Altered Expression of Multiple Genes Involved in Retinoic Acid Biosynthesis in Human Colorectal Cancer
All-trans-retinoic acid (atRA), the oxidized form of vitamin A (retinol), regulates a wide variety of biological processes, such as cell proliferation and differentiation. Multiple alcohol, retinol and retinaldehyde dehydrogenases (ADHs, RDHs, RALDHs) as well as aldo-keto reductases (AKRs) catalyze...
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| Veröffentlicht in: | Pathology oncology research 2014-07, Vol.20 (3), p.707-717 |
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| creator | Kropotova, Ekaterina S. Zinovieva, Olga L. Zyryanova, Alisa F. Dybovaya, Vera I. Prasolov, Vladimir S. Beresten, Sergey F. Oparina, Nina Yu Mashkova, Tamara D. |
| description | All-trans-retinoic acid (atRA), the oxidized form of vitamin A (retinol), regulates a wide variety of biological processes, such as cell proliferation and differentiation. Multiple alcohol, retinol and retinaldehyde dehydrogenases (ADHs, RDHs, RALDHs) as well as aldo-keto reductases (AKRs) catalyze atRA production. The reduced atRA biosynthesis has been observed in several human tumors, including colorectal cancer. However, subsets of atRA-synthesizing enzymes have not been determined in colorectal tumors. We investigated the expression patterns of genes involved in atRA biosynthesis in normal human colorectal tissues, primary carcinomas and cancer cell lines by RT-PCR. These genes were identified using transcriptomic data analysis (expressed sequence tags, RNA-sequencing, microarrays). Our results indicate that each step of the atRA biosynthesis pathway is dysregulated in colorectal cancer. Frequent and significant decreases in the mRNA levels of the
ADH1B
,
ADH1C
,
RDHL
,
RDH5
and
AKR1B10
genes were observed in a majority of colorectal carcinomas. The expression levels of the
RALDH1
gene were reduced, and the expression levels of the cytochrome
CYP26A1
gene increased. The human colon cancer cell lines showed a similar pattern of changes in the mRNA levels of these genes. A dramatic reduction in the expression of genes encoding the predominant retinol-oxidizing enzymes could impair atRA production. The most abundant of these genes,
ADH1B
and
ADH1C
, display decreased expression during progression from adenoma to early and more advanced stage of colorectal carcinomas. The diminished atRA biosynthesis may lead to alteration of cell growth and differentiation in the colon and rectum, thus contributing to the progression of colorectal cancer. |
| doi_str_mv | 10.1007/s12253-014-9751-4 |
| format | Article |
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ADH1B
,
ADH1C
,
RDHL
,
RDH5
and
AKR1B10
genes were observed in a majority of colorectal carcinomas. The expression levels of the
RALDH1
gene were reduced, and the expression levels of the cytochrome
CYP26A1
gene increased. The human colon cancer cell lines showed a similar pattern of changes in the mRNA levels of these genes. A dramatic reduction in the expression of genes encoding the predominant retinol-oxidizing enzymes could impair atRA production. The most abundant of these genes,
ADH1B
and
ADH1C
, display decreased expression during progression from adenoma to early and more advanced stage of colorectal carcinomas. The diminished atRA biosynthesis may lead to alteration of cell growth and differentiation in the colon and rectum, thus contributing to the progression of colorectal cancer.</description><identifier>ISSN: 1219-4956</identifier><identifier>EISSN: 1532-2807</identifier><identifier>DOI: 10.1007/s12253-014-9751-4</identifier><identifier>PMID: 24599561</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>3-Hydroxysteroid Dehydrogenases - genetics ; Adenoma - genetics ; Adenoma - pathology ; Alcohol Dehydrogenase - genetics ; Alcohol Oxidoreductases - genetics ; Aldehyde Reductase - genetics ; Biomarkers, Tumor - genetics ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Case-Control Studies ; Colon - metabolism ; Colorectal cancer ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - pathology ; Databases, Factual ; Gene Expression Profiling ; Humans ; Immunology ; Oligonucleotide Array Sequence Analysis ; Oncology ; Pathology ; Prognosis ; Rectum - metabolism ; Tretinoin - metabolism</subject><ispartof>Pathology oncology research, 2014-07, Vol.20 (3), p.707-717</ispartof><rights>Arányi Lajos Foundation 2014</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c475t-c7ee4c5905a66a319744eb7af8d0548401529064d9a3ef6f0ee2c335841865353</citedby><cites>FETCH-LOGICAL-c475t-c7ee4c5905a66a319744eb7af8d0548401529064d9a3ef6f0ee2c335841865353</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/s12253-014-9751-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12253-014-9751-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24599561$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kropotova, Ekaterina S.</creatorcontrib><creatorcontrib>Zinovieva, Olga L.</creatorcontrib><creatorcontrib>Zyryanova, Alisa F.