Circ_0008717 promotes renal cell carcinoma progression by upregulating FBXO17 via targeting miR‐217
Background Renal cell carcinoma (RCC) is a common lethal urological malignancy. Circular RNAs are assumed to play important roles in cancer development. The objective of the present study was to investigate the role and action mechanism of circ_0008717 in RCC. Methods The expression of circ_0008717,...
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Veröffentlicht in: | The journal of gene medicine 2022-11, Vol.24 (11), p.e3418-n/a |
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description | Background
Renal cell carcinoma (RCC) is a common lethal urological malignancy. Circular RNAs are assumed to play important roles in cancer development. The objective of the present study was to investigate the role and action mechanism of circ_0008717 in RCC.
Methods
The expression of circ_0008717, miR‐217 and F‐box protein 17 (FBXO17) mRNA was detected by a real‐time quantitative polymerase chain reaction. Cell proliferation was examined using a cell counting kit‐8 assay and an 5‐ethynyl‐2′‐deoxyuridine assay. Cell apoptosis was assessed by a flow cytometry assay. Cell migration and cell invasion were investigated using a transwell assay. Glycolysis progression was assessed according to the levels of glucose uptake and lactate production. The expression of glycolysis‐related proteins and FBXO17 protein was quantified by western blotting. The targets were analyzed by the bioinformatics tools (starBase and circinteractome) and validated by a dual‐luciferase reporter assay, RNA pull‐down assay and RNA immunoprecipitation assay. A xenograft model was established to monitor the role of circ_0008717 in vivo.
Results
Circ_0008717 was upregulated in RCC tissues and cells. Silencing circ_0008717 suppressed RCC cell proliferation, migration, invasion and glycolysis but promoted cell apoptosis. MiR‐217 was a target of circ_0008717 and bound to the FBXO17 3′ untranslated region. The expression of FBXO17 was positively regulated by circ_0008717 but impaired by miR‐217 reintroduction. The inhibitory effects of circ_0008717 knockdown on RCC cell malignant behaviors were reversed by miR‐217 inhibition or FBXO17 overexpression. Circ_0008717 knockdown inhibited tumor growth in vivo by regulating miR‐217 and FBXO17.
Conclusions
Circ_0008717 aggravated the progression of RCC by activating FBXO17 through targeting miR‐217, which provided a novel mechanism for circ_0008717 to participate in RCC progression.
Circ_0008717 and FBXO17 are upregulated, whereas miR‐217 is downregulated in RCC. Circ_0008717 acts as miR‐217 sponges to decoy miR‐217 and thus regulate FBXO17 expression, thus affecting proliferation, migration, invasion, glycolysis and apoptosis in RCC development. |
doi_str_mv | 10.1002/jgm.3418 |
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Renal cell carcinoma (RCC) is a common lethal urological malignancy. Circular RNAs are assumed to play important roles in cancer development. The objective of the present study was to investigate the role and action mechanism of circ_0008717 in RCC.
Methods
The expression of circ_0008717, miR‐217 and F‐box protein 17 (FBXO17) mRNA was detected by a real‐time quantitative polymerase chain reaction. Cell proliferation was examined using a cell counting kit‐8 assay and an 5‐ethynyl‐2′‐deoxyuridine assay. Cell apoptosis was assessed by a flow cytometry assay. Cell migration and cell invasion were investigated using a transwell assay. Glycolysis progression was assessed according to the levels of glucose uptake and lactate production. The expression of glycolysis‐related proteins and FBXO17 protein was quantified by western blotting. The targets were analyzed by the bioinformatics tools (starBase and circinteractome) and validated by a dual‐luciferase reporter assay, RNA pull‐down assay and RNA immunoprecipitation assay. A xenograft model was established to monitor the role of circ_0008717 in vivo.
Results
Circ_0008717 was upregulated in RCC tissues and cells. Silencing circ_0008717 suppressed RCC cell proliferation, migration, invasion and glycolysis but promoted cell apoptosis. MiR‐217 was a target of circ_0008717 and bound to the FBXO17 3′ untranslated region. The expression of FBXO17 was positively regulated by circ_0008717 but impaired by miR‐217 reintroduction. The inhibitory effects of circ_0008717 knockdown on RCC cell malignant behaviors were reversed by miR‐217 inhibition or FBXO17 overexpression. Circ_0008717 knockdown inhibited tumor growth in vivo by regulating miR‐217 and FBXO17.
