STIM1 overexpression promotes colorectal cancer progression, cell motility and COX-2 expression
Tumor metastasis is the major cause of death among cancer patients, with >90% of cancer-related death attributable to the spreading of metastatic cells to secondary organs. Store-operated Ca 2+ entry (SOCE) is the predominant Ca 2+ entry mechanism in most cancer cells, and stromal interaction mol...
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| Veröffentlicht in: | Oncogene 2015-08, Vol.34 (33), p.4358-4367 |
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| creator | Wang, J-Y Sun, J Huang, M-Y Wang, Y-S Hou, M-F Sun, Y He, H Krishna, N Chiu, S-J Lin, S Yang, S Chang, W-C |
| description | Tumor metastasis is the major cause of death among cancer patients, with >90% of cancer-related death attributable to the spreading of metastatic cells to secondary organs. Store-operated Ca
2+
entry (SOCE) is the predominant Ca
2+
entry mechanism in most cancer cells, and stromal interaction molecule 1 (STIM1) is the endoplasmic reticulum (ER) Ca
2+
sensor for store-operated channels. Here we reported that the STIM1 was overexpressed in colorectal cancer (CRC) patients. STIM1 overexpression in CRC was significantly associated with tumor size, depth of invasion, lymph node metastasis status and serum levels of carcinoembryonic antigen. Furthermore, ectopic expression of STIM1 promoted CRC cell motility, while depletion of STIM1 with short hairpin RNA inhibited CRC cell migration. Our data further suggested that STIM1 promoted CRC cell migration through increasing the expression of cyclooxygenase-2 (COX-2) and production of prostaglandin E2 (PGE2). Importantly, ectopically expressed COX-2 or exogenous PGE2 were able to rescue migration defect in STIM1 knockdown CRC cells, and inhibition of COX-2 with ibuprofen and indomethacin abrogated STIM1-mediated CRC cell motility. In short, our data provided clinicopathological significance for STIM1 and SOCE in CRC progression, and implicated a role for COX-2 in STIM1-mediated CRC metastasis. Our studies also suggested a new approach to inhibit STIM1-mediated metastasis with COX-2 inhibitors. |
| doi_str_mv | 10.1038/onc.2014.366 |
| format | Article |
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2+
entry (SOCE) is the predominant Ca
2+
entry mechanism in most cancer cells, and stromal interaction molecule 1 (STIM1) is the endoplasmic reticulum (ER) Ca
2+
sensor for store-operated channels. Here we reported that the STIM1 was overexpressed in colorectal cancer (CRC) patients. STIM1 overexpression in CRC was significantly associated with tumor size, depth of invasion, lymph node metastasis status and serum levels of carcinoembryonic antigen. Furthermore, ectopic expression of STIM1 promoted CRC cell motility, while depletion of STIM1 with short hairpin RNA inhibited CRC cell migration. Our data further suggested that STIM1 promoted CRC cell migration through increasing the expression of cyclooxygenase-2 (COX-2) and production of prostaglandin E2 (PGE2). Importantly, ectopically expressed COX-2 or exogenous PGE2 were able to rescue migration defect in STIM1 knockdown CRC cells, and inhibition of COX-2 with ibuprofen and indomethacin abrogated STIM1-mediated CRC cell motility. In short, our data provided clinicopathological significance for STIM1 and SOCE in CRC progression, and implicated a role for COX-2 in STIM1-mediated CRC metastasis. Our studies also suggested a new approach to inhibit STIM1-mediated metastasis with COX-2 inhibitors.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2014.366</identifier><identifier>PMID: 25381814</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>38 ; 631/67/1504/1885 ; 631/80/84 ; 82 ; 82/1 ; 82/80 ; 96 ; 96/21 ; 96/95 ; Apoptosis ; Caco-2 Cells ; Calcium (reticular) ; Calcium channels ; Calcium influx ; Cancer ; Carcinoembryonic antigen ; Carcinoembryonic Antigen - blood ; Cell adhesion & migration ; Cell Biology ; Cell Line, Tumor ; Cell migration ; Cell Movement - genetics ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - blood ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - pathology ; Cyclooxygenase 2 - genetics ; Cyclooxygenase-2 ; Development and progression ; Dinoprostone - genetics ; Disease Progression ; Ectopic expression ; Endoplasmic reticulum ; Female ; Genetic aspects ; HCT116 Cells ; HT29 Cells ; Human Genetics ; Humans ; Ibuprofen ; Indomethacin ; Internal Medicine ; Invasiveness ; Lymph nodes ; Lymphatic Metastasis - genetics ; Lymphatic Metastasis - pathology ; Male ; Medicine ; Medicine & Public Health ; Membrane Proteins - genetics ; Metastases ; Metastasis ; Middle Aged ; Motility ; Neoplasm Proteins - genetics ; Oncology ; Oncology, Experimental ; original-article ; Patient outcomes ; Prostaglandin E2 ; Ribonucleic acid ; RNA ; RNA, Small Interfering - genetics ; Serum levels ; STIM1 protein ; Stromal Interaction Molecule 1 ; Tumors</subject><ispartof>Oncogene, 2015-08, Vol.34 (33), p.4358-4367</ispartof><rights>Macmillan Publishers Limited 2015</rights><rights>COPYRIGHT 2015 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Aug 13, 2015</rights><rights>Macmillan Publishers Limited 2015.