GTSE1 promotes prostate cancer cell proliferation via the SP1/FOXM1 signaling pathway
G2 and S phase-expressed-1 (GTSE1) has been implicated in the pathogenesis of several malignant tumors. However, its specific role in prostate cancer (PCa) remains unclear. In this study, RNA-Seq data from patients with PCa and controls were downloaded from the FIREBROWSE database, and it was found...
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description | G2 and S phase-expressed-1 (GTSE1) has been implicated in the pathogenesis of several malignant tumors. However, its specific role in prostate cancer (PCa) remains unclear. In this study, RNA-Seq data from patients with PCa and controls were downloaded from the FIREBROWSE database, and it was found that the GTSE1 mRNA level was significantly upregulated in PCa. Moreover, patients with higher GTSE1 mRNA levels had higher Gleason scores (P < 0.001), a more advanced pT stage (P = 0.011), and a more advanced pN stage (P = 0.006) as well as a shorter time to biochemical recurrence (P = 0.005). In addition, overexpression of GTSE1 could promote proliferation in LNCaP cells, whereas silencing GTSE1 could inhibit the growth of C4-2 cells in vitro and in vivo. Mechanistically, GTSE1 enhanced the expression of FOXM1 by upregulating the SP1 protein level, a transcription factor of FOXM1, which ultimately promoted PCa cell proliferation. In summary, GTSE1 is a new candidate oncogene in the development and progression of PCa, and it can promote PCa cell proliferation via the SP1/FOXM1 signaling pathway. |
doi_str_mv | 10.1038/s41374-020-00510-4 |
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However, its specific role in prostate cancer (PCa) remains unclear. In this study, RNA-Seq data from patients with PCa and controls were downloaded from the FIREBROWSE database, and it was found that the GTSE1 mRNA level was significantly upregulated in PCa. Moreover, patients with higher GTSE1 mRNA levels had higher Gleason scores (P < 0.001), a more advanced pT stage (P = 0.011), and a more advanced pN stage (P = 0.006) as well as a shorter time to biochemical recurrence (P = 0.005). In addition, overexpression of GTSE1 could promote proliferation in LNCaP cells, whereas silencing GTSE1 could inhibit the growth of C4-2 cells in vitro and in vivo. Mechanistically, GTSE1 enhanced the expression of FOXM1 by upregulating the SP1 protein level, a transcription factor of FOXM1, which ultimately promoted PCa cell proliferation. In summary, GTSE1 is a new candidate oncogene in the development and progression of PCa, and it can promote PCa cell proliferation via the SP1/FOXM1 signaling pathway.</description><identifier>ISSN: 0023-6837</identifier><identifier>EISSN: 1530-0307</identifier><identifier>DOI: 10.1038/s41374-020-00510-4</identifier><identifier>PMID: 33328578</identifier><language>eng</language><publisher>New York: Elsevier Inc</publisher><subject>13/1 ; 13/109 ; 13/31 ; 13/89 ; 14/34 ; 14/5 ; 38/77 ; 631/67/395 ; 631/67/589/466 ; 631/80/304 ; 64/60 ; 692/53/2422 ; 82/51 ; Animals ; Cell growth ; Cell Line, Tumor ; Cell Proliferation ; Forkhead Box Protein M1 - metabolism ; Humans ; Laboratory Medicine ; Male ; Medicine ; Medicine & Public Health ; Mice, Inbred BALB C ; Mice, Nude ; Microtubule-Associated Proteins - genetics ; Pathogenesis ; Pathology ; Prostate cancer ; Prostatic Neoplasms - etiology ; Prostatic Neoplasms - metabolism ; S phase ; Signal Transduction ; Signaling ; Sp1 protein ; Sp1 Transcription Factor - metabolism ; Tumorigenesis ; Tumors</subject><ispartof>Laboratory investigation, 2021-05, Vol.101 (5), p.554-563</ispartof><rights>2020 United States & Canadian Academy of Pathology</rights><rights>The Author(s), under exclusive licence to United States and Canadian Academy of Pathology 2020</rights><rights>The Author(s), under exclusive licence to United States and Canadian Academy of Pathology 2020.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c472t-6cae98a83b99db236bdaa6467d6150069c459900ac891c5a6adb9f2fed60fbc13</citedby><cites>FETCH-LOGICAL-c472t-6cae98a83b99db236bdaa6467d6150069c459900ac891c5a6adb9f2fed60fbc13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33328578$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lai, Wenjie</creatorcontrib><creatorcontrib>Zhu, Weian</creatorcontrib><creatorcontrib>Li, Xiaojuan</creatorcontrib><creatorcontrib>Han, Yuefu</creatorcontrib><creatorcontrib>Wang, Yu</creatorcontrib><creatorcontrib>Leng, Qu</creatorcontrib><creatorcontrib>Li, Mingzhao</creatorcontrib><creatorcontrib>Wen, Xingqiao</creatorcontrib><title>GTSE1 promotes prostate cancer cell proliferation via the SP1/FOXM1 signaling