Regulatory role of osteopontin in malignant transformation of endometrial cancer
Osteopontin (OPN) involves in the tumor-promoting or metastasis in human endometrial cancer. Depletion of OPN gene expression in endometrial cancer cells was significantly decreased in cell viability and the cells undergo apoptotic cell death. The status of OPN in THESC, RL95, Hec1A and Ishikawa cel...
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Veröffentlicht in: | Molecular biology reports 2013-05, Vol.40 (5), p.3623-3629 |
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creator | Ramachandran, Sabarish Kwon, Kun-Young Shin, So-Jin Kwon, Sang-Hoon Cha, Soon-Do Lee, Hyun-Gyo Hong, Young-Bin Bae, Insoo Lee, Gun-Ho Cho, Chi-Heum |
description | Osteopontin (OPN) involves in the tumor-promoting or metastasis in human endometrial cancer. Depletion of OPN gene expression in endometrial cancer cells was significantly decreased in cell viability and the cells undergo apoptotic cell death. The status of OPN in THESC, RL95, Hec1A and Ishikawa cell lines were analyzed by RT-PCR and western blot. After OPN-siRNA transfection, mRNA and protein expression levels of OPN were determined in Hec1A and Ishikawa cells. Cell proliferation and cell cycle distribution were observed by MTT and flow cytometry analysis. DNA fragmentation assay was used to measure cell apoptosis. Cell migration was assessed by wound healing assay. Depletion of OPN gene expression in endometrial cancer cell lines (Hec1A and Ishikawa cells) reproducibly changed their ability of proliferation. Concomitant changes were seen in the expression of OPN binding cell surface receptors, cell cycle-regulatory genes, cell invasion and colony formation nature of the tumor cells. Decreased colonizing potential in the absence of OPN was reversed in the presence of recombinant OPN. Inhibition of anchorage-independent growth was observed in the presence of metabolic inhibitors of the PI3K, Src and integrin signaling cascades, which was ameliorated in the presence of exogenously added OPN. Our result showed the role of OPN in endometrial cancer, in particular on the malignancy-promoting aspects of OPN that may pave way for new approaches to the clinical management of endometrial cancer. |
doi_str_mv | 10.1007/s11033-012-2436-8 |
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Depletion of OPN gene expression in endometrial cancer cells was significantly decreased in cell viability and the cells undergo apoptotic cell death. The status of OPN in THESC, RL95, Hec1A and Ishikawa cell lines were analyzed by RT-PCR and western blot. After OPN-siRNA transfection, mRNA and protein expression levels of OPN were determined in Hec1A and Ishikawa cells. Cell proliferation and cell cycle distribution were observed by MTT and flow cytometry analysis. DNA fragmentation assay was used to measure cell apoptosis. Cell migration was assessed by wound healing assay. Depletion of OPN gene expression in endometrial cancer cell lines (Hec1A and Ishikawa cells) reproducibly changed their ability of proliferation. Concomitant changes were seen in the expression of OPN binding cell surface receptors, cell cycle-regulatory genes, cell invasion and colony formation nature of the tumor cells. Decreased colonizing potential in the absence of OPN was reversed in the presence of recombinant OPN. Inhibition of anchorage-independent growth was observed in the presence of metabolic inhibitors of the PI3K, Src and integrin signaling cascades, which was ameliorated in the presence of exogenously added OPN. Our result showed the role of OPN in endometrial cancer, in particular on the malignancy-promoting aspects of OPN that may pave way for new approaches to the clinical management of endometrial cancer.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-012-2436-8</identifier><identifier>PMID: 23269624</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Animal Anatomy ; Animal Biochemistry ; Apoptosis ; Apoptosis Regulatory Proteins - metabolism ; Biomedical and Life Sciences ; Cell Cycle Proteins - metabolism ; Cell Line ; Cell Line, Tumor ; Cell Proliferation ; Cell Transformation, Neoplastic - genetics ; Cell Transformation, Neoplastic - metabolism ; Endometrial cancer ; Endometrial Neoplasms - genetics ; Endometrial Neoplasms - metabolism ; Female ; Gene expression ; Gene Expression Regulation, Neoplastic ; Histology ; Humans ; Life Sciences ; Morphology ; Neoplasm Metastasis - genetics ; Osteopontin - genetics ; Osteopontin - metabolism ; Ribonucleic acid ; RNA</subject><ispartof>Molecular biology reports, 2013-05, Vol.40 (5), p.3623-3629</ispartof><rights>Springer Science+Business Media Dordrecht 2012</rights><rights>Springer Science+Business Media Dordrecht 