colon cancer cells were treated with inhibitors of ERK, Akt, and mTOR signaling pathways and the resulting effects on PDF and MAP1D mRNA levels were determined by qPCR for colon and lung cancer cell lines. Finally, the effects of a PDF inhibitor, actinonin, on the proliferation of breast, colon, and prostate cell lines were determined using the CyQUANT assay.
PDF and MAP1D mRNA levels were elevated in cancer cell lines compared to non-cancer lines. PDF mRNA levels were significantly increased in breast, colon, and lung cancer samples while MAP1D mRNA levels were increased in just colon cancers. The expression of PDF and MAP1D varied with stage in these cancers. Further, PDF protein expression was elevated in colon cancer tissue samples. Inhibition of the MEK/ERK, but not PI3K or mTOR, pathway reduced the expression of PDF and MAP1D in both colon and lung cancer cell lines. Further, inhibition of PDF with actinonin resulted in greater reduction of breast, colon, and prostate cancer cell proliferation than non-cancer cell lines.
This is the first report showing that PDF is over-expressed in breast, colon, and lung cancers, and the first evidence that the MEK/ERK pathway plays a role in regulating the expression of PDF and MAP1D. The over-expression of PDF in several cancers and the inhibition of cancer cell growth by a PDF inhibitor suggest this enzyme may act as an oncogene to promote cancer cell proliferation.</description><subject>Amidohydrolases - analysis</subject><subject>Amidohydrolases - biosynthesis</subject><subject>Aminopeptidases - analysis</subject><subject>Aminopeptidases - biosynthesis</subject><subject>Biomarkers, Tumor - analysis</subject><subject>Biotechnology industry</subject><subject>Blotting, Western</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - metabolism</subject><subject>Cancer</subject><subject>Colon</subject><subject>Colon cancer</subject><subject>Colonic Neoplasms - metabolism</subject><subject>Colorectal cancer</subject><subject>Development and progression</subject><subject>Enzymes</subject><subject>Female</subject><subject>Humans</subject><subject>Kinases</subject><subject>Lung Neoplasms - metabolism</subject><subject>Male</subject><subject>Medical research</subject><subject>Mitochondrial DNA</subject><subject>Physiological aspects</subject><subject>Prevention</subject><subject>Prostate cancer</subject><subject>Proteins</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Signal Transduction - physiology</subject><subject>Tissue Array Analysis</subject><issn>1471-2407</issn><issn>1471-2407</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNp1ks1r3DAQxU1paT7ae0_FUCgtxKlGkm3lUghL2gQCgX6chSyPdxVkyZXskPz3ldl0uy4pOkjM_N6TeJosewPkFEBUn4DXUFBO6gJYwSg8yw53ped754PsKMZbQqAWRLzMDigTUApBD7PLmzsMeD8EjNF4l_suH3AYTYt5i50P_YNVEXPj8iagiuNJrr317iRXrs3t5Na5Vk5jiK-yF52yEV8_7sfZzy8XP1aXxfXN16vV-XXRVIKOBdccGmg00JorbFXV6UrXogLCuO6aDkDXleaU6LKsKJYtrWqqGOeqJhyIZsfZ563vMDU9thrdGJSVQzC9Cg_SKyOXHWc2cu3vJKspJcCTwWpr0Bj_H4NlR_tezknKOUkJTKagk8uHx2cE_2vCOMreRI3WKod-ikkAtCxFKUhC3_2D3vopuBTSTDFGas7P_lJrZVEa1_l0uZ5N5XnJeAWUs5k6fYJKq8XeaO-wM6m-EHxcCBIz4v24VlOM8ur7tyX7fo_doLLjJno7jWkw4hIkW1AHH2PAbpceEDkP5lN5vd3_tp3gzySy31ZX2mc</recordid><startdate>20130701</startdate><enddate>20130701</enddate><creator>Randhawa, Harsharan</creator><creator>Chikara, Shireen</creator><creator>Gehring, Drew</creator><creator>Yildirim, Tuba</creator><creator>Menon, Jyotsana</creator><creator>Reindl, Katie M</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>ISR</scope><scope>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20130701</creationdate><title>Overexpression of peptide deformylase in breast, colon, and lung cancers</title><author>Randhawa, Harsharan ; Chikara, Shireen ; Gehring, Drew ; Yildirim, Tuba ; Menon, Jyotsana ; Reindl, Katie M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b682t-4c41b1bc1274aeda6fc6c7861034cfbf11c76c420c5562e5d2672a344a70410c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Amidohydrolases - analysis</topic><topic>Amidohydrolases - biosynthesis</topic><topic>Aminopeptidases - analysis</topic><topic>Aminopeptidases - biosynthesis</topic><topic>Biomarkers, Tumor - analysis</topic><topic>Biotechnology industry</topic><topic>Blotting, Western</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - metabolism</topic><topic>Cancer</topic><topic>Colon</topic><topic>Colon cancer</topic><topic>Colonic Neoplasms - metabolism</topic><topic>Colorectal cancer</topic><topic>Development and progression</topic><topic>Enzymes</topic><topic>Female</topic><topic>Humans</topic><topic>Kinases</topic><topic>Lung