Variation in dermcidin expression in a range of primary human tumours and in hypoxic/oxidatively stressed human cell lines
Dermcidin acts as a survival factor in a variety of cancer cell lines under hypoxia or oxidative stress. The aim of this study was to evaluate dermcidin expression in cell lines following simulation of tumour microenvironmental conditions and in a range of primary tumours. Tumour tissues were collec...
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| Veröffentlicht in: | British journal of cancer 2008-07, Vol.99 (1), p.126-132 |
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| creator | Stewart, G D Skipworth, R J E Pennington, C J Lowrie, A G Deans, D A C Edwards, D R Habib, F K Riddick, A C P Fearon, K C H Ross, J A |
| description | Dermcidin acts as a survival factor in a variety of cancer cell lines under hypoxia or oxidative stress. The aim of this study was to evaluate dermcidin expression in cell lines following simulation of tumour microenvironmental conditions and in a range of primary tumours. Tumour tissues were collected from patients with oesophageal (28 samples), gastric (20), pancreatic (five), bile duct (one) and prostatic (52) carcinomas as well as 30 benign tissue samples, for assessment of dermcidin mRNA levels using real-time PCR. Dermcidin expression was assessed in prostatic and pancreatic cancer cell lines, with and without induction of hypoxia or oxidative stress. Dermcidin mRNA expression was very low or absent in both unstressed and stressed prostate cell lines. None of the primary prostate tissue, benign or malignant, expressed dermcidin mRNA. Only two (4%) of the gastro-oesophageal cancer samples expressed moderate quantities of dermcidin mRNA. However, three (60%) of the pancreatic cancer samples and the single cholangiocarcinoma specimen had moderate/high levels of dermcidin expression. Of the two pancreatic cancer cell lines, one expressed dermcidin moderately but neither showed a response to hypoxia or oxidative stress. Expression of dermcidin in human primary tumours appears highly variable and is not induced substantially by hypoxia/oxidative stress in cell line model systems. The relationship of these findings to dermcidin protein levels and cell survival remains to be determined. |
| doi_str_mv | 10.1038/sj.bjc.6604458 |
| format | Article |
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The aim of this study was to evaluate dermcidin expression in cell lines following simulation of tumour microenvironmental conditions and in a range of primary tumours. Tumour tissues were collected from patients with oesophageal (28 samples), gastric (20), pancreatic (five), bile duct (one) and prostatic (52) carcinomas as well as 30 benign tissue samples, for assessment of dermcidin mRNA levels using real-time PCR. Dermcidin expression was assessed in prostatic and pancreatic cancer cell lines, with and without induction of hypoxia or oxidative stress. Dermcidin mRNA expression was very low or absent in both unstressed and stressed prostate cell lines. None of the primary prostate tissue, benign or malignant, expressed dermcidin mRNA. Only two (4%) of the gastro-oesophageal cancer samples expressed moderate quantities of dermcidin mRNA. However, three (60%) of the pancreatic cancer samples and the single cholangiocarcinoma specimen had moderate/high levels of dermcidin expression. Of the two pancreatic cancer cell lines, one expressed dermcidin moderately but neither showed a response to hypoxia or oxidative stress. Expression of dermcidin in human primary tumours appears highly variable and is not induced substantially by hypoxia/oxidative stress in cell line model systems. The relationship of these findings to dermcidin protein levels and cell survival remains to be determined.</description><identifier>ISSN: 0007-0920</identifier><identifier>EISSN: 1532-1827</identifier><identifier>DOI: 10.1038/sj.bjc.6604458</identifier><identifier>PMID: 18594538</identifier><identifier>CODEN: BJCAAI</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Amino acids ; Bile ducts ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Breast cancer ; Cancer Research ; Cell growth ; Cell Line ; Cell Line, Tumor ; Drug Resistance ; Epidemiology ; Esophageal cancer ; Humans ; Hypoxia ; Hypoxia - physiopathology ; Medical research ; Medical sciences ; Molecular Medicine ; Neoplasms - metabolism ; Nephrology. Urinary tract diseases ; Nerve Tissue Proteins - biosynthesis ; Oncology ; Oxidative stress ; Oxidative Stress - physiology ; Pancreatic cancer ; Peptides ; Polymerase Chain Reaction ; Polypeptides ; Prostate