Conclusions
Circ_0008717 aggravated the progression of RCC by activating FBXO17 through targeting miR‐217, which provided a novel mechanism for circ_0008717 to participate in RCC progression.
Circ_0008717 and FBXO17 are upregulated, whereas miR‐217 is downregulated in RCC. Circ_0008717 acts as miR‐217 sponges to decoy miR‐217 and thus regulate FBXO17 expression, thus affecting proliferation, migration, invasion, glycolysis and apoptosis in RCC development.</description><identifier>ISSN: 1099-498X</identifier><identifier>EISSN: 1521-2254</identifier><identifier>DOI: 10.1002/jgm.3418</identifier><identifier>PMID: 35357059</identifier><language>eng</language><publisher>England: Wiley Periodicals Inc</publisher><subject>3' Untranslated regions ; Apoptosis ; Bioinformatics ; Cell growth ; Cell migration ; Cell proliferation ; circ_0008717 ; FBXO17 ; Flow cytometry ; Gene therapy ; Glycolysis ; Immunoprecipitation ; Kidney cancer ; Kinases ; Lactic acid ; Malignancy ; miR‐217 ; mRNA ; RCC ; Renal cell carcinoma ; Tumors ; Western blotting ; Xenografts</subject><ispartof>The journal of gene medicine, 2022-11, Vol.24 (11), p.e3418-n/a</ispartof><rights>2022 John Wiley & Sons, Ltd.</rights><rights>This article is protected by copyright. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3498-470581b4931ab935f77c68aef31232d7305f85b4e3a1ff588ed30a31dc5578703</citedby><cites>FETCH-LOGICAL-c3498-470581b4931ab935f77c68aef31232d7305f85b4e3a1ff588ed30a31dc5578703</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjgm.3418$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjgm.3418$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35357059$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shen, Siyao</creatorcontrib><creatorcontrib>Jiang, Ming</creatorcontrib><creatorcontrib>Deng, Wen</creatorcontrib><creatorcontrib>Liu, Xiaoqiang</creatorcontrib><creatorcontrib>Xiong, Junhui</creatorcontrib><creatorcontrib>Zeng, Zhigang</creatorcontrib><creatorcontrib>Zhao, Hong</creatorcontrib><creatorcontrib>Zeng, Xiaochun</creatorcontrib><creatorcontrib>Fu, Bin</creatorcontrib><title>Circ_0008717 promotes renal cell carcinoma progression by upregulating FBXO17 via targeting miR‐217</title><title>The journal of gene medicine</title><addtitle>J Gene Med</addtitle><description>Background
Renal cell carcinoma (RCC) is a common lethal urological malignancy. Circular RNAs are assumed to play important roles in cancer development. The objective of the present study was to investigate the role and action mechanism of circ_0008717 in RCC.
Methods
The expression of circ_0008717, miR‐217 and F‐box protein 17 (FBXO17) mRNA was detected by a real‐time quantitative polymerase chain reaction. Cell proliferation was examined using a cell counting kit‐8 assay and an 5‐ethynyl‐2′‐deoxyuridine assay. Cell apoptosis was assessed by a flow cytometry assay. Cell migration and cell invasion were investigated using a transwell assay. Glycolysis progression was assessed according to the levels of glucose uptake and lactate production. The expression of glycolysis‐related proteins and FBXO17 protein was quantified by western blotting. The targets were analyzed by the bioinformatics tools (starBase and circinteractome) and validated by a dual‐luciferase reporter assay, RNA pull‐down assay and RNA immunoprecipitation assay. A xenograft model was established to monitor the role of circ_0008717 in vivo.
Results
Circ_0008717 was upregulated in RCC tissues and cells. Silencing circ_0008717 suppressed RCC cell proliferation, migration, invasion and glycolysis but promoted cell apoptosis. MiR‐217 was a target of circ_0008717 and bound to the FBXO17 3′ untranslated region. The expression of FBXO17 was positively regulated by circ_0008717 but impaired by miR‐217 reintroduction. The inhibitory effects of circ_0008717 knockdown on RCC cell malignant behaviors were reversed by miR‐217 inhibition or FBXO17 overexpression. Circ_0008717 knockdown inhibited tumor growth in vivo by regulating miR‐217 and FBXO17.