</creatorcontrib><creatorcontrib>Dybovaya, Vera I.</creatorcontrib><creatorcontrib>Prasolov, Vladimir S.</creatorcontrib><creatorcontrib>Beresten, Sergey F.</creatorcontrib><creatorcontrib>Oparina, Nina Yu</creatorcontrib><creatorcontrib>Mashkova, Tamara D.</creatorcontrib><title>Altered Expression of Multiple Genes Involved in Retinoic Acid Biosynthesis in Human Colorectal Cancer</title><title>Pathology oncology research</title><addtitle>Pathol. Oncol. Res</addtitle><addtitle>Pathol Oncol Res</addtitle><description>All-trans-retinoic acid (atRA), the oxidized form of vitamin A (retinol), regulates a wide variety of biological processes, such as cell proliferation and differentiation. Multiple alcohol, retinol and retinaldehyde dehydrogenases (ADHs, RDHs, RALDHs) as well as aldo-keto reductases (AKRs) catalyze atRA production. The reduced atRA biosynthesis has been observed in several human tumors, including colorectal cancer. However, subsets of atRA-synthesizing enzymes have not been determined in colorectal tumors. We investigated the expression patterns of genes involved in atRA biosynthesis in normal human colorectal tissues, primary carcinomas and cancer cell lines by RT-PCR. These genes were identified using transcriptomic data analysis (expressed sequence tags, RNA-sequencing, microarrays). Our results indicate that each step of the atRA biosynthesis pathway is dysregulated in colorectal cancer. Frequent and significant decreases in the mRNA levels of the
ADH1B
,
ADH1C
,
RDHL
,
RDH5
and
AKR1B10
genes were observed in a majority of colorectal carcinomas. The expression levels of the
RALDH1
gene were reduced, and the expression levels of the cytochrome
CYP26A1
gene increased. The human colon cancer cell lines showed a similar pattern of changes in the mRNA levels of these genes. A dramatic reduction in the expression of genes encoding the predominant retinol-oxidizing enzymes could impair atRA production. The most abundant of these genes,
ADH1B
and
ADH1C
, display decreased expression during progression from adenoma to early and more advanced stage of colorectal carcinomas. The diminished atRA biosynthesis may lead to alteration of cell growth and differentiation in the colon and rectum, thus contributing to the progression of colorectal cancer.</description><subject>3-Hydroxysteroid Dehydrogenases - genetics</subject><subject>Adenoma - genetics</subject><subject>Adenoma - pathology</subject><subject>Alcohol Dehydrogenase - genetics</subject><subject>Alcohol Oxidoreductases - genetics</subject><subject>Aldehyde Reductase - genetics</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Case-Control Studies</subject><subject>Colon - metabolism</subject><subject>Colorectal cancer</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Databases, Factual</subject><subject>Gene Expression Profiling</subject><subject>Humans</subject><subject>Immunology</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Oncology</subject><subject>Pathology</subject><subject>Prognosis</subject><subject>Rectum - metabolism</subject><subject>Tretinoin - metabolism</subject><issn>1219-4956</issn><issn>1532-2807</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkU1rFTEUhoMo9kN_gBsJuHEzNd-ZLK-XfkFFkHYd0syZmpKbXJOZ0v57M9y2FKG4Ssh53vcQHoQ-UXJECdHfKmVM8o5Q0RktaSfeoH0qOetYT_TbdmfUdMJItYcOar0lLaOMeo_2mJCmPdN9NK7iBAUGfHy_LVBryAnnEf-Y4xS2EfApJKj4PN3leNeokPAvmELKweOVDwP-HnJ9SNNvqKEu07N54xJe55gL-MlFvHbJQ_mA3o0uVvj4eB6iq5Pjy_VZd_Hz9Hy9uui80HLqvAYQXhoinVKOU6OFgGvtxn4gUvSCUMkMUWIwjsOoRgLAPOeyF7RXkkt-iL7uercl_5mhTnYTqocYXYI8V0tVr5UShNP_o5IboQzjpKFf_kFv81xS-8hCaSqNMEsh3VG-5FoLjHZbwsaVB0uJXXzZnS_bfNnFlxUt8_mxeb7ewPCceBLUALYDahulGygvVr_a-hfOIJ5B</recordid><startdate>20140701</startdate><enddate>20140701</enddate><creator>Kropotova, Ekaterina S.</creator><creator>Zinovieva, Olga L.</creator><creator>Zyryanova, Alisa F.</creator><creator>Dybovaya, Vera I.</creator><creator>Prasolov, Vladimir S.</creator><creator>Beresten, Sergey F.</creator><creator>Oparina, Nina Yu</creator><creator>Mashkova, Tamara D.</creator><general>Springer Netherlands</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>7RV</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</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>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20140701</creationdate><title>Altered Expression of Multiple Genes Involved in Retinoic Acid Biosynthesis in Human Colorectal Cancer</title><author>Kropotova, Ekaterina S. ; Zinovieva, Olga L. ; Zyryanova, Alisa F. ; Dybovaya, Vera I. ; Prasolov, Vladimir S. ; Beresten, Sergey F. ; Oparina, Nina Yu ; Mashkova, Tamara D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c475t-c7ee4c5905a66a319744eb7af8d0548401529064d9a3ef6f0ee2c335841865353</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>3-Hydroxysteroid Dehydrogenases - genetics</topic><topic>Adenoma - genetics</topic><topic>Adenoma - pathology</topic><topic>Alcohol Dehydrogenase - genetics</topic><topic>Alcohol Oxidoreductases - genetics</topic><topic>Aldehyde Reductase - genetics</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Case-Control Studies</topic><topic>Colon - metabolism</topic><topic>Colorectal cancer</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Databases, Factual</topic><topic>Gene Expression Profiling</topic><topic>Humans</topic><topic>Immunology</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Oncology</topic><topic>Pathology</topic><topic>Prognosis</topic><topic>Rectum - metabolism</topic><topic>Tretinoin - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kropotova, Ekaterina S.