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Propofol inhibited gastric cancer proliferation via the hsa-miR-328-3p/STAT3 pathway

Purpose The aim of the present study was to elucidate the functional role of hsa-miR-328-3p/STAT3 pathway in the effects of propofol on gastric cancer proliferation. Methods Bioinformatics was used to analyze the molecular expression differences of hsa-miR-328-3p/STAT3 axis in stomach adenocarcinoma...

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Published in:Clinical & translational oncology 2021-09, Vol.23 (9), p.1866-1873
Main Authors: Bai, Z. M., Li, X. F., Yang, Y., Yang, Y. F., Lv, D. R., Tang, L. L.
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cited_by cdi_FETCH-LOGICAL-c347t-1a425b78c36e677424349c994b4b1274735d389b331cf3cdbfa3039f9008b0763
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container_issue 9
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container_title Clinical & translational oncology
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creator Bai, Z. M.
Li, X. F.
Yang, Y.
Yang, Y. F.
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Tang, L. L.
description Purpose The aim of the present study was to elucidate the functional role of hsa-miR-328-3p/STAT3 pathway in the effects of propofol on gastric cancer proliferation. Methods Bioinformatics was used to analyze the molecular expression differences of hsa-miR-328-3p/STAT3 axis in stomach adenocarcinoma ( n  = 435) and normal samples ( n  = 41) from TCGA database. The expression of the above molecules in gastric cancer cells SGC-7901 and normal gastric mucosal cells GES-1 was verified via qPCR. The dual-luciferase assay was carried out to confirm the interaction between hsa-miR-328-3p and STAT3. Subsequently, the cell proliferation and the expression of the above molecules in SGC-7901 and GES-1 cells were evaluated after 10 μM propofol treatment. Finally, we analyzed whether propofol still inhibited the proliferation of gastric cancer by suppressing STAT3 pathway after hsa-miR-328-3p down-regulation. Results Compared with normal samples, the expression of hsa-miR-328-3p was significantly down-regulated in stomach adenocarcinoma samples, while the expression of STAT3 and downstream target genes (MMP2, CCND1 and COX2) was up-regulated. The results were consistent with those in GES-1 and SGC-7901 cell lines. Meanwhile, we found that hsa-miR-328-3p can bind to the 3′-UTR of the potential target gene STAT3. Furthermore, propofol significantly inhibited the proliferation of gastric cancer cell line SGC-7901, where hsa-miR-328-3p was up-regulated and the expression of STAT3 and downstream proliferation-related target genes were down-regulated. However, the growth inhibition of propofol on SGC-7901 cell was significantly reversed after the inhibition of hsa-miR-328-3p. Conclusions To sum up, propofol suppressed the STAT3 pathway via up-regulating hsa-miR-328-3p to inhibit gastric cancer proliferation.
doi_str_mv 10.1007/s12094-021-02595-9
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M. ; Li, X. F. ; Yang, Y. ; Yang, Y. F. ; Lv, D. R. ; Tang, L. L.</creator><creatorcontrib>Bai, Z. M. ; Li, X. F. ; Yang, Y. ; Yang, Y. F. ; Lv, D. R. ; Tang, L. L.</creatorcontrib><description>Purpose The aim of the present study was to elucidate the functional role of hsa-miR-328-3p/STAT3 pathway in the effects of propofol on gastric cancer proliferation. Methods Bioinformatics was used to analyze the molecular expression differences of hsa-miR-328-3p/STAT3 axis in stomach adenocarcinoma ( n  = 435) and normal samples ( n  = 41) from TCGA database. The expression of the above molecules in gastric cancer cells SGC-7901 and normal gastric mucosal cells GES-1 was verified via qPCR. The dual-luciferase assay was carried out to confirm the interaction between hsa-miR-328-3p and STAT3. Subsequently, the cell proliferation and the expression of the above molecules in SGC-7901 and