LncRNA SNHG3 Facilitates the Malignant Phenotype of Cholangiocarcinoma Cells via the miR-3173–5p/ERG Axis
Background Long noncoding RNA (lncRNA) small nucleolar RNA host gene 3 (SNHG3) is an oncogenic lncRNA that has been reported in many cancers, but the role of SNHG3 in cholangiocarcinoma (CCA) remains largely unknown. Bioinformatic analysis revealed a regulatory relationship among SNHG3, miR-3173–5p,...
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Veröffentlicht in: | Journal of gastrointestinal surgery 2022-04, Vol.26 (4), p.802-812 |
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creator | Sun, Zeng-Peng Tan, Zhi-Guo Peng, Chuang Yi, Wei-Min |
description | Background
Long noncoding RNA (lncRNA) small nucleolar RNA host gene 3 (SNHG3) is an oncogenic lncRNA that has been reported in many cancers, but the role of SNHG3 in cholangiocarcinoma (CCA) remains largely unknown. Bioinformatic analysis revealed a regulatory relationship among SNHG3, miR-3173–5p, and ERG. miR-3173–5p is a tumour suppressive miRNA, while ERG is an oncogene. In the present study, we focused on the regulatory effects and molecular mechanisms of SNHG3 in CCA.
Method
The expression of SNHG3 and miR-3173–5p was evaluated using qRT–PCR analysis. Knockdown of SNHG3 was achieved by shRNA. Cell viability was assessed by MTT assay. Migration and invasion were determined by Transwell assay. Flow cytometry was used to assess cell apoptosis. Western blots were applied to quantify protein levels. Furthermore, using RNA pulldown and dual luciferase assays, the interactions between SNHG3 and miR-3173–5p and between miR-3173–5p and ERG in CCA cells were validated.
Results
SNHG3 was significantly upregulated in CCA cells compared with normal human intrahepatic biliary epithelial cells. Knockdown of SNHG3 inhibited the proliferation and migration of CCA cells
.
Mechanistically, SNHG3-sponged miR-3173–5p, thus releasing the repression of ERG by miR-3173–5p. Rescue experiments showed that the miR-3173–5p/ERG axis mediated the oncogenic effect of SNHG3.
Conclusion
Taken together, our data suggest that SNHG3 is a pleiotropic oncogenic lncRNA in CCA. Knockdown of SNHG3 expression suppressed malignant phenotypes in CCA cells via the miR-3173–5p/ERG axis. |
doi_str_mv | 10.1007/s11605-021-05160-5 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2582110353</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2582110353</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-b134c82711eceec0e61e0653a1025bcd2750f548f68ff5aefa7b61ce71ca8c9c3</originalsourceid><addsrcrecordid>eNp9kc9OGzEQxi1UxL_yAhyQpV56cfHYa3s5RhGESgGqtJW4WY6ZTUx37XS9qcqNd-gb9knqEv5IPfQ0I83v-2Y0HyFHwD8A5-YkA2iuGBfAuCotU1tkD2ojWaWFflN6fgpMKHWzS_ZzvuMcDId6h-zKSldGCL1Hvk2jn12N6Oeri4mk586HNgxuwEyHJdJL14ZFdHGgn5YY03C_QpoaOl6m1sVFSN71PsTUOTrGts30R3CPui7MmAQjfz_8UquTs9mEjn6G_JZsN67NePhUD8jX87Mv4ws2vZ58HI-mzEujBjYHWflaGAD0iJ6jBuRaSQdcqLm_FUbxRlV1o-umUQ4bZ-YaPBrwrvanXh6Q9xvfVZ--rzEPtgvZlwNdxLTOVqhaAHCpZEHf_YPepXUfy3VWaCWMlFLzQokN5fuUc4-NXfWhc_29BW7_RmE3UdgShX2MwqoiOn6yXs87vH2RPP--AHID5DKKC-xfd__H9g98MJK5</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2652733360</pqid></control><display><type>article</type><title>LncRNA SNHG3 Facilitates the Malignant Phenotype of Cholangiocarcinoma Cells via the miR-3173–5p/ERG Axis</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Sun, Zeng-Peng ; Tan, Zhi-Guo ; Peng, Chuang ; Yi, Wei-Min</creator><creatorcontrib>Sun, Zeng-Peng ; Tan, Zhi-Guo ; Peng, Chuang ; Yi, Wei-Min</creatorcontrib><description>Background
Long noncoding RNA (lncRNA) small nucleolar RNA host gene 3 (SNHG3) is an oncogenic lncRNA that has been reported in many cancers, but the role of SNHG3 in cholangiocarcinoma (CCA) remains largely unknown. Bioinformatic analysis revealed a regulatory relationship among SNHG3, miR-3173–5p, and ERG. miR-3173–5p is a tumour suppressive miRNA, while ERG is an oncogene. In the present study, we focused on the regulatory effects and molecular mechanisms of SNHG3 in CCA.