cancer ; Proteins ; RNA, Messenger - biosynthesis ; Translational Therapeutics ; Tumors ; Tumors of the urinary system ; Urinary tract. Prostate gland</subject><ispartof>British journal of cancer, 2008-07, Vol.99 (1), p.126-132</ispartof><rights>The Author(s) 2008</rights><rights>2008 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jul 8, 2008</rights><rights>Copyright © 2008 Cancer Research UK 2008 Cancer Research UK</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c485t-271c2305fd983fa1afbdd6e0dcbf6801a30203cb6875a87fa6725575bf33a1033</citedby><cites>FETCH-LOGICAL-c485t-271c2305fd983fa1afbdd6e0dcbf6801a30203cb6875a87fa6725575bf33a1033</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/PMC2453008/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2453008/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,41464,42533,51294,53766,53768</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20509083$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18594538$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Stewart, G D</creatorcontrib><creatorcontrib>Skipworth, R J E</creatorcontrib><creatorcontrib>Pennington, C J</creatorcontrib><creatorcontrib>Lowrie, A G</creatorcontrib><creatorcontrib>Deans, D A C</creatorcontrib><creatorcontrib>Edwards, D R</creatorcontrib><creatorcontrib>Habib, F K</creatorcontrib><creatorcontrib>Riddick, A C P</creatorcontrib><creatorcontrib>Fearon, K C H</creatorcontrib><creatorcontrib>Ross, J A</creatorcontrib><title>Variation in dermcidin expression in a range of primary human tumours and in hypoxic/oxidatively stressed human cell lines</title><title>British journal of cancer</title><addtitle>Br J Cancer</addtitle><addtitle>Br J Cancer</addtitle><description>Dermcidin acts as a survival factor in a variety of cancer cell lines under hypoxia or oxidative stress. The aim of this study was to evaluate dermcidin expression in cell lines following simulation of tumour microenvironmental conditions and in a range of primary tumours. Tumour tissues were collected from patients with oesophageal (28 samples), gastric (20), pancreatic (five), bile duct (one) and prostatic (52) carcinomas as well as 30 benign tissue samples, for assessment of dermcidin mRNA levels using real-time PCR. Dermcidin expression was assessed in prostatic and pancreatic cancer cell lines, with and without induction of hypoxia or oxidative stress. Dermcidin mRNA expression was very low or absent in both unstressed and stressed prostate cell lines. None of the primary prostate tissue, benign or malignant, expressed dermcidin mRNA. Only two (4%) of the gastro-oesophageal cancer samples expressed moderate quantities of dermcidin mRNA. However, three (60%) of the pancreatic cancer samples and the single cholangiocarcinoma specimen had moderate/high levels of dermcidin expression. Of the two pancreatic cancer cell lines, one expressed dermcidin moderately but neither showed a response to hypoxia or oxidative stress. Expression of dermcidin in human primary tumours appears highly variable and is not induced substantially by hypoxia/oxidative stress in cell line model systems. The relationship of these findings to dermcidin protein levels and cell survival remains to be determined.</description><subject>Amino acids</subject><subject>Bile ducts</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Breast cancer</subject><subject>Cancer Research</subject><subject>Cell growth</subject><subject>Cell Line</subject><subject>Cell Line, Tumor</subject><subject>Drug Resistance</subject><subject>Epidemiology</subject><subject>Esophageal cancer</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Hypoxia - physiopathology</subject><subject>Medical research</subject><subject>Medical sciences</subject><subject>Molecular Medicine</subject><subject>Neoplasms - metabolism</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nerve Tissue Proteins - biosynthesis</subject><subject>Oncology</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - physiology</subject><subject>Pancreatic cancer</subject><subject>Peptides</subject><subject>Polymerase Chain Reaction</subject><subject>Polypeptides</subject><subject>Prostate cancer</subject><subject>Proteins</subject><subject>RNA, Messenger - biosynthesis</subject><subject>Translational Therapeutics</subject><subject>Tumors</subject><subject>Tumors of the urinary system</subject><subject>Urinary tract. 