Long non-coding RNA small nucleolar RNA host gene 6 aggravates pancreatic cancer through upregulation of far upstream element binding protein 1 by sponging microRNA-26a-5p

Pancreatic cancer (PC) is a highly deadly malignancy with few effective therapies. We aimed to unmask the role that long non-coding RNA small nucleolar RNA host gene 6 (SNHG6) plays in PC cells by targeting far upstream element binding protein 1 (FUBP1) via microRNA-26a-5p (miR-26a-5p). SNHG6 expres...

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Published in:Chinese medical journal 2020-05, Vol.133 (10), p.1211-1220
Main Authors: Zhang, Xing-Xing, Chen, Hua, Li, Hui-Ying, Chen, Rui, He, Lei, Yang, Juan-Li, Xiao, Lin-Lin, Chen, Jin-Lian
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container_title Chinese medical journal
container_volume 133
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Chen, Hua
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Chen, Rui
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Xiao, Lin-Lin
Chen, Jin-Lian
description Pancreatic cancer (PC) is a highly deadly malignancy with few effective therapies. We aimed to unmask the role that long non-coding RNA small nucleolar RNA host gene 6 (SNHG6) plays in PC cells by targeting far upstream element binding protein 1 (FUBP1) via microRNA-26a-5p (miR-26a-5p). SNHG6 expression was predicted by bioinformatics, followed by verification via reverse transcription quantitative polymerase chain reaction. Then, the interactions among SNHG6, miR-26a-5p, and FUBP1 were detected through online software analysis, dual luciferase reporter assay and RNA pull-down. After that, cells were treated with different small interfering RNAs and/or mimic to determine the interactions among SNHG6, miR-26a-5p, and FUBP1 and their roles in PC cells. Finally, the role of SNHG6 in tumor growth in vivo was evaluated by measuring the growth and weight of transplanted tumors in nude mice. A t-test, one-way and two-way analysis of variance were used for data analysis. Compared with that in normal tissues, SNHG6 was highly expressed in PC tissues (1.00 ± 0.05 vs. 1.56 ± 0.06, t = 16.03, P 
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We aimed to unmask the role that long non-coding RNA small nucleolar RNA host gene 6 (SNHG6) plays in PC cells by targeting far upstream element binding protein 1 (FUBP1) via microRNA-26a-5p (miR-26a-5p). SNHG6 expression was predicted by bioinformatics, followed by verification via reverse transcription quantitative polymerase chain reaction. Then, the interactions among SNHG6, miR-26a-5p, and FUBP1 were detected through online software analysis, dual luciferase reporter assay and RNA pull-down. After that, cells were treated with different small interfering RNAs and/or mimic to determine the interactions among SNHG6, miR-26a-5p, and FUBP1 and their roles in PC cells. Finally, the role of SNHG6 in tumor growth in vivo was evaluated by measuring the growth and weight of transplanted tumors in nude mice. A t-test, one-way and two-way analysis of variance were used for data analysis. Compared with that in normal tissues, SNHG6 was highly expressed in PC tissues (1.00 ± 0.05 vs. 1.56 ± 0.06, t = 16.03, P < 0.001). Compared with that in HPDE6-C7 cells, SNHG6 showed the highest expression in PANC-1 cells (1.00 ± 0.06 vs. 3.87 ± 0.13, t = 34.72, P < 0.001) and the lowest expression in MIAPACA-2 cells (1.00 ± 0.06 vs. 1.41 ± 0.07, t = 7.70, P = 0.0015). Compared with the levels in the si-negative control group, SNHG6 (0.97 ± 0.05 vs. 0.21 ± 0.06, t = 16.85, P < 0.001), N-cadherin (0.74 ± 0.05 vs. 0.41 ± 0.04, t = 8.93, P < 0.001), Vimentin (0.55 ± 0.04 vs. 0.25 ± 0.03, t = 10.39, P < 0.001), and β-catenin (0.62 ± 0.05 vs. 0.32 ± 0.03, t = 8.91, P < 0.001) were decreased, while E-cadherin (0.65 ± 0.06 vs. 1.36 ± 0.07, t = 13.34, P < 0.001) was increased after SNHG6 knockdown or miR-26a-5p overexpression, accompanied by inhibited cell proliferation, migration, and invasion. SNHG6 overexpression exerted the opposite effects. SNHG6 upregulated FUBP1 expression by sponging miR-26a-5p. Silencing SNHG6 blocked the growth of PC in vivo. Silencing SNHG6 might ameliorate PC through inhibition of FUBP1 by sponging miR-26a-5p, thus providing further supporting evidence for its use in PC treatment.]]