Neoplasms - metabolism</topic><topic>Male</topic><topic>Medical research</topic><topic>Mitochondrial DNA</topic><topic>Physiological aspects</topic><topic>Prevention</topic><topic>Prostate cancer</topic><topic>Proteins</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Signal Transduction - physiology</topic><topic>Tissue Array Analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Randhawa, Harsharan</creatorcontrib><creatorcontrib>Chikara, Shireen</creatorcontrib><creatorcontrib>Gehring, Drew</creatorcontrib><creatorcontrib>Yildirim, Tuba</creatorcontrib><creatorcontrib>Menon, Jyotsana</creatorcontrib><creatorcontrib>Reindl, Katie M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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 Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Publicly Available Content 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><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BMC cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Randhawa, Harsharan</au><au>Chikara, Shireen</au><au>Gehring, Drew</au><au>Yildirim, Tuba</au><au>Menon, Jyotsana</au><au>Reindl, Katie M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overexpression of peptide deformylase in breast, colon, and lung cancers</atitle><jtitle>BMC cancer</jtitle><addtitle>BMC Cancer</addtitle><date>2013-07-01</date><risdate>2013</risdate><volume>13</volume><issue>1</issue><spage>321</spage><epage>321</epage><pages>321-321</pages><artnum>321</artnum><issn>1471-2407</issn><eissn>1471-2407</eissn><abstract>Human mitochondrial peptide deformylase (PDF) has been proposed as a novel cancer therapeutic target. However, very little is known about its expression and regulation in human tissues. The purpose of this study was to characterize the expression pattern of PDF in cancerous tissues and to identify mechanisms that regulate its expression.
The mRNA expression levels of PDF and methionine aminopeptidase 1D (MAP1D), an enzyme involved in a related pathway with PDF, were determined using tissue panels containing cDNA from patients with various types of cancer (breast, colon, kidney, liver, lung, ovarian, prostate, or thyroid) and human cell lines. Protein levels of PDF were also determined in 2 colon cancer patients via western blotting. Colon cancer cells were treated with inhibitors of ERK, Akt, and mTOR signaling pathways and the resulting effects on PDF and MAP1D mRNA levels were determined by qPCR for colon and lung cancer cell lines. Finally, the effects of a PDF inhibitor, actinonin, on the proliferation of breast, colon, and prostate cell lines were determined using the CyQUANT assay.
PDF and MAP1D mRNA levels were elevated in cancer cell lines compared to non-cancer lines. PDF mRNA levels were significantly increased in breast, colon, and lung cancer samples while MAP1D mRNA levels were increased in just colon cancers. The expression of PDF and MAP1D varied with stage in these cancers. Further, PDF protein expression was elevated in colon cancer tissue samples. Inhibition of the MEK/ERK, but not PI3K or mTOR, pathway reduced the expression of PDF and MAP1D in both colon and lung cancer cell lines. Further, inhibition of PDF with actinonin resulted in greater reduction of breast, colon, and prostate cancer cell proliferation than non-cancer cell lines.
This is the first report showing that PDF is over-expressed in breast, colon, and lung cancers, and the first evidence that the MEK/ERK pathway plays a role in regulating the expression of PDF and MAP1D. The over-expression of PDF in several cancers and the inhibition of cancer cell growth by a PDF inhibitor suggest this enzyme may act as an oncogene to promote cancer cell proliferation.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>23815882</pmid><doi>10.1186/1471-2407-13-321</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Amidohydrolases - analysis Amidohydrolases - biosynthesis Aminopeptidases - analysis Aminopeptidases - biosynthesis Biomarkers, Tumor - analysis Biotechnology industry Blotting, Western Breast cancer Breast Neoplasms - metabolism Cancer Colon Colon cancer Colonic Neoplasms - metabolism Colorectal cancer Development and progression Enzymes Female Humans Kinases Lung Neoplasms - metabolism Male Medical research Mitochondrial DNA Physiological aspects Prevention Prostate cancer Proteins Reverse Transcriptase Polymerase Chain Reaction Signal Transduction - physiology Tissue Array Analysis |
| title | Overexpression of peptide deformylase in breast, colon, and lung cancers |
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