pathway</title><title>Laboratory investigation</title><addtitle>Lab Invest</addtitle><addtitle>Lab Invest</addtitle><description>G2 and S phase-expressed-1 (GTSE1) has been implicated in the pathogenesis of several malignant tumors. However, its specific role in prostate cancer (PCa) remains unclear. In this study, RNA-Seq data from patients with PCa and controls were downloaded from the FIREBROWSE database, and it was found that the GTSE1 mRNA level was significantly upregulated in PCa. Moreover, patients with higher GTSE1 mRNA levels had higher Gleason scores (P < 0.001), a more advanced pT stage (P = 0.011), and a more advanced pN stage (P = 0.006) as well as a shorter time to biochemical recurrence (P = 0.005). In addition, overexpression of GTSE1 could promote proliferation in LNCaP cells, whereas silencing GTSE1 could inhibit the growth of C4-2 cells in vitro and in vivo. Mechanistically, GTSE1 enhanced the expression of FOXM1 by upregulating the SP1 protein level, a transcription factor of FOXM1, which ultimately promoted PCa cell proliferation. In summary, GTSE1 is a new candidate oncogene in the development and progression of PCa, and it can promote PCa cell proliferation via the SP1/FOXM1 signaling pathway.</description><subject>13/1</subject><subject>13/109</subject><subject>13/31</subject><subject>13/89</subject><subject>14/34</subject><subject>14/5</subject><subject>38/77</subject><subject>631/67/395</subject><subject>631/67/589/466</subject><subject>631/80/304</subject><subject>64/60</subject><subject>692/53/2422</subject><subject>82/51</subject><subject>Animals</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Forkhead Box Protein M1 - metabolism</subject><subject>Humans</subject><subject>Laboratory Medicine</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Microtubule-Associated Proteins - genetics</subject><subject>Pathogenesis</subject><subject>Pathology</subject><subject>Prostate cancer</subject><subject>Prostatic Neoplasms - 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Academic</collection><jtitle>Laboratory investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lai, Wenjie</au><au>Zhu, Weian</au><au>Li, Xiaojuan</au><au>Han, Yuefu</au><au>Wang, Yu</au><au>Leng, Qu</au><au>Li, Mingzhao</au><au>Wen, Xingqiao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>GTSE1 promotes prostate cancer cell proliferation via the SP1/FOXM1 signaling pathway</atitle><jtitle>Laboratory investigation</jtitle><stitle>Lab Invest</stitle><addtitle>Lab Invest</addtitle><date>2021-05-01</date><risdate>2021</risdate><volume>101</volume><issue>5</issue><spage>554</spage><epage>563</epage><pages>554-563</pages><issn>0023-6837</issn><eissn>1530-0307</eissn><abstract>G2 and S phase-expressed-1 (GTSE1) has been implicated in the pathogenesis of several malignant tumors. However, its specific role in prostate cancer (PCa) remains unclear. In this study, RNA-Seq data from patients with PCa and controls were downloaded from the FIREBROWSE database, and it was found that the GTSE1 mRNA level was significantly upregulated in PCa. Moreover, patients with higher GTSE1 mRNA levels had higher Gleason scores (P < 0.001), a more advanced pT stage (P = 0.011), and a more advanced pN stage (P = 0.006) as well as a shorter time to biochemical recurrence (P = 0.005). In addition, overexpression of GTSE1 could promote proliferation in LNCaP cells, whereas silencing GTSE1 could inhibit the growth of C4-2 cells in vitro and in vivo. Mechanistically, GTSE1 enhanced the expression of FOXM1 by upregulating the SP1 protein level, a transcription factor of FOXM1, which ultimately promoted PCa cell proliferation. In summary, GTSE1 is a new candidate oncogene in the development and progression of PCa, and it can promote PCa cell proliferation via the SP1/FOXM1 signaling pathway.</abstract><cop>New York</cop><pub>Elsevier Inc</pub><pmid>33328578</pmid><doi>10.1038/s41374-020-00510-4</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 13/1 13/109 13/31 13/89 14/34 14/5 38/77 631/67/395 631/67/589/466 631/80/304 64/60 692/53/2422 82/51 Animals Cell growth Cell Line, Tumor Cell Proliferation Forkhead Box Protein M1 - metabolism Humans Laboratory Medicine Male Medicine Medicine & Public Health Mice, Inbred BALB C Mice, Nude Microtubule-Associated Proteins - genetics Pathogenesis Pathology Prostate cancer Prostatic Neoplasms - etiology Prostatic Neoplasms - metabolism S phase Signal Transduction Signaling Sp1 protein Sp1 Transcription Factor - metabolism Tumorigenesis Tumors |
title | GTSE1 promotes prostate cancer cell proliferation via the SP1/FOXM1 signaling pathway |
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