REC8 inhibits EMT by downregulating EGR1 in gastric cancer cells
REC8 is a component of the meiotic cohesion complex that plays a critical role in chromosome dynamics during meiosis. However, the functional role of REC8 in gastric cancer has not been elucidated. In the present study, REC8 suppressed the growth and metastasis of gastric cancer cells in vitro. Whol...
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| Veröffentlicht in: | Oncology reports 2018-04, Vol.39 (4), p.1583-1590 |
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| creator | Zhao, Junhong Geng, Lanlan Duan, Gaoyang Xu, Wanfu Cheng, Yang Huang, Zhiliang Zhou, Zhenwen Gong, Sitang |
| description | REC8 is a component of the meiotic cohesion complex that plays a critical role in chromosome dynamics during meiosis. However, the functional role of REC8 in gastric cancer has not been elucidated. In the present study, REC8 suppressed the growth and metastasis of gastric cancer cells in vitro. Whole Human Genome Oligo Microarray results revealed that a wide range of genes with broad function were targeted by REC8. Among them early growth response-1 (EGR1), a transcription factor and an epithelial-mesenchymal transition (EMT)-associated protein in the AGR-RAGE pathway was significantly downregulated when REC8 was overexpressed in gastric cancer cells. We hypothesized that REC8 inhibits EMT by downregulating EGR1 in gastric cancer cells. Consistent with our prediction, REC8 overexpression decreased EMT in gastric cancer cells, whereas the REC8 ablation reversed these effects. In addition, the phenotypes of EGR1 overexpressed cells were similar to the phenotypes of REC8 ablated cells. Furthermore, we determined that REC8 interacted with EGR1, and inhibited EMT in gastric cancer cells. We thus propose further studies of the pathways associated with REC8 and EGR1 to potentially find novel targets in the treatment for gastric cancer. |
| doi_str_mv | 10.3892/or.2018.6244 |
| format | Article |
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However, the functional role of REC8 in gastric cancer has not been elucidated. In the present study, REC8 suppressed the growth and metastasis of gastric cancer cells in vitro. Whole Human Genome Oligo Microarray results revealed that a wide range of genes with broad function were targeted by REC8. Among them early growth response-1 (EGR1), a transcription factor and an epithelial-mesenchymal transition (EMT)-associated protein in the AGR-RAGE pathway was significantly downregulated when REC8 was overexpressed in gastric cancer cells. We hypothesized that REC8 inhibits EMT by downregulating EGR1 in gastric cancer cells. Consistent with our prediction, REC8 overexpression decreased EMT in gastric cancer cells, whereas the REC8 ablation reversed these effects. In addition, the phenotypes of EGR1 overexpressed cells were similar to the phenotypes of REC8 ablated cells. Furthermore, we determined that REC8 interacted with EGR1, and inhibited EMT in gastric cancer cells. We thus propose further studies of the pathways associated with REC8 and EGR1 to potentially find novel targets in the treatment for gastric cancer.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2018.6244</identifier><identifier>PMID: 29393474</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Biomarkers, Tumor - genetics ; Cancer therapies ; Care and treatment ; Cell adhesion & migration ; Cell cycle ; Cell Cycle Proteins - genetics ; Cell growth ; Cell Line, Tumor ; Development and progression ; Early Growth Response Protein 1 - genetics ; Epigenetics ; Epithelial-Mesenchymal Transition ; Gastric cancer ; Gene expression ; Gene Expression Regulation, Neoplastic ; Genetic aspects ; Genomes ; Health aspects ; Humans ; Metastasis ; Motility ; Proteins ; Stomach cancer ; Stomach Neoplasms - genetics ; Stomach Neoplasms - pathology ; Studies ; Transcription factors ; Tumors ; Wound healing</subject><ispartof>Oncology reports, 2018-04, Vol.39 (4), p.1583-1590</ispartof><rights>COPYRIGHT 2018 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><rights>Copyright: © Zhao et al. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c510t-1608ab4e0de56c4a3e3fc62b1b293c6046bb8c982957233b0907766776ca80fb3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29393474$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Junhong</creatorcontrib><creatorcontrib>Geng, Lanlan</creatorcontrib><creatorcontrib>Duan, Gaoyang</creatorcontrib><creatorcontrib>Xu, Wanfu</creatorcontrib><creatorcontrib>Cheng, Yang</creatorcontrib><creatorcontrib>Huang, Zhiliang</creatorcontrib><creatorcontrib>Zhou, Zhenwen</creatorcontrib><creatorcontrib>Gong, Sitang</creatorcontrib><title>REC8 inhibits EMT by downregulating EGR1 in gastric cancer cells</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>REC8 is a component of the meiotic cohesion complex that plays a critical role in chromosome dynamics during meiosis. However, the functional role of REC8 in