></description><identifier>ISSN: 0366-6999</identifier><identifier>EISSN: 2542-5641</identifier><identifier>DOI: 10.1097/CM9.0000000000000758</identifier><identifier>PMID: 32265427</identifier><language>eng</language><publisher>China: Wolters Kluwer</publisher><ispartof>Chinese medical journal, 2020-05, Vol.133 (10), p.1211-1220</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3348-e6278c61bb5d406b2529c36b3c726543e98fc025e9adc22b82cd79def14299b43</citedby><cites>FETCH-LOGICAL-c3348-e6278c61bb5d406b2529c36b3c726543e98fc025e9adc22b82cd79def14299b43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924,37012</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32265427$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Xing-Xing</creatorcontrib><creatorcontrib>Chen, Hua</creatorcontrib><creatorcontrib>Li, Hui-Ying</creatorcontrib><creatorcontrib>Chen, Rui</creatorcontrib><creatorcontrib>He, Lei</creatorcontrib><creatorcontrib>Yang, Juan-Li</creatorcontrib><creatorcontrib>Xiao, Lin-Lin</creatorcontrib><creatorcontrib>Chen, Jin-Lian</creatorcontrib><title>Long non-coding RNA small nucleolar RNA host gene 6 aggravates pancreatic cancer through upregulation of far upstream element binding protein 1 by sponging microRNA-26a-5p</title><title>Chinese medical journal</title><addtitle>Chin Med J (Engl)</addtitle><description><![CDATA[Pancreatic cancer (PC) is a highly deadly malignancy with few effective therapies. We aimed to unmask the role that long non-coding RNA small nucleolar RNA host gene 6 (SNHG6) plays in PC cells by targeting far upstream element binding protein 1 (FUBP1) via microRNA-26a-5p (miR-26a-5p). SNHG6 expression was predicted by bioinformatics, followed by verification via reverse transcription quantitative polymerase chain reaction. Then, the interactions among SNHG6, miR-26a-5p, and FUBP1 were detected through online software analysis, dual luciferase reporter assay and RNA pull-down. After that, cells were treated with different small interfering RNAs and/or mimic to determine the interactions among SNHG6, miR-26a-5p, and FUBP1 and their roles in PC cells. Finally, the role of SNHG6 in tumor growth in vivo was evaluated by measuring the growth and weight of transplanted tumors in nude mice. A t-test, one-way and two-way analysis of variance were used for data analysis. Compared with that in normal tissues, SNHG6 was highly expressed in PC tissues (1.00 ± 0.05 vs. 1.56 ± 0.06, t = 16.03, P < 0.001). Compared with that in HPDE6-C7 cells, SNHG6 showed the highest expression in PANC-1 cells (1.00 ± 0.06 vs. 3.87 ± 0.13, t = 34.72, P < 0.001) and the lowest expression in MIAPACA-2 cells (1.00 ± 0.06 vs. 1.41 ± 0.07, t = 7.70, P = 0.0015). Compared with the levels in the si-negative control group, SNHG6 (0.97 ± 0.05 vs. 0.21 ± 0.06, t = 16.85, P < 0.001), N-cadherin (0.74 ± 0.05 vs. 0.41 ± 0.04, t = 8.93, P < 0.001), Vimentin (0.55 ± 0.04 vs. 0.25 ± 0.03, t = 10.39, P < 0.001), and β-catenin (0.62 ± 0.05 vs. 0.32 ± 0.03, t = 8.91, P < 0.001) were decreased, while E-cadherin (0.65 ± 0.06 vs. 1.36 ± 0.07, t = 13.34, P < 0.001) was increased after SNHG6 knockdown or miR-26a-5p overexpression, accompanied by inhibited cell proliferation, migration, and invasion. SNHG6 overexpression exerted the opposite effects. SNHG6 upregulated FUBP1 expression by sponging miR-26a-5p. Silencing SNHG6 blocked the growth of PC in vivo. Silencing SNHG6 might ameliorate PC through inhibition of FUBP1 by sponging miR-26a-5p, thus providing further supporting evidence for its use in PC treatment.]]></description><issn>0366-6999</issn><issn>2542-5641</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNpdUcuO1DAQtBCIHQb-ACEfuWRx_Mr4uBrxWGkACcHZ8qOTycqxg50g7Tfxk3hmlhXCB7tV7q5yuRB63ZLrlqju3f6zuib_rk7snqANFZw2QvL2KdoQJmUjlVJX6EUpd4RQITr5HF0xSmXt6zbo9yHFAccUG5f8WMtvX25wmUwIOK4uQAomn7FjKgseIAKW2AxDNr_MAgXPJroMZhkddrWEjJdjTutwxOucYVhDvUoRpx73lWidy1K7JwwBJogLtmM8q845LTBG3GJ7j8tc33RCp9HlVMUbKk0j5pfoWW9CgVcP5xb9-PD--_5Tc_j68XZ_c2gcY3zXgKTdzsnWWuE5kZYKqhyTlrnu5JqB2vWufgUo4x2ldked75SHvuVUKcvZFt1eeH0yd3rO42TyvU5m1Gcg5UGbXB0H0L61pvVAFLWWAyXGsY5x6Jhl1nDhK9fbC1d1-HOFsuhpLA5CMBHSWjTlRDBGZN22iF9aq-lSMvSP0i3Rp8h1jVz_H3kde_OgsNoJ_OPQ34zZH4fhp9Y</recordid><startdate>20200520</startdate><enddate>20200520</enddate><creator>Zhang, Xing-Xing</creator><creator>Chen, Hua</creator><creator>Li, Hui-Ying</creator><creator>Chen, Rui</creator><creator>He, Lei</creator><creator>Yang, Juan-Li</creator><creator>Xiao, Lin-Lin</creator><creator>Chen, Jin-Lian</creator><general>Wolters