GES-1 cells were evaluated after 10 μM propofol treatment. Finally, we analyzed whether propofol still inhibited the proliferation of gastric cancer by suppressing STAT3 pathway after hsa-miR-328-3p down-regulation. Results Compared with normal samples, the expression of hsa-miR-328-3p was significantly down-regulated in stomach adenocarcinoma samples, while the expression of STAT3 and downstream target genes (MMP2, CCND1 and COX2) was up-regulated. The results were consistent with those in GES-1 and SGC-7901 cell lines. Meanwhile, we found that hsa-miR-328-3p can bind to the 3′-UTR of the potential target gene STAT3. Furthermore, propofol significantly inhibited the proliferation of gastric cancer cell line SGC-7901, where hsa-miR-328-3p was up-regulated and the expression of STAT3 and downstream proliferation-related target genes were down-regulated. However, the growth inhibition of propofol on SGC-7901 cell was significantly reversed after the inhibition of hsa-miR-328-3p. Conclusions To sum up, propofol suppressed the STAT3 pathway via up-regulating hsa-miR-328-3p to inhibit gastric cancer proliferation.</description><identifier>ISSN: 1699-048X</identifier><identifier>EISSN: 1699-3055</identifier><identifier>DOI: 10.1007/s12094-021-02595-9</identifier><identifier>PMID: 33772723</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Medicine ; Medicine &amp; Public Health ; Oncology ; Research Article</subject><ispartof>Clinical &amp; translational oncology, 2021-09, Vol.23 (9), p.1866-1873</ispartof><rights>Federación de Sociedades Españolas de Oncología (FESEO) 2021</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c347t-1a425b78c36e677424349c994b4b1274735d389b331cf3cdbfa3039f9008b0763</citedby><cites>FETCH-LOGICAL-c347t-1a425b78c36e677424349c994b4b1274735d389b331cf3cdbfa3039f9008b0763</cites><orcidid>0000-0002-1478-901X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33772723$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bai, Z. M.</creatorcontrib><creatorcontrib>Li, X. F.</creatorcontrib><creatorcontrib>Yang, Y.</creatorcontrib><creatorcontrib>Yang, Y. F.</creatorcontrib><creatorcontrib>Lv, D. R.</creatorcontrib><creatorcontrib>Tang, L. L.</creatorcontrib><title>Propofol inhibited gastric cancer proliferation via the hsa-miR-328-3p/STAT3 pathway</title><title>Clinical &amp; translational oncology</title><addtitle>Clin Transl Oncol</addtitle><addtitle>Clin Transl Oncol</addtitle><description>Purpose The aim of the present study was to elucidate the functional role of hsa-miR-328-3p/STAT3 pathway in the effects of propofol on gastric cancer proliferation. Methods Bioinformatics was used to analyze the molecular expression differences of hsa-miR-328-3p/STAT3 axis in stomach adenocarcinoma ( n  = 435) and normal samples ( n  = 41) from TCGA database. The expression of the above molecules in gastric cancer cells SGC-7901 and normal gastric mucosal cells GES-1 was verified via qPCR. The dual-luciferase assay was carried out to confirm the interaction between hsa-miR-328-3p and STAT3. Subsequently, the cell proliferation and the expression of the above molecules in SGC-7901 and GES-1 cells were evaluated after 10 μM propofol treatment. Finally, we analyzed whether propofol still inhibited the proliferation of gastric cancer by suppressing STAT3 pathway after hsa-miR-328-3p down-regulation. Results Compared with normal samples, the expression of hsa-miR-328-3p was significantly down-regulated in stomach adenocarcinoma samples, while the expression of STAT3 and downstream target genes (MMP2, CCND1 and COX2) was up-regulated. The results were consistent with those in GES-1 and SGC-7901 cell lines. Meanwhile, we found that hsa-miR-328-3p can bind to the 3′-UTR of the potential target gene STAT3. Furthermore, propofol significantly inhibited the proliferation of gastric cancer cell line SGC-7901, where hsa-miR-328-3p was up-regulated and the expression of STAT3 and downstream proliferation-related target genes were down-regulated. However, the growth inhibition of propofol on SGC-7901 cell was significantly reversed after the inhibition of hsa-miR-328-3p. Conclusions To sum up, propofol suppressed the STAT3 pathway via up-regulating hsa-miR-328-3p to inhibit gastric cancer proliferation.