Deleted in liver cancer 3 (DLC-3), a novel Rho GTPase-activating protein, is downregulated in cancer and inhibits tumor cell growth
Two related Rho GTPase-activating proteins, DLC-1 (deleted in liver cancer 1) and DLC-2, are emerging as bona fide tumor suppressor genes that inhibit cancer cell growth. In this report, we characterized a gene on chromosome Xq13 that encodes DLC-3 (also known as KIAA0189 and STARD8 ), a third membe...
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| Veröffentlicht in: | Oncogene 2007-07, Vol.26 (31), p.4580-4589 |
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| creator | Durkin, M E Ullmannova, V Guan, M Popescu, N C |
| description | Two related Rho GTPase-activating proteins, DLC-1 (deleted in liver cancer 1) and DLC-2, are emerging as bona fide tumor suppressor genes that inhibit cancer cell growth. In this report, we characterized a gene on chromosome Xq13 that encodes DLC-3 (also known as KIAA0189 and
STARD8
), a third member of the DLC family. The DLC-3 gene has transcripts with alternative 5′ ends, one of which, DLC-3
α
, encodes an 1103-amino acid polypeptide highly similar to DLC-1 and DLC-2. A second isoform (DLC-3
β
) would yield a protein lacking the N-terminal sterile alpha motif domain. The DLC-3 gene is widely expressed in normal tissues, but DLC-3 mRNA levels were low or absent in a significant number of breast, ovarian, liver and prostate cancer cell lines. Using a cancer profiling array to compare matched tumor and normal human tissues, downregulation of DLC-3 mRNA was observed in kidney, lung, ovarian, uterine and breast cancer samples. By quantitative reverse transcriptase–polymerase chain reaction, DLC-3 expression was reduced in primary prostate carcinomas relative to normal prostate tissue. Transfection of human breast and prostate cancer cells with a DLC-3
α
expression vector inhibited cell proliferation, colony formation and growth in soft agar. These results indicate that deregulation of DLC-3 may contribute to breast and prostate tumorigenesis. |
| doi_str_mv | 10.1038/sj.onc.1210244 |
| format | Article |
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α
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STARD8
), a third member of the DLC family. The DLC-3 gene has transcripts with alternative 5′ ends, one of which, DLC-3
α
, encodes an 1103-amino acid polypeptide highly similar to DLC-1 and DLC-2. A second isoform (DLC-3
β
) would yield a protein lacking the N-terminal sterile alpha motif domain. The DLC-3 gene is widely expressed in normal tissues, but DLC-3 mRNA levels were low or absent in a significant number of breast, ovarian, liver and prostate cancer cell lines. Using a cancer profiling array to compare matched tumor and normal human tissues, downregulation of DLC-3 mRNA was observed in kidney, lung, ovarian, uterine and breast cancer samples. By quantitative reverse transcriptase–polymerase chain reaction, DLC-3 expression was reduced in primary prostate carcinomas relative to normal prostate tissue. Transfection of human breast and prostate cancer cells with a DLC-3
α
expression vector inhibited cell proliferation, colony formation and growth in soft agar. These results indicate that deregulation of DLC-3 may contribute to breast and prostate tumorigenesis.</description><subject>Amino Acid Sequence</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Breast - metabolism</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - metabolism</subject><subject>Cancer</subject><subject>Carcinogenesis</subject><subject>Causes of</subject><subject>Cell Biology</subject><subject>Cell growth</subject><subject>Cell physiology</subject><subject>Cell Proliferation</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Chromosomes</subject><subject>Down-Regulation</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene expression</subject><subject>Genes, Tumor Suppressor</subject><subject>Genetic aspects</subject><subject>Genetics</subject><subject>GTPase-activating protein</subject><subject>GTPase-Activating Proteins - metabolism</subject><subject>Health aspects</subject><subject>Hepatocytes</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Liver cancer</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Molecular and cellular biology</subject><subject>Molecular Sequence Data</subject><subject>Neoplasms - metabolism</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Oncology</subject><subject>original-article</subject><subject>Ovarian cancer</subject><subject>Ovaries</subject><subject>Polymerase chain reaction</subject><subject>Prostate - metabolism</subject><subject>Prostate cancer</subject><subject>Prostate carcinoma</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA-directed DNA polymerase</subject><subject>Transfection</subject><subject>Tumor cell lines</subject><subject>Tumor suppressor genes</subject><subject>Tumor Suppressor Proteins - genetics</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><subject>Tumors of the urinary system</subject><subject>Urinary tract. 