Conclusions
Circ_0008717 aggravated the progression of RCC by activating FBXO17 through targeting miR‐217, which provided a novel mechanism for circ_0008717 to participate in RCC progression.
Circ_0008717 and FBXO17 are upregulated, whereas miR‐217 is downregulated in RCC. Circ_0008717 acts as miR‐217 sponges to decoy miR‐217 and thus regulate FBXO17 expression, thus affecting proliferation, migration, invasion, glycolysis and apoptosis in RCC development.</description><subject>3' Untranslated regions</subject><subject>Apoptosis</subject><subject>Bioinformatics</subject><subject>Cell growth</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>circ_0008717</subject><subject>FBXO17</subject><subject>Flow cytometry</subject><subject>Gene therapy</subject><subject>Glycolysis</subject><subject>Immunoprecipitation</subject><subject>Kidney cancer</subject><subject>Kinases</subject><subject>Lactic acid</subject><subject>Malignancy</subject><subject>miR‐217</subject><subject>mRNA</subject><subject>RCC</subject><subject>Renal cell carcinoma</subject><subject>Tumors</subject><subject>Western blotting</subject><subject>Xenografts</subject><issn>1099-498X</issn><issn>1521-2254</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><recordid>eNp1kM1KAzEURoMotlbBJ5ABN26mJrmTJrPUYqtSKYhCdyEzzQwp81OTjtKdj-Az-iRm2qoguEnCzeHw3Q-hU4L7BGN6ucjLPkRE7KEuYZSElLJo379xHIdRLGYddOTcAmPChYgPUQcYMI5Z3EV6aGwqMcaCEx4sbV3WK-0CqytVBKku_KFsaqq6VO1vbrVzpq6CZB00S6vzplArU-XB6Ho29YJXo4KVsrneDEvz-Pn-QQk_RgeZKpw-2d099Dy6eRrehpPp-G54NQlT8DHDyGcSJIliICqJgWWcpwOhdAaEAp1zwCwTLIk0KJJlTAg9B6yAzFPGuOAYeuhi6_VRXxrtVrI0rt1CVbpunKSDiAkWU0E8ev4HXdSN9Vt7igMBCoLBrzC1tXNWZ3JpTansWhIs2-qlr1621Xv0bCdsklLPf8Dvrj0QboE3U-j1vyJ5P37YCL8ApA-K2w</recordid><startdate>202211</startdate><enddate>202211</enddate><creator>Shen, Siyao</creator><creator>Jiang, Ming</creator><creator>Deng, Wen</creator><creator>Liu, Xiaoqiang</creator><creator>Xiong, Junhui</creator><creator>Zeng, Zhigang</creator><creator>Zhao, Hong</creator><creator>Zeng, Xiaochun</creator><creator>Fu, Bin</creator><general>Wiley Periodicals Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>202211</creationdate><title>Circ_0008717 promotes renal cell carcinoma progression by upregulating FBXO17 via targeting miR‐217</title><author>Shen, Siyao ; Jiang, Ming ; Deng, Wen ; Liu, Xiaoqiang ; Xiong, Junhui ; Zeng, Zhigang ; Zhao, Hong ; Zeng, Xiaochun ; Fu, Bin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3498-470581b4931ab935f77c68aef31232d7305f85b4e3a1ff588ed30a31dc5578703</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>3' Untranslated regions</topic><topic>Apoptosis</topic><topic>Bioinformatics</topic><topic>Cell growth</topic><topic>Cell migration</topic><topic>Cell proliferation</topic><topic>circ_0008717</topic><topic>FBXO17</topic><topic>Flow cytometry</topic><topic>Gene therapy</topic><topic>Glycolysis</topic><topic>Immunoprecipitation</topic><topic>Kidney cancer</topic><topic>Kinases</topic><topic>Lactic acid</topic><topic>Malignancy</topic><topic>miR‐217</topic><topic>mRNA</topic><topic>RCC</topic><topic>Renal cell carcinoma</topic><topic>Tumors</topic><topic>Western blotting</topic><topic>Xenografts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shen, Siyao</creatorcontrib><creatorcontrib>Jiang, Ming</creatorcontrib><creatorcontrib>Deng, Wen</creatorcontrib><creatorcontrib>Liu, Xiaoqiang</creatorcontrib><creatorcontrib>Xiong, Junhui</creatorcontrib><creatorcontrib>Zeng, Zhigang</creatorcontrib><creatorcontrib>Zhao, Hong</creatorcontrib><creatorcontrib>Zeng, Xiaochun</creatorcontrib><creatorcontrib>Fu, Bin</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The