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c714t-b026519831729a8594ee033dd72d71ffa56124b987143c266b75e4640cd63a4b3</citedby><cites>FETCH-LOGICAL-c714t-b026519831729a8594ee033dd72d71ffa56124b987143c266b75e4640cd63a4b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/onc.2014.366$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/onc.2014.366$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27903,27904,41467,42536,51298</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25381814$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, J-Y</creatorcontrib><creatorcontrib>Sun, J</creatorcontrib><creatorcontrib>Huang, M-Y</creatorcontrib><creatorcontrib>Wang, Y-S</creatorcontrib><creatorcontrib>Hou, M-F</creatorcontrib><creatorcontrib>Sun, Y</creatorcontrib><creatorcontrib>He, H</creatorcontrib><creatorcontrib>Krishna, N</creatorcontrib><creatorcontrib>Chiu, S-J</creatorcontrib><creatorcontrib>Lin, S</creatorcontrib><creatorcontrib>Yang, S</creatorcontrib><creatorcontrib>Chang, W-C</creatorcontrib><title>STIM1 overexpression promotes colorectal cancer progression, cell motility and COX-2 expression</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Tumor metastasis is the major cause of death among cancer patients, with >90% of cancer-related death attributable to the spreading of metastatic cells to secondary organs. Store-operated Ca
2+
entry (SOCE) is the predominant Ca
2+
entry mechanism in most cancer cells, and stromal interaction molecule 1 (STIM1) is the endoplasmic reticulum (ER) Ca
2+
sensor for store-operated channels. Here we reported that the STIM1 was overexpressed in colorectal cancer (CRC) patients. STIM1 overexpression in CRC was significantly associated with tumor size, depth of invasion, lymph node metastasis status and serum levels of carcinoembryonic antigen. Furthermore, ectopic expression of STIM1 promoted CRC cell motility, while depletion of STIM1 with short hairpin RNA inhibited CRC cell migration. Our data further suggested that STIM1 promoted CRC cell migration through increasing the expression of cyclooxygenase-2 (COX-2) and production of prostaglandin E2 (PGE2). Importantly, ectopically expressed COX-2 or exogenous PGE2 were able to rescue migration defect in STIM1 knockdown CRC cells, and inhibition of COX-2 with ibuprofen and indomethacin abrogated STIM1-mediated CRC cell motility. In short, our data provided clinicopathological significance for STIM1 and SOCE in CRC progression, and implicated a role for COX-2 in STIM1-mediated CRC metastasis. Our studies also suggested a new approach to inhibit STIM1-mediated metastasis with COX-2 inhibitors.</description><subject>38</subject><subject>631/67/1504/1885</subject><subject>631/80/84</subject><subject>82</subject><subject>82/1</subject><subject>82/80</subject><subject>96</subject><subject>96/21</subject><subject>96/95</subject><subject>Apoptosis</subject><subject>Caco-2 Cells</subject><subject>Calcium (reticular)</subject><subject>Calcium channels</subject><subject>Calcium influx</subject><subject>Cancer</subject><subject>Carcinoembryonic antigen</subject><subject>Carcinoembryonic Antigen - blood</subject><subject>Cell adhesion & migration</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement - genetics</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - blood</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Cyclooxygenase 2 - genetics</subject><subject>Cyclooxygenase-2</subject><subject>Development and progression</subject><subject>Dinoprostone - genetics</subject><subject>Disease Progression</subject><subject>Ectopic expression</subject><subject>Endoplasmic reticulum</subject><subject>Female</subject><subject>Genetic aspects</subject><subject>HCT116 Cells</subject><subject>HT29 Cells</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Ibuprofen</subject><subject>Indomethacin</subject><subject>Internal Medicine</subject><subject>Invasiveness</subject><subject>Lymph