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Action of oncogenes and antioncogenes</topic><topic>Chromosomes</topic><topic>Down-Regulation</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene expression</topic><topic>Genes, Tumor Suppressor</topic><topic>Genetic aspects</topic><topic>Genetics</topic><topic>GTPase-activating protein</topic><topic>GTPase-Activating Proteins - metabolism</topic><topic>Health aspects</topic><topic>Hepatocytes</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Liver cancer</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Molecular and cellular biology</topic><topic>Molecular Sequence Data</topic><topic>Neoplasms - metabolism</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Oncology</topic><topic>original-article</topic><topic>Ovarian cancer</topic><topic>Ovaries</topic><topic>Polymerase chain reaction</topic><topic>Prostate - metabolism</topic><topic>Prostate cancer</topic><topic>Prostate carcinoma</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA-directed DNA polymerase</topic><topic>Transfection</topic><topic>Tumor cell lines</topic><topic>Tumor suppressor genes</topic><topic>Tumor Suppressor Proteins - genetics</topic><topic>Tumorigenesis</topic><topic>Tumors</topic><topic>Tumors of the urinary system</topic><topic>Urinary tract. Prostate gland</topic><topic>Uterine cancer</topic><topic>Uterus</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Durkin, M E</creatorcontrib><creatorcontrib>Ullmannova, V</creatorcontrib><creatorcontrib>Guan, M</creatorcontrib><creatorcontrib>Popescu, N C</creatorcontrib><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>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>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research 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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</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>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</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>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Durkin, M E</au><au>Ullmannova, V</au><au>Guan, M</au><au>Popescu, N C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Deleted in liver cancer 3 (DLC-3), a novel Rho GTPase-activating protein, is downregulated in cancer and inhibits tumor cell growth</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2007-07-05</date><risdate>2007</risdate><volume>26</volume><issue>31</issue><spage>4580</spage><epage>4589</epage><pages>4580-4589</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>Two related Rho GTPase-activating proteins, DLC-1 (deleted in liver cancer 1) and DLC-2, are emerging as bona fide tumor suppressor genes that inhibit cancer cell growth. In this report, we characterized a gene on chromosome Xq13 that encodes DLC-3 (also known as KIAA0189 and
STARD8
), a third member of the DLC family. The DLC-3 gene has transcripts with alternative 5′ ends, one of which, DLC-3
α
, encodes an 1103-amino acid polypeptide highly similar to DLC-1 and DLC-2. A second isoform (DLC-3
β
) would yield a protein lacking the N-terminal sterile alpha motif domain. The DLC-3 gene is widely expressed in normal tissues, but DLC-3 mRNA levels were low or absent in a significant number of breast, ovarian, liver and prostate cancer cell lines. Using a cancer profiling array to compare matched tumor and normal human tissues, downregulation of DLC-3 mRNA was observed in kidney, lung, ovarian, uterine and breast cancer samples. By quantitative reverse transcriptase–polymerase chain reaction, DLC-3 expression was reduced in primary prostate carcinomas relative to normal prostate tissue. Transfection of human breast and prostate cancer cells with a DLC-3
α
expression vector inhibited cell proliferation, colony formation and growth in soft agar. These results indicate that deregulation of DLC-3 may contribute to breast and prostate tumorigenesis.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>17297465</pmid><doi>10.1038/sj.onc.1210244</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 0950-9232 1476-5594 |
| language | eng |
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| source | MEDLINE; Nature; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Amino Acid Sequence Apoptosis Biological and medical sciences Breast - metabolism Breast cancer Breast Neoplasms - metabolism Cancer Carcinogenesis Causes of Cell Biology Cell growth Cell physiology Cell Proliferation Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Chromosomes Down-Regulation Female Fundamental and applied biological sciences. Psychology Gastroenterology. Liver. Pancreas. Abdomen Gene expression Genes, Tumor Suppressor Genetic aspects Genetics GTPase-activating protein GTPase-Activating Proteins - metabolism Health aspects Hepatocytes Human Genetics Humans Internal Medicine Liver cancer Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Medicine Medicine & Public Health Molecular and cellular biology Molecular Sequence Data Neoplasms - metabolism Nephrology. Urinary tract diseases Oncology original-article Ovarian cancer Ovaries Polymerase chain reaction Prostate - metabolism Prostate cancer Prostate carcinoma Prostatic Neoplasms - metabolism Reverse Transcriptase Polymerase Chain Reaction RNA-directed DNA polymerase Transfection Tumor cell lines Tumor suppressor genes Tumor Suppressor Proteins - genetics Tumorigenesis Tumors Tumors of the urinary system Urinary tract. Prostate gland Uterine cancer Uterus |
| title | Deleted in liver cancer 3 (DLC-3), a novel Rho GTPase-activating protein, is downregulated in cancer and inhibits tumor cell growth |
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