</description><subject>Medicine</subject><subject>Medicine &amp; Public Health</subject><subject>Oncology</subject><subject>Research Article</subject><issn>1699-048X</issn><issn>1699-3055</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNp9kE1PwzAMhiMEYmPwBzigHrmEJXHaNMdp4kuaBIIhcYvSNF0zdW1JWtD-PR0bHDlYtuzXr-wHoUtKbighYhooI5JjwugQsYyxPEJjmkiJgcTx8aEmPH0fobMQ1mToJpSeohGAEEwwGKPls2_apmiqyNWly1xn82ilQ-ediYyujfVR65vKFdbrzjV19Ol01JU2KoPGG_eCgaUY2unrcraEqNVd-aW35-ik0FWwF4c8QW93t8v5A1483T_OZwtsgIsOU81ZnInUQGITITjjwKWRkmc8o0xwAXEOqcwAqCnA5FmhgYAsJCFpRkQCE3S99x1O_Oht6NTGBWOrSte26YNiMUmYkILupGwvNb4JwdtCtd5ttN8qStSOptrTVANN9UNTyWHp6uDfZxub_6384hsEsBeEYVSvrFfrpvf18PN_tt9R5H3O</recordid><startdate>20210901</startdate><enddate>20210901</enddate><creator>Bai, Z. 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L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c347t-1a425b78c36e677424349c994b4b1274735d389b331cf3cdbfa3039f9008b0763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Medicine</topic><topic>Medicine &amp; Public Health</topic><topic>Oncology</topic><topic>Research Article</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bai, Z. M.</creatorcontrib><creatorcontrib>Li, X. F.</creatorcontrib><creatorcontrib>Yang, Y.</creatorcontrib><creatorcontrib>Yang, Y. F.</creatorcontrib><creatorcontrib>Lv, D. R.</creatorcontrib><creatorcontrib>Tang, L. L.</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical &amp; translational oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bai, Z. M.</au><au>Li, X. F.</au><au>Yang, Y.</au><au>Yang, Y. F.</au><au>Lv, D. R.</au><au>Tang, L. L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Propofol inhibited gastric cancer proliferation via the hsa-miR-328-3p/STAT3 pathway</atitle><jtitle>Clinical &amp; translational oncology</jtitle><stitle>Clin Transl Oncol</stitle><addtitle>Clin Transl Oncol</addtitle><date>2021-09-01</date><risdate>2021</risdate><volume>23</volume><issue>9</issue><spage>1866</spage><epage>1873</epage><pages>1866-1873</pages><issn>1699-048X</issn><eissn>1699-3055</eissn><abstract>Purpose The aim of the present study was to elucidate the functional role of hsa-miR-328-3p/STAT3 pathway in the effects of propofol on gastric cancer proliferation. Methods Bioinformatics was used to analyze the molecular expression differences of hsa-miR-328-3p/STAT3 axis in stomach adenocarcinoma ( n  = 435) and normal samples ( n  = 41) from TCGA database. The expression of the above molecules in gastric cancer cells SGC-7901 and normal gastric mucosal cells GES-1 was verified via qPCR. The dual-luciferase assay was carried out to confirm the interaction between hsa-miR-328-3p and STAT3. Subsequently, the cell proliferation and the expression of the above molecules in SGC-7901 and GES-1 cells were evaluated after 10 μM propofol treatment. Finally, we analyzed whether propofol still inhibited the proliferation of gastric cancer by suppressing STAT3 pathway after hsa-miR-328-3p down-regulation. Results Compared with normal samples, the expression of hsa-miR-328-3p was significantly down-regulated in stomach adenocarcinoma samples, while the expression of STAT3 and downstream target genes (MMP2, CCND1 and COX2) was up-regulated. The results were consistent with those in GES-1 and SGC-7901 cell lines. Meanwhile, we found that hsa-miR-328-3p can bind to the 3′-UTR of the potential target gene STAT3. 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Medicine & Public Health
Oncology
Research Article
title Propofol inhibited gastric cancer proliferation via the hsa-miR-328-3p/STAT3 pathway
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