nodes</subject><subject>Lymphatic Metastasis - genetics</subject><subject>Lymphatic Metastasis - pathology</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Membrane Proteins - genetics</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Middle Aged</subject><subject>Motility</subject><subject>Neoplasm Proteins - genetics</subject><subject>Oncology</subject><subject>Oncology, Experimental</subject><subject>original-article</subject><subject>Patient outcomes</subject><subject>Prostaglandin E2</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Small Interfering - genetics</subject><subject>Serum levels</subject><subject>STIM1 protein</subject><subject>Stromal Interaction Molecule 1</subject><subject>Tumors</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFks9rFDEUx4Modq3ePMuAlx46a34ncxHKYrVQ6cEK3kIm82ZNmUnWZLbY_74Zdu0PKUoOgbzP--Z9H1-E3hK8JJjpDzG4JcWEL5mUz9CCcCVrIRr-HC1wI3DdUEYP0KucrzDGqsH0JTqggmmiCV8g8-3y7Cup4jUk-L1JkLOPodqkOMYJcuXiEBO4yQ6Vs8FBmkvrPXZcORiGqpB-8NNNZUNXrS5-1LS6l3qNXvR2yPBmfx-i76efLldf6vOLz2erk_PaKcKnusVUCtJoRhRtrC7jA2DGuk7RTpG-t0ISyttGF5o5KmWrBHDJsesks7xlh-jjTnezbUfoHIQp2cFskh9tujHRevO4EvxPs47XhnMqqeBF4GgvkOKvLeTJjD7P_myAuM2mDEaJlE1Z5_9RzJnAhOKCvv8LvYrbFMomDGWMSKIp4_-iihYTWmit7qm1HcD40MdixM1fm5NiQlNJ1Ky1fIIqp4PRuxig9-X9UcPxrsGlmHOC_m5pBJs5YaYkzMwJMyVhBX_3cNF38J9IFaDeAbmUwhrSAzNPCd4CZpfX4w</recordid><startdate>20150813</startdate><enddate>20150813</enddate><creator>Wang, J-Y</creator><creator>Sun, J</creator><creator>Huang, M-Y</creator><creator>Wang, Y-S</creator><creator>Hou, M-F</creator><creator>Sun, Y</creator><creator>He, H</creator><creator>Krishna, N</creator><creator>Chiu, S-J</creator><creator>Lin, S</creator><creator>Yang, S</creator><creator>Chang, W-C</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</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>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150813</creationdate><title>STIM1 overexpression promotes colorectal cancer progression, cell motility and COX-2 expression</title><author>Wang, J-Y ; Sun, J ; Huang, M-Y ; Wang, Y-S ; Hou, M-F ; Sun, Y ; He, H ; Krishna, N ; Chiu, S-J ; Lin, S ; Yang, S ; Chang, W-C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c714t-b026519831729a8594ee033dd72d71ffa56124b987143c266b75e4640cd63a4b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>38</topic><topic>631/67/1504/1885</topic><topic>631/80/84</topic><topic>82</topic><topic>82/1</topic><topic>82/80</topic><topic>96</topic><topic>96/21</topic><topic>96/95</topic><topic>Apoptosis</topic><topic>Caco-2 Cells</topic><topic>Calcium (reticular)</topic><topic>Calcium channels</topic><topic>Calcium influx</topic><topic>Cancer</topic><topic>Carcinoembryonic antigen</topic><topic>Carcinoembryonic Antigen - blood</topic><topic>Cell adhesion & migration</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement - genetics</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Colorectal Neoplasms - blood</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Cyclooxygenase 2 - genetics</topic><topic>Cyclooxygenase-2</topic><topic>Development and progression</topic><topic>Dinoprostone - genetics</topic><topic>Disease Progression</topic><topic>Ectopic expression</topic><topic>Endoplasmic reticulum</topic><topic>Female</topic><topic>Genetic aspects</topic><topic>HCT116 Cells</topic><topic>HT29 Cells</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Ibuprofen</topic><topic>Indomethacin</topic><topic>Internal Medicine</topic><topic>Invasiveness</topic><topic>Lymph nodes</topic><topic>Lymphatic Metastasis - genetics</topic><topic>Lymphatic Metastasis - pathology</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Membrane Proteins - genetics</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Middle Aged</topic><topic>Motility</topic><topic>Neoplasm Proteins - genetics</topic><topic>Oncology</topic><topic>Oncology, Experimental</topic><topic>original-article</topic><topic>Patient outcomes</topic><topic>Prostaglandin E2</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA, Small Interfering - genetics</topic><topic>Serum levels</topic><topic>STIM1 protein</topic><topic>Stromal Interaction Molecule 1</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, J-Y</creatorcontrib><creatorcontrib>Sun, J</creatorcontrib><creatorcontrib>Huang, M-Y</creatorcontrib><creatorcontrib>Wang, Y-S</creatorcontrib><creatorcontrib>Hou, M-F</creatorcontrib><creatorcontrib>Sun, Y</creatorcontrib><creatorcontrib>He, H</creatorcontrib><creatorcontrib>Krishna, N</creatorcontrib><creatorcontrib>Chiu, S-J</creatorcontrib><creatorcontrib>Lin, S</creatorcontrib><creatorcontrib>Yang, S</creatorcontrib><creatorcontrib>Chang, W-C</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>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 Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, J-Y</au><au>Sun, J</au><au>Huang, M-Y</au><au>Wang, Y-S</au><au>Hou, M-F</au><au>Sun, Y</au><au>He, H</au><au>Krishna, N</au><au>Chiu, S-J</au><au>Lin, S</au><au>Yang, S</au><au>Chang, W-C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>STIM1 overexpression promotes colorectal cancer progression, cell motility and COX-2 expression</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2015-08-13</date><risdate>2015</risdate><volume>34</volume><issue>33</issue><spage>4358</spage><epage>4367</epage><pages>4358-4367</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>Tumor metastasis is the major cause of death among cancer patients, with >90% of cancer-related death attributable to the spreading of metastatic cells to secondary organs. Store-operated Ca
2+
entry (SOCE) is the predominant Ca
2+
entry mechanism in most cancer cells, and stromal interaction molecule 1 (STIM1) is the endoplasmic reticulum (ER) Ca
2+
sensor for store-operated channels. Here we reported that the STIM1 was overexpressed in colorectal cancer (CRC) patients. STIM1 overexpression in CRC was significantly associated with tumor size, depth of invasion, lymph node metastasis status and serum levels of carcinoembryonic antigen. Furthermore, ectopic expression of STIM1 promoted CRC cell motility, while depletion of STIM1 with short hairpin RNA inhibited CRC cell migration. Our data further suggested that STIM1 promoted CRC cell migration through increasing the expression of cyclooxygenase-2 (COX-2) and production of prostaglandin E2 (PGE2). Importantly, ectopically expressed COX-2 or exogenous PGE2 were able to rescue migration defect in STIM1 knockdown CRC cells, and inhibition of COX-2 with ibuprofen and indomethacin abrogated STIM1-mediated CRC cell motility. In short, our data provided clinicopathological significance for STIM1 and SOCE in CRC progression, and implicated a role for COX-2 in STIM1-mediated CRC metastasis. Our studies also suggested a new approach to inhibit STIM1-mediated metastasis with COX-2 inhibitors.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>25381814</pmid><doi>10.1038/onc.2014.366</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0950-9232 |
| ispartof | Oncogene, 2015-08, Vol.34 (33), p.4358-4367 |
| issn | 0950-9232 1476-5594 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4426254 |
| source | MEDLINE; Nature; Springer Nature - Complete Springer Journals; EZB-FREE-00999 freely available EZB journals |
| subjects | 38 631/67/1504/1885 631/80/84 82 82/1 82/80 96 96/21 96/95 Apoptosis Caco-2 Cells Calcium (reticular) Calcium channels Calcium influx Cancer Carcinoembryonic antigen Carcinoembryonic Antigen - blood Cell adhesion & migration Cell Biology Cell Line, Tumor Cell migration Cell Movement - genetics Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - blood Colorectal Neoplasms - genetics Colorectal Neoplasms - pathology Cyclooxygenase 2 - genetics Cyclooxygenase-2 Development and progression Dinoprostone - genetics Disease Progression Ectopic expression Endoplasmic reticulum Female Genetic aspects HCT116 Cells HT29 Cells Human Genetics Humans Ibuprofen Indomethacin Internal Medicine Invasiveness Lymph nodes Lymphatic Metastasis - genetics Lymphatic Metastasis - pathology Male Medicine Medicine & Public Health Membrane Proteins - genetics Metastases Metastasis Middle Aged Motility Neoplasm Proteins - genetics Oncology Oncology, Experimental original-article Patient outcomes Prostaglandin E2 Ribonucleic acid RNA RNA, Small Interfering - genetics Serum levels STIM1 protein Stromal Interaction Molecule 1 Tumors |
| title | STIM1 overexpression promotes colorectal cancer progression, cell motility and COX-2 expression |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-22T07%3A52%3A42IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=STIM1%20overexpression%20promotes%20colorectal%20cancer%20progression,%20cell%20motility%20and%20COX-2%20expression&rft.jtitle=Oncogene&rft.au=Wang,%20J-Y&rft.date=2015-08-13&rft.volume=34&rft.issue=33&rft.spage=4358&rft.epage=4367&rft.pages=4358-4367&rft.issn=0950-9232&rft.eissn=1476-5594&rft.coden=ONCNES&rft_id=info:doi/10.1038/onc.2014.366&rft_dat=%3Cgale_pubme%3EA426826174%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1703585887&rft_id=info:pmid/25381814&rft_galeid=A426826174&rfr_iscdi=true |