gastric cancer has not been elucidated. In the present study, REC8 suppressed the growth and metastasis of gastric cancer cells in vitro. Whole Human Genome Oligo Microarray results revealed that a wide range of genes with broad function were targeted by REC8. Among them early growth response-1 (EGR1), a transcription factor and an epithelial-mesenchymal transition (EMT)-associated protein in the AGR-RAGE pathway was significantly downregulated when REC8 was overexpressed in gastric cancer cells. We hypothesized that REC8 inhibits EMT by downregulating EGR1 in gastric cancer cells. Consistent with our prediction, REC8 overexpression decreased EMT in gastric cancer cells, whereas the REC8 ablation reversed these effects. In addition, the phenotypes of EGR1 overexpressed cells were similar to the phenotypes of REC8 ablated cells. Furthermore, we determined that REC8 interacted with EGR1, and inhibited EMT in gastric cancer cells. We thus propose further studies of the pathways associated with REC8 and EGR1 to potentially find novel targets in the treatment for gastric cancer.</description><subject>Biomarkers, Tumor - genetics</subject><subject>Cancer therapies</subject><subject>Care and treatment</subject><subject>Cell adhesion & migration</subject><subject>Cell cycle</subject><subject>Cell Cycle Proteins - genetics</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Development and progression</subject><subject>Early Growth Response Protein 1 - genetics</subject><subject>Epigenetics</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>Gastric cancer</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Metastasis</subject><subject>Motility</subject><subject>Proteins</subject><subject>Stomach cancer</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - pathology</subject><subject>Studies</subject><subject>Transcription factors</subject><subject>Tumors</subject><subject>Wound healing</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkttLHDEUxkOx1Fvf-lwGCuKDs81tcnkRZVltQSmIQt9Cks3MRmYTTWZa_O-bqda6IiHkkPzOl3M-DgCfEJwRIfHXmGYYIjFjmNJ3YAdxiWpMCdoqMcSoJqT5uQ12c76FEHPI5AewjSWRhHK6A06uFnNR-bDyxg-5WlxeV-ahWsbfIblu7PXgQ1ctzq9QYapO5yF5W1kdrEuVdX2f98H7VvfZfXw698DN2eJ6_q2--HH-fX56UdsGwaFGDAptqINL1zBLNXGktQwbZEotlkHKjBFWCiwbjgkxUELOGSvbagFbQ_bA8aPu3WjWbmldGJLu1V3ya50eVNRebb4Ev1Jd_KUawQThpAgcPgmkeD-6PKi1z1MLOrg4ZoVkMUVIgVBBv7xCb-OYQmlPTVZLwSnm_6lO90750Mbyr51E1WlDKBWioU2hZm9QZS3d2tsYXOvL_UbCwYuEldP9sMqxHwcfQ94Ejx5Bm2LOybXPZiCoptFQMf2tV02jUfDPLw18hv_NAvkDZVSv4w</recordid><startdate>20180401</startdate><enddate>20180401</enddate><creator>Zhao, Junhong</creator><creator>Geng, Lanlan</creator><creator>Duan, Gaoyang</creator><creator>Xu, Wanfu</creator><creator>Cheng, Yang</creator><creator>Huang, Zhiliang</creator><creator>Zhou, Zhenwen</creator><creator>Gong, Sitang</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. 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However, the functional role of REC8 in gastric cancer has not been elucidated. In the present study, REC8 suppressed the growth and metastasis of gastric cancer cells in vitro. Whole Human Genome Oligo Microarray results revealed that a wide range of genes with broad function were targeted by REC8. Among them early growth response-1 (EGR1), a transcription factor and an epithelial-mesenchymal transition (EMT)-associated protein in the AGR-RAGE pathway was significantly downregulated when REC8 was overexpressed in gastric cancer cells. We hypothesized that REC8 inhibits EMT by downregulating EGR1 in gastric cancer cells. Consistent with our prediction, REC8 overexpression decreased EMT in gastric cancer cells, whereas the REC8 ablation reversed these effects. In addition, the phenotypes of EGR1 overexpressed cells were similar to the phenotypes of REC8 ablated cells. Furthermore, we determined that REC8 interacted with EGR1, and inhibited EMT in gastric cancer cells. We thus propose further studies of the pathways associated with REC8 and EGR1 to potentially find novel targets in the treatment for gastric cancer.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>29393474</pmid><doi>10.3892/or.2018.6244</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Oncology reports, 2018-04, Vol.39 (4), p.1583-1590 |
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| subjects | Biomarkers, Tumor - genetics Cancer therapies Care and treatment Cell adhesion & migration Cell cycle Cell Cycle Proteins - genetics Cell growth Cell Line, Tumor Development and progression Early Growth Response Protein 1 - genetics Epigenetics Epithelial-Mesenchymal Transition Gastric cancer Gene expression Gene Expression Regulation, Neoplastic Genetic aspects Genomes Health aspects Humans Metastasis Motility Proteins Stomach cancer Stomach Neoplasms - genetics Stomach Neoplasms - pathology Studies Transcription factors Tumors Wound healing |
| title | REC8 inhibits EMT by downregulating EGR1 in gastric cancer cells |
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