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Urinary tract diseases</topic><topic>Nerve Tissue Proteins - biosynthesis</topic><topic>Oncology</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - physiology</topic><topic>Pancreatic cancer</topic><topic>Peptides</topic><topic>Polymerase Chain Reaction</topic><topic>Polypeptides</topic><topic>Prostate cancer</topic><topic>Proteins</topic><topic>RNA, Messenger - biosynthesis</topic><topic>Translational Therapeutics</topic><topic>Tumors</topic><topic>Tumors of the urinary system</topic><topic>Urinary tract. Prostate gland</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Stewart, G D</creatorcontrib><creatorcontrib>Skipworth, R J E</creatorcontrib><creatorcontrib>Pennington, C J</creatorcontrib><creatorcontrib>Lowrie, A G</creatorcontrib><creatorcontrib>Deans, D A C</creatorcontrib><creatorcontrib>Edwards, D R</creatorcontrib><creatorcontrib>Habib, F K</creatorcontrib><creatorcontrib>Riddick, A C P</creatorcontrib><creatorcontrib>Fearon, K C H</creatorcontrib><creatorcontrib>Ross, J A</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Pascal-Francis</collection><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>Nursing & Allied Health Database</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</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>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</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>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</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>British journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Stewart, G D</au><au>Skipworth, R J E</au><au>Pennington, C J</au><au>Lowrie, A G</au><au>Deans, D A C</au><au>Edwards, D R</au><au>Habib, F K</au><au>Riddick, A C P</au><au>Fearon, K C H</au><au>Ross, J A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Variation in dermcidin expression in a range of primary human tumours and in hypoxic/oxidatively stressed human cell lines</atitle><jtitle>British journal of cancer</jtitle><stitle>Br J Cancer</stitle><addtitle>Br J Cancer</addtitle><date>2008-07-08</date><risdate>2008</risdate><volume>99</volume><issue>1</issue><spage>126</spage><epage>132</epage><pages>126-132</pages><issn>0007-0920</issn><eissn>1532-1827</eissn><coden>BJCAAI</coden><abstract>Dermcidin acts as a survival factor in a variety of cancer cell lines under hypoxia or oxidative stress. The aim of this study was to evaluate dermcidin expression in cell lines following simulation of tumour microenvironmental conditions and in a range of primary tumours. Tumour tissues were collected from patients with oesophageal (28 samples), gastric (20), pancreatic (five), bile duct (one) and prostatic (52) carcinomas as well as 30 benign tissue samples, for assessment of dermcidin mRNA levels using real-time PCR. Dermcidin expression was assessed in prostatic and pancreatic cancer cell lines, with and without induction of hypoxia or oxidative stress. Dermcidin mRNA expression was very low or absent in both unstressed and stressed prostate cell lines. None of the primary prostate tissue, benign or malignant, expressed dermcidin mRNA. Only two (4%) of the gastro-oesophageal cancer samples expressed moderate quantities of dermcidin mRNA. However, three (60%) of the pancreatic cancer samples and the single cholangiocarcinoma specimen had moderate/high levels of dermcidin expression. Of the two pancreatic cancer cell lines, one expressed dermcidin moderately but neither showed a response to hypoxia or oxidative stress. Expression of dermcidin in human primary tumours appears highly variable and is not induced substantially by hypoxia/oxidative stress in cell line model systems. The relationship of these findings to dermcidin protein levels and cell survival remains to be determined.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>18594538</pmid><doi>10.1038/sj.bjc.6604458</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Amino acids Bile ducts Biological and medical sciences Biomedical and Life Sciences Biomedicine Breast cancer Cancer Research Cell growth Cell Line Cell Line, Tumor Drug Resistance Epidemiology Esophageal cancer Humans Hypoxia Hypoxia - physiopathology Medical research Medical sciences Molecular Medicine Neoplasms - metabolism Nephrology. Urinary tract diseases Nerve Tissue Proteins - biosynthesis Oncology Oxidative stress Oxidative Stress - physiology Pancreatic cancer Peptides Polymerase Chain Reaction Polypeptides Prostate cancer Proteins RNA, Messenger - biosynthesis Translational Therapeutics Tumors Tumors of the urinary system Urinary tract. Prostate gland |
| title | Variation in dermcidin expression in a range of primary human tumours and in hypoxic/oxidatively stressed human cell lines |
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