</creatorcontrib><creatorcontrib>Zinovieva, Olga L.</creatorcontrib><creatorcontrib>Zyryanova, Alisa F.</creatorcontrib><creatorcontrib>Dybovaya, Vera I.</creatorcontrib><creatorcontrib>Prasolov, Vladimir S.</creatorcontrib><creatorcontrib>Beresten, Sergey F.</creatorcontrib><creatorcontrib>Oparina, Nina Yu</creatorcontrib><creatorcontrib>Mashkova, Tamara D.</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>Proquest Nursing & Allied Health Source</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</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>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>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</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>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Pathology oncology research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kropotova, Ekaterina S.</au><au>Zinovieva, Olga L.</au><au>Zyryanova, Alisa F.</au><au>Dybovaya, Vera I.</au><au>Prasolov, Vladimir S.</au><au>Beresten, Sergey F.</au><au>Oparina, Nina Yu</au><au>Mashkova, Tamara D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Altered Expression of Multiple Genes Involved in Retinoic Acid Biosynthesis in Human Colorectal Cancer</atitle><jtitle>Pathology oncology research</jtitle><stitle>Pathol. Oncol. Res</stitle><addtitle>Pathol Oncol Res</addtitle><date>2014-07-01</date><risdate>2014</risdate><volume>20</volume><issue>3</issue><spage>707</spage><epage>717</epage><pages>707-717</pages><issn>1219-4956</issn><eissn>1532-2807</eissn><abstract>All-trans-retinoic acid (atRA), the oxidized form of vitamin A (retinol), regulates a wide variety of biological processes, such as cell proliferation and differentiation. Multiple alcohol, retinol and retinaldehyde dehydrogenases (ADHs, RDHs, RALDHs) as well as aldo-keto reductases (AKRs) catalyze atRA production. The reduced atRA biosynthesis has been observed in several human tumors, including colorectal cancer. However, subsets of atRA-synthesizing enzymes have not been determined in colorectal tumors. We investigated the expression patterns of genes involved in atRA biosynthesis in normal human colorectal tissues, primary carcinomas and cancer cell lines by RT-PCR. These genes were identified using transcriptomic data analysis (expressed sequence tags, RNA-sequencing, microarrays). Our results indicate that each step of the atRA biosynthesis pathway is dysregulated in colorectal cancer. Frequent and significant decreases in the mRNA levels of the
ADH1B
,
ADH1C
,
RDHL
,
RDH5
and
AKR1B10
genes were observed in a majority of colorectal carcinomas. The expression levels of the
RALDH1
gene were reduced, and the expression levels of the cytochrome
CYP26A1
gene increased. The human colon cancer cell lines showed a similar pattern of changes in the mRNA levels of these genes. A dramatic reduction in the expression of genes encoding the predominant retinol-oxidizing enzymes could impair atRA production. The most abundant of these genes,
ADH1B
and
ADH1C
, display decreased expression during progression from adenoma to early and more advanced stage of colorectal carcinomas. The diminished atRA biosynthesis may lead to alteration of cell growth and differentiation in the colon and rectum, thus contributing to the progression of colorectal cancer.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>24599561</pmid><doi>10.1007/s12253-014-9751-4</doi><tpages>11</tpages></addata></record> |
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| ispartof | Pathology oncology research, 2014-07, Vol.20 (3), p.707-717 |
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| language | eng |
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| source | MEDLINE; SpringerNature Journals |
| subjects | 3-Hydroxysteroid Dehydrogenases - genetics Adenoma - genetics Adenoma - pathology Alcohol Dehydrogenase - genetics Alcohol Oxidoreductases - genetics Aldehyde Reductase - genetics Biomarkers, Tumor - genetics Biomedical and Life Sciences Biomedicine Cancer Research Case-Control Studies Colon - metabolism Colorectal cancer Colorectal Neoplasms - genetics Colorectal Neoplasms - pathology Databases, Factual Gene Expression Profiling Humans Immunology Oligonucleotide Array Sequence Analysis Oncology Pathology Prognosis Rectum - metabolism Tretinoin - metabolism |
| title | Altered Expression of Multiple Genes Involved in Retinoic Acid Biosynthesis in Human Colorectal Cancer |
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