Method
The expression of SNHG3 and miR-3173–5p was evaluated using qRT–PCR analysis. Knockdown of SNHG3 was achieved by shRNA. Cell viability was assessed by MTT assay. Migration and invasion were determined by Transwell assay. Flow cytometry was used to assess cell apoptosis. Western blots were applied to quantify protein levels. Furthermore, using RNA pulldown and dual luciferase assays, the interactions between SNHG3 and miR-3173–5p and between miR-3173–5p and ERG in CCA cells were validated.
Results
SNHG3 was significantly upregulated in CCA cells compared with normal human intrahepatic biliary epithelial cells. Knockdown of SNHG3 inhibited the proliferation and migration of CCA cells
.
Mechanistically, SNHG3-sponged miR-3173–5p, thus releasing the repression of ERG by miR-3173–5p. Rescue experiments showed that the miR-3173–5p/ERG axis mediated the oncogenic effect of SNHG3.
Conclusion
Taken together, our data suggest that SNHG3 is a pleiotropic oncogenic lncRNA in CCA. Knockdown of SNHG3 expression suppressed malignant phenotypes in CCA cells via the miR-3173–5p/ERG axis.</description><identifier>ISSN: 1091-255X</identifier><identifier>EISSN: 1873-4626</identifier><identifier>DOI: 10.1007/s11605-021-05160-5</identifier><identifier>PMID: 34647226</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Apoptosis ; Bile Duct Neoplasms - pathology ; Bile Ducts, Intrahepatic - pathology ; Binding sites ; Cancer ; Cell culture ; Cell Line, Tumor ; Cell Movement - genetics ; Cell Proliferation - genetics ; Cholangiocarcinoma ; Cholangiocarcinoma - genetics ; Cholangiocarcinoma - pathology ; Flow cytometry ; Gastroenterology ; Gastrointestinal surgery ; Gene expression ; Gene Expression Regulation, Neoplastic ; Genotype & phenotype ; Humans ; Leukemia ; Medicine ; Medicine & Public Health ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Original Article ; Phenotype ; Plasmids ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Surgery ; Transcriptional Regulator ERG - genetics ; Transcriptional Regulator ERG - metabolism</subject><ispartof>Journal of gastrointestinal surgery, 2022-04, Vol.26 (4), p.802-812</ispartof><rights>The Society for Surgery of the Alimentary Tract 2021</rights><rights>2021. The Society for Surgery of the Alimentary Tract.</rights><rights>The Society for Surgery of the Alimentary Tract 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-b134c82711eceec0e61e0653a1025bcd2750f548f68ff5aefa7b61ce71ca8c9c3</citedby><cites>FETCH-LOGICAL-c375t-b134c82711eceec0e61e0653a1025bcd2750f548f68ff5aefa7b61ce71ca8c9c3</cites><orcidid>0000-0002-4906-1301</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11605-021-05160-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11605-021-05160-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51298</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34647226$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sun, Zeng-Peng</creatorcontrib><creatorcontrib>Tan, Zhi-Guo</creatorcontrib><creatorcontrib>Peng, Chuang</creatorcontrib><creatorcontrib>Yi, Wei-Min</creatorcontrib><title>LncRNA SNHG3 Facilitates the Malignant Phenotype of Cholangiocarcinoma Cells via the miR-3173–5p/ERG Axis</title><title>Journal of gastrointestinal surgery</title><addtitle>J Gastrointest Surg</addtitle><addtitle>J Gastrointest Surg</addtitle><description>Background
Long noncoding RNA (lncRNA) small nucleolar RNA host gene 3 (SNHG3) is an oncogenic lncRNA that has been reported in many cancers, but the role of SNHG3 in cholangiocarcinoma (CCA) remains largely unknown. Bioinformatic analysis revealed a regulatory relationship among SNHG3, miR-3173–5p, and ERG. miR-3173–5p is a tumour suppressive miRNA, while ERG is an oncogene. In the present study, we focused on the regulatory effects and molecular mechanisms of SNHG3 in CCA.