Kluwer</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>DOA</scope></search><sort><creationdate>20200520</creationdate><title>Long non-coding RNA small nucleolar RNA host gene 6 aggravates pancreatic cancer through upregulation of far upstream element binding protein 1 by sponging microRNA-26a-5p</title><author>Zhang, Xing-Xing ; Chen, Hua ; Li, Hui-Ying ; Chen, Rui ; He, Lei ; Yang, Juan-Li ; Xiao, Lin-Lin ; Chen, Jin-Lian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3348-e6278c61bb5d406b2529c36b3c726543e98fc025e9adc22b82cd79def14299b43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Xing-Xing</creatorcontrib><creatorcontrib>Chen, Hua</creatorcontrib><creatorcontrib>Li, Hui-Ying</creatorcontrib><creatorcontrib>Chen, Rui</creatorcontrib><creatorcontrib>He, Lei</creatorcontrib><creatorcontrib>Yang, Juan-Li</creatorcontrib><creatorcontrib>Xiao, Lin-Lin</creatorcontrib><creatorcontrib>Chen, Jin-Lian</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Chinese medical journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Xing-Xing</au><au>Chen, Hua</au><au>Li, Hui-Ying</au><au>Chen, Rui</au><au>He, Lei</au><au>Yang, Juan-Li</au><au>Xiao, Lin-Lin</au><au>Chen, Jin-Lian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Long non-coding RNA small nucleolar RNA host gene 6 aggravates pancreatic cancer through upregulation of far upstream element binding protein 1 by sponging microRNA-26a-5p</atitle><jtitle>Chinese medical journal</jtitle><addtitle>Chin Med J (Engl)</addtitle><date>2020-05-20</date><risdate>2020</risdate><volume>133</volume><issue>10</issue><spage>1211</spage><epage>1220</epage><pages>1211-1220</pages><issn>0366-6999</issn><eissn>2542-5641</eissn><abstract><![CDATA[Pancreatic cancer (PC) is a highly deadly malignancy with few effective therapies. We aimed to unmask the role that long non-coding RNA small nucleolar RNA host gene 6 (SNHG6) plays in PC cells by targeting far upstream element binding protein 1 (FUBP1) via microRNA-26a-5p (miR-26a-5p). SNHG6 expression was predicted by bioinformatics, followed by verification via reverse transcription quantitative polymerase chain reaction. Then, the interactions among SNHG6, miR-26a-5p, and FUBP1 were detected through online software analysis, dual luciferase reporter assay and RNA pull-down. After that, cells were treated with different small interfering RNAs and/or mimic to determine the interactions among SNHG6, miR-26a-5p, and FUBP1 and their roles in PC cells. Finally, the role of SNHG6 in tumor growth in vivo was evaluated by measuring the growth and weight of transplanted tumors in nude mice. A t-test, one-way and two-way analysis of variance were used for data analysis. Compared with that in normal tissues, SNHG6 was highly expressed in PC tissues (1.00 ± 0.05 vs. 1.56 ± 0.06, t = 16.03, P < 0.001). Compared with that in HPDE6-C7 cells, SNHG6 showed the highest expression in PANC-1 cells (1.00 ± 0.06 vs. 3.87 ± 0.13, t = 34.72, P < 0.001) and the lowest expression in MIAPACA-2 cells (1.00 ± 0.06 vs. 1.41 ± 0.07, t = 7.70, P = 0.0015). Compared with the levels in the si-negative control group, SNHG6 (0.97 ± 0.05 vs. 0.21 ± 0.06, t = 16.85, P < 0.001), N-cadherin (0.74 ± 0.05 vs. 0.41 ± 0.04, t = 8.93, P < 0.001), Vimentin (0.55 ± 0.04 vs. 0.25 ± 0.03, t = 10.39, P < 0.001), and β-catenin (0.62 ± 0.05 vs. 0.32 ± 0.03, t = 8.91, P < 0.001) were decreased, while E-cadherin (0.65 ± 0.06 vs. 1.36 ± 0.07, t = 13.34, P < 0.001) was increased after SNHG6 knockdown or miR-26a-5p overexpression, accompanied by inhibited cell proliferation, migration, and invasion. SNHG6 overexpression exerted the opposite effects. SNHG6 upregulated FUBP1 expression by sponging miR-26a-5p. Silencing SNHG6 blocked the growth of PC in vivo. Silencing SNHG6 might ameliorate PC through inhibition of FUBP1 by sponging miR-26a-5p, thus providing further supporting evidence for its use in PC treatment.]]></abstract><cop>China</cop><pub>Wolters Kluwer</pub><pmid>32265427</pmid><doi>10.1097/CM9.0000000000000758</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record>
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title Long non-coding RNA small nucleolar RNA host gene 6 aggravates pancreatic cancer through upregulation of far upstream element binding protein 1 by sponging microRNA-26a-5p
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