2013</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-2467ec322d50903318a50245c11a7b6d1a5e6bda9fe661751535b8c453f4ba543</citedby><cites>FETCH-LOGICAL-c372t-2467ec322d50903318a50245c11a7b6d1a5e6bda9fe661751535b8c453f4ba543</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/s11033-012-2436-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11033-012-2436-8$$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/23269624$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ramachandran, Sabarish</creatorcontrib><creatorcontrib>Kwon, Kun-Young</creatorcontrib><creatorcontrib>Shin, So-Jin</creatorcontrib><creatorcontrib>Kwon, Sang-Hoon</creatorcontrib><creatorcontrib>Cha, Soon-Do</creatorcontrib><creatorcontrib>Lee, Hyun-Gyo</creatorcontrib><creatorcontrib>Hong, Young-Bin</creatorcontrib><creatorcontrib>Bae, Insoo</creatorcontrib><creatorcontrib>Lee, Gun-Ho</creatorcontrib><creatorcontrib>Cho, Chi-Heum</creatorcontrib><title>Regulatory role of osteopontin in malignant transformation of endometrial cancer</title><title>Molecular biology reports</title><addtitle>Mol Biol Rep</addtitle><addtitle>Mol Biol Rep</addtitle><description>Osteopontin (OPN) involves in the tumor-promoting or metastasis in human endometrial cancer. Depletion of OPN gene expression in endometrial cancer cells was significantly decreased in cell viability and the cells undergo apoptotic cell death. The status of OPN in THESC, RL95, Hec1A and Ishikawa cell lines were analyzed by RT-PCR and western blot. After OPN-siRNA transfection, mRNA and protein expression levels of OPN were determined in Hec1A and Ishikawa cells. Cell proliferation and cell cycle distribution were observed by MTT and flow cytometry analysis. DNA fragmentation assay was used to measure cell apoptosis. Cell migration was assessed by wound healing assay. Depletion of OPN gene expression in endometrial cancer cell lines (Hec1A and Ishikawa cells) reproducibly changed their ability of proliferation. Concomitant changes were seen in the expression of OPN binding cell surface receptors, cell cycle-regulatory genes, cell invasion and colony formation nature of the tumor cells. Decreased colonizing potential in the absence of OPN was reversed in the presence of recombinant OPN. Inhibition of anchorage-independent growth was observed in the presence of metabolic inhibitors of the PI3K, Src and integrin signaling cascades, which was ameliorated in the presence of exogenously added OPN. Our result showed the role of OPN in endometrial cancer, in particular on the malignancy-promoting aspects of OPN that may pave way for new approaches to the clinical management of endometrial cancer.</description><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Apoptosis</subject><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>Biomedical and Life Sciences</subject><subject>Cell Cycle Proteins - metabolism</subject><subject>Cell Line</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Endometrial cancer</subject><subject>Endometrial Neoplasms - genetics</subject><subject>Endometrial Neoplasms - metabolism</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Histology</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>Morphology</subject><subject>Neoplasm Metastasis - genetics</subject><subject>Osteopontin - genetics</subject><subject>Osteopontin - metabolism</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><issn>0301-4851</issn><issn>1573-4978</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><sourceid>GNUQQ</sourceid><recordid>eNp1kE1LxDAQhoMo7rr6A7xIwXM1k6-mR1lcFRYU0XNI23Tp0iZrkh7235ulq3gRBnKYZ96ZPAhdA74DjIv7AIApzTGQnDAqcnmC5sALmrOykKdojimGnEkOM3QRwhZjzKDg52hGKBGlIGyO3t7NZux1dH6fedebzLWZC9G4nbOxs1mqQffdxmobs-i1Da3zg46dswfU2MYNJvpO91mtbW38JTprdR_M1fFdoM_V48fyOV-_Pr0sH9Z5TQsS072iMDUlpOG4TJ8AqTkmjNcAuqhEA5obUTW6bI0Q6WjglFeyZpy2rNKc0QW6nXJ33n2NJkS1daO3aaWCFMuxZBISBRNVexeCN63a-W7Qfq8Aq4NDNTlUyaE6OFQyzdwck8dqMM3vxI-0BJAJCKllN8b_Wf1v6jdcmXvY</recordid><startdate>20130501</startdate><enddate>20130501</enddate><creator>Ramachandran, Sabarish</creator><creator>Kwon, Kun-Young</creator><creator>Shin, So-Jin</creator><creator>Kwon, Sang-Hoon</creator><creator>Cha, Soon-Do</creator><creator>Lee, Hyun-Gyo</creator><creator>Hong, Young-Bin</creator><creator>Bae, Insoo</creator><creator>Lee, Gun-Ho</creator><creator>Cho, Chi-Heum</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>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope></search><sort><creationdate>20130501</creationdate><title>Regulatory role of osteopontin in malignant transformation of endometrial cancer</title><author>Ramachandran, Sabarish ; Kwon, Kun-Young ; Shin, So-Jin ; Kwon, Sang-Hoon ; Cha, Soon-Do ; Lee, Hyun-Gyo ; Hong, Young-Bin ; Bae, Insoo ; Lee, Gun-Ho ; Cho, Chi-Heum</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-2467ec322d50903318a50245c11a7b6d1a5e6bda9fe661751535b8c453f4ba543</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Apoptosis</topic><topic>Apoptosis