Method
The expression of SNHG3 and miR-3173–5p was evaluated using qRT–PCR analysis. Knockdown of SNHG3 was achieved by shRNA. Cell viability was assessed by MTT assay. Migration and invasion were determined by Transwell assay. Flow cytometry was used to assess cell apoptosis. Western blots were applied to quantify protein levels. Furthermore, using RNA pulldown and dual luciferase assays, the interactions between SNHG3 and miR-3173–5p and between miR-3173–5p and ERG in CCA cells were validated.
Results
SNHG3 was significantly upregulated in CCA cells compared with normal human intrahepatic biliary epithelial cells. Knockdown of SNHG3 inhibited the proliferation and migration of CCA cells
.
Mechanistically, SNHG3-sponged miR-3173–5p, thus releasing the repression of ERG by miR-3173–5p. Rescue experiments showed that the miR-3173–5p/ERG axis mediated the oncogenic effect of SNHG3.
Conclusion
Taken together, our data suggest that SNHG3 is a pleiotropic oncogenic lncRNA in CCA. Knockdown of SNHG3 expression suppressed malignant phenotypes in CCA cells via the miR-3173–5p/ERG axis.</description><subject>Apoptosis</subject><subject>Bile Duct Neoplasms - pathology</subject><subject>Bile Ducts, Intrahepatic - pathology</subject><subject>Binding sites</subject><subject>Cancer</subject><subject>Cell culture</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Cell Proliferation - genetics</subject><subject>Cholangiocarcinoma</subject><subject>Cholangiocarcinoma - genetics</subject><subject>Cholangiocarcinoma - pathology</subject><subject>Flow cytometry</subject><subject>Gastroenterology</subject><subject>Gastrointestinal surgery</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genotype & phenotype</subject><subject>Humans</subject><subject>Leukemia</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Original Article</subject><subject>Phenotype</subject><subject>Plasmids</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Surgery</subject><subject>Transcriptional Regulator ERG - genetics</subject><subject>Transcriptional Regulator ERG - metabolism</subject><issn>1091-255X</issn><issn>1873-4626</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kc9OGzEQxi1UxL_yAhyQpV56cfHYa3s5RhGESgGqtJW4WY6ZTUx37XS9qcqNd-gb9knqEv5IPfQ0I83v-2Y0HyFHwD8A5-YkA2iuGBfAuCotU1tkD2ojWaWFflN6fgpMKHWzS_ZzvuMcDId6h-zKSldGCL1Hvk2jn12N6Oeri4mk586HNgxuwEyHJdJL14ZFdHGgn5YY03C_QpoaOl6m1sVFSN71PsTUOTrGts30R3CPui7MmAQjfz_8UquTs9mEjn6G_JZsN67NePhUD8jX87Mv4ws2vZ58HI-mzEujBjYHWflaGAD0iJ6jBuRaSQdcqLm_FUbxRlV1o-umUQ4bZ-YaPBrwrvanXh6Q9xvfVZ--rzEPtgvZlwNdxLTOVqhaAHCpZEHf_YPepXUfy3VWaCWMlFLzQokN5fuUc4-NXfWhc_29BW7_RmE3UdgShX2MwqoiOn6yXs87vH2RPP--AHID5DKKC-xfd__H9g98MJK5</recordid><startdate>20220401</startdate><enddate>20220401</enddate><creator>Sun, Zeng-Peng</creator><creator>Tan, Zhi-Guo</creator><creator>Peng, Chuang</creator><creator>Yi, Wei-Min</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4906-1301</orcidid></search><sort><creationdate>20220401</creationdate><title>LncRNA SNHG3 Facilitates the Malignant Phenotype of Cholangiocarcinoma Cells via the miR-3173–5p/ERG Axis</title><author>Sun, Zeng-Peng ; Tan, Zhi-Guo ; Peng, Chuang ; Yi, Wei-Min</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-b134c82711eceec0e61e0653a1025bcd2750f548f68ff5aefa7b61ce71ca8c9c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Apoptosis</topic><topic>Bile Duct Neoplasms - pathology</topic><topic>Bile Ducts, Intrahepatic - pathology</topic><topic>Binding sites</topic><topic>Cancer</topic><topic>Cell culture</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - genetics</topic><topic>Cell Proliferation - genetics</topic><topic>Cholangiocarcinoma</topic><topic>Cholangiocarcinoma - genetics</topic><topic>Cholangiocarcinoma - pathology</topic><topic>Flow cytometry</topic><topic>Gastroenterology</topic><topic>Gastrointestinal surgery</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genotype & phenotype</topic><topic>Humans</topic><topic>Leukemia</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Original Article</topic><topic>Phenotype</topic><topic>Plasmids</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Surgery</topic><topic>Transcriptional Regulator ERG - genetics</topic><topic>Transcriptional Regulator ERG - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sun, Zeng-Peng</creatorcontrib><creatorcontrib>Tan, Zhi-Guo</creatorcontrib><creatorcontrib>Peng, Chuang</creatorcontrib><creatorcontrib>Yi, Wei-Min</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Nursing & Allied Health Database</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of gastrointestinal surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sun, Zeng-Peng</au><au>Tan, Zhi-Guo</au><au>Peng, Chuang</au><au>Yi, Wei-Min</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>LncRNA SNHG3 Facilitates the Malignant Phenotype of Cholangiocarcinoma Cells via the miR-3173–5p/ERG Axis</atitle><jtitle>Journal of gastrointestinal surgery</jtitle><stitle>J Gastrointest Surg</stitle><addtitle>J Gastrointest Surg</addtitle><date>2022-04-01</date><risdate>2022</risdate><volume>26</volume><issue>4</issue><spage>802</spage><epage>812</epage><pages>802-812</pages><issn>1091-255X</issn><eissn>1873-4626</eissn><abstract>Background
Long noncoding RNA (lncRNA) small nucleolar RNA host gene 3 (SNHG3) is an oncogenic lncRNA that has been reported in many cancers, but the role of SNHG3 in cholangiocarcinoma (CCA) remains largely unknown. Bioinformatic analysis revealed a regulatory relationship among SNHG3, miR-3173–5p, and ERG. miR-3173–5p is a tumour suppressive miRNA, while ERG is an oncogene. In the present study, we focused on the regulatory effects and molecular mechanisms of SNHG3 in CCA.
Method
The expression of SNHG3 and miR-3173–5p was evaluated using qRT–PCR analysis. Knockdown of SNHG3 was achieved by shRNA. Cell viability was assessed by MTT assay. Migration and invasion were determined by Transwell assay. Flow cytometry was used to assess cell apoptosis. Western blots were applied to quantify protein levels. Furthermore, using RNA pulldown and dual luciferase assays, the interactions between SNHG3 and miR-3173–5p and between miR-3173–5p and ERG in CCA cells were validated.
Results
SNHG3 was significantly upregulated in CCA cells compared with normal human intrahepatic biliary epithelial cells. Knockdown of SNHG3 inhibited the proliferation and migration of CCA cells
.
Mechanistically, SNHG3-sponged miR-3173–5p, thus releasing the repression of ERG by miR-3173–5p. Rescue experiments showed that the miR-3173–5p/ERG axis mediated the oncogenic effect of SNHG3.
Conclusion
Taken together, our data suggest that SNHG3 is a pleiotropic oncogenic lncRNA in CCA. Knockdown of SNHG3 expression suppressed malignant phenotypes in CCA cells via the miR-3173–5p/ERG axis.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>34647226</pmid><doi>10.1007/s11605-021-05160-5</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-4906-1301</orcidid></addata></record> |
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subjects | Apoptosis Bile Duct Neoplasms - pathology Bile Ducts, Intrahepatic - pathology Binding sites Cancer Cell culture Cell Line, Tumor Cell Movement - genetics Cell Proliferation - genetics Cholangiocarcinoma Cholangiocarcinoma - genetics Cholangiocarcinoma - pathology Flow cytometry Gastroenterology Gastrointestinal surgery Gene expression Gene Expression Regulation, Neoplastic Genotype & phenotype Humans Leukemia Medicine Medicine & Public Health MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism Original Article Phenotype Plasmids RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Surgery Transcriptional Regulator ERG - genetics Transcriptional Regulator ERG - metabolism |
title | LncRNA SNHG3 Facilitates the Malignant Phenotype of Cholangiocarcinoma Cells via the miR-3173–5p/ERG Axis |
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