journal of gene medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shen, Siyao</au><au>Jiang, Ming</au><au>Deng, Wen</au><au>Liu, Xiaoqiang</au><au>Xiong, Junhui</au><au>Zeng, Zhigang</au><au>Zhao, Hong</au><au>Zeng, Xiaochun</au><au>Fu, Bin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Circ_0008717 promotes renal cell carcinoma progression by upregulating FBXO17 via targeting miR‐217</atitle><jtitle>The journal of gene medicine</jtitle><addtitle>J Gene Med</addtitle><date>2022-11</date><risdate>2022</risdate><volume>24</volume><issue>11</issue><spage>e3418</spage><epage>n/a</epage><pages>e3418-n/a</pages><issn>1099-498X</issn><eissn>1521-2254</eissn><abstract>Background
Renal cell carcinoma (RCC) is a common lethal urological malignancy. Circular RNAs are assumed to play important roles in cancer development. The objective of the present study was to investigate the role and action mechanism of circ_0008717 in RCC.
Methods
The expression of circ_0008717, miR‐217 and F‐box protein 17 (FBXO17) mRNA was detected by a real‐time quantitative polymerase chain reaction. Cell proliferation was examined using a cell counting kit‐8 assay and an 5‐ethynyl‐2′‐deoxyuridine assay. Cell apoptosis was assessed by a flow cytometry assay. Cell migration and cell invasion were investigated using a transwell assay. Glycolysis progression was assessed according to the levels of glucose uptake and lactate production. The expression of glycolysis‐related proteins and FBXO17 protein was quantified by western blotting. The targets were analyzed by the bioinformatics tools (starBase and circinteractome) and validated by a dual‐luciferase reporter assay, RNA pull‐down assay and RNA immunoprecipitation assay. A xenograft model was established to monitor the role of circ_0008717 in vivo.
Results
Circ_0008717 was upregulated in RCC tissues and cells. Silencing circ_0008717 suppressed RCC cell proliferation, migration, invasion and glycolysis but promoted cell apoptosis. MiR‐217 was a target of circ_0008717 and bound to the FBXO17 3′ untranslated region. The expression of FBXO17 was positively regulated by circ_0008717 but impaired by miR‐217 reintroduction. The inhibitory effects of circ_0008717 knockdown on RCC cell malignant behaviors were reversed by miR‐217 inhibition or FBXO17 overexpression. Circ_0008717 knockdown inhibited tumor growth in vivo by regulating miR‐217 and FBXO17.
Conclusions
Circ_0008717 aggravated the progression of RCC by activating FBXO17 through targeting miR‐217, which provided a novel mechanism for circ_0008717 to participate in RCC progression.
Circ_0008717 and FBXO17 are upregulated, whereas miR‐217 is downregulated in RCC. Circ_0008717 acts as miR‐217 sponges to decoy miR‐217 and thus regulate FBXO17 expression, thus affecting proliferation, migration, invasion, glycolysis and apoptosis in RCC development.</abstract><cop>England</cop><pub>Wiley Periodicals Inc</pub><pmid>35357059</pmid><doi>10.1002/jgm.3418</doi><tpages>13</tpages></addata></record> |
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subjects | 3' Untranslated regions Apoptosis Bioinformatics Cell growth Cell migration Cell proliferation circ_0008717 FBXO17 Flow cytometry Gene therapy Glycolysis Immunoprecipitation Kidney cancer Kinases Lactic acid Malignancy miR‐217 mRNA RCC Renal cell carcinoma Tumors Western blotting Xenografts |
title | Circ_0008717 promotes renal cell carcinoma progression by upregulating FBXO17 via targeting miR‐217 |
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