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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 |
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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. Lv, D. R. 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 |
format | article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2506279716</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2506279716</sourcerecordid><originalsourceid>FETCH-LOGICAL-c347t-1a425b78c36e677424349c994b4b1274735d389b331cf3cdbfa3039f9008b0763</originalsourceid><addsrcrecordid>eNp9kE1PwzAMhiMEYmPwBzigHrmEJXHaNMdp4kuaBIIhcYvSNF0zdW1JWtD-PR0bHDlYtuzXr-wHoUtKbighYhooI5JjwugQsYyxPEJjmkiJgcTx8aEmPH0fobMQ1mToJpSeohGAEEwwGKPls2_apmiqyNWly1xn82ilQ-ediYyujfVR65vKFdbrzjV19Ol01JU2KoPGG_eCgaUY2unrcraEqNVd-aW35-ik0FWwF4c8QW93t8v5A1483T_OZwtsgIsOU81ZnInUQGITITjjwKWRkmc8o0xwAXEOqcwAqCnA5FmhgYAsJCFpRkQCE3S99x1O_Oht6NTGBWOrSte26YNiMUmYkILupGwvNb4JwdtCtd5ttN8qStSOptrTVANN9UNTyWHp6uDfZxub_6384hsEsBeEYVSvrFfrpvf18PN_tt9R5H3O</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2506279716</pqid></control><display><type>article</type><title>Propofol inhibited gastric cancer proliferation via the hsa-miR-328-3p/STAT3 pathway</title><source>Springer Nature</source><creator>Bai, Z. 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 & Public Health ; Oncology ; Research Article</subject><ispartof>Clinical & 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 & 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 & 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. M.</creator><creator>Li, X. F.</creator><creator>Yang, Y.</creator><creator>Yang, Y. F.</creator><creator>Lv, D. R.</creator><creator>Tang, L. L.</creator><general>Springer International Publishing</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-1478-901X</orcidid></search><sort><creationdate>20210901</creationdate><title>Propofol inhibited gastric cancer proliferation via the hsa-miR-328-3p/STAT3 pathway</title><author>Bai, Z. M. ; Li, X. F. ; Yang, Y. ; Yang, Y. F. ; Lv, D. R. ; Tang, L. 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 & 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 & 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 & 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. 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.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>33772723</pmid><doi>10.1007/s12094-021-02595-9</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-1478-901X</orcidid></addata></record> |
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subjects | Medicine Medicine & Public Health Oncology Research Article |
title | Propofol inhibited gastric cancer proliferation via the hsa-miR-328-3p/STAT3 pathway |
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