Regulatory Proteins - metabolism</topic><topic>Biomedical and Life Sciences</topic><topic>Cell Cycle Proteins - metabolism</topic><topic>Cell Line</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Cell Transformation, Neoplastic - genetics</topic><topic>Cell Transformation, Neoplastic - metabolism</topic><topic>Endometrial cancer</topic><topic>Endometrial Neoplasms - genetics</topic><topic>Endometrial Neoplasms - metabolism</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Histology</topic><topic>Humans</topic><topic>Life Sciences</topic><topic>Morphology</topic><topic>Neoplasm Metastasis - genetics</topic><topic>Osteopontin - genetics</topic><topic>Osteopontin - metabolism</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ramachandran, Sabarish</creatorcontrib><creatorcontrib>Kwon, Kun-Young</creatorcontrib><creatorcontrib>Shin, So-Jin</creatorcontrib><creatorcontrib>Kwon, Sang-Hoon</creatorcontrib><creatorcontrib>Cha, Soon-Do</creatorcontrib><creatorcontrib>Lee, Hyun-Gyo</creatorcontrib><creatorcontrib>Hong, Young-Bin</creatorcontrib><creatorcontrib>Bae, Insoo</creatorcontrib><creatorcontrib>Lee, Gun-Ho</creatorcontrib><creatorcontrib>Cho, Chi-Heum</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>Neurosciences Abstracts</collection><collection>Nucleic Acids 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>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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>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>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>Science Database</collection><collection>Biological Science Database</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>Molecular biology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ramachandran, Sabarish</au><au>Kwon, Kun-Young</au><au>Shin, So-Jin</au><au>Kwon, Sang-Hoon</au><au>Cha, Soon-Do</au><au>Lee, Hyun-Gyo</au><au>Hong, Young-Bin</au><au>Bae, Insoo</au><au>Lee, Gun-Ho</au><au>Cho, Chi-Heum</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulatory role of osteopontin in malignant transformation of endometrial cancer</atitle><jtitle>Molecular biology reports</jtitle><stitle>Mol Biol Rep</stitle><addtitle>Mol Biol Rep</addtitle><date>2013-05-01</date><risdate>2013</risdate><volume>40</volume><issue>5</issue><spage>3623</spage><epage>3629</epage><pages>3623-3629</pages><issn>0301-4851</issn><eissn>1573-4978</eissn><abstract>Osteopontin (OPN) involves in the tumor-promoting or metastasis in human endometrial cancer. Depletion of OPN gene expression in endometrial cancer cells was significantly decreased in cell viability and the cells undergo apoptotic cell death. The status of OPN in THESC, RL95, Hec1A and Ishikawa cell lines were analyzed by RT-PCR and western blot. After OPN-siRNA transfection, mRNA and protein expression levels of OPN were determined in Hec1A and Ishikawa cells. Cell proliferation and cell cycle distribution were observed by MTT and flow cytometry analysis. DNA fragmentation assay was used to measure cell apoptosis. Cell migration was assessed by wound healing assay. Depletion of OPN gene expression in endometrial cancer cell lines (Hec1A and Ishikawa cells) reproducibly changed their ability of proliferation. Concomitant changes were seen in the expression of OPN binding cell surface receptors, cell cycle-regulatory genes, cell invasion and colony formation nature of the tumor cells. Decreased colonizing potential in the absence of OPN was reversed in the presence of recombinant OPN. Inhibition of anchorage-independent growth was observed in the presence of metabolic inhibitors of the PI3K, Src and integrin signaling cascades, which was ameliorated in the presence of exogenously added OPN. Our result showed the role of OPN in endometrial cancer, in particular on the malignancy-promoting aspects of OPN that may pave way for new approaches to the clinical management of endometrial cancer.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>23269624</pmid><doi>10.1007/s11033-012-2436-8</doi><tpages>7</tpages></addata></record> |
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subjects | Animal Anatomy Animal Biochemistry Apoptosis Apoptosis Regulatory Proteins - metabolism Biomedical and Life Sciences Cell Cycle Proteins - metabolism Cell Line Cell Line, Tumor Cell Proliferation Cell Transformation, Neoplastic - genetics Cell Transformation, Neoplastic - metabolism Endometrial cancer Endometrial Neoplasms - genetics Endometrial Neoplasms - metabolism Female Gene expression Gene Expression Regulation, Neoplastic Histology Humans Life Sciences Morphology Neoplasm Metastasis - genetics Osteopontin - genetics Osteopontin - metabolism Ribonucleic acid RNA |
title | Regulatory role of osteopontin in malignant transformation of endometrial cancer |
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