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LINC01088/miR-22/CDC6 Axis Regulates Prostate Cancer Progression by Activating the PI3K/AKT Pathway
Background. Prostate cancer (PCa) harms the male reproductive system, and lncRNA may play an important role in it. Here, we report that the LINC01088/microRNA- (miRNA/miR-) 22/cell division cycle 6 (CDC6) axis regulated through the phosphatidylinositide 3-kinases- (PI3K-) protein kinase B (AKT) sign...
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Published in: | Mediators of inflammation 2023-07, Vol.2023, p.9207148-14 |
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description | Background. Prostate cancer (PCa) harms the male reproductive system, and lncRNA may play an important role in it. Here, we report that the LINC01088/microRNA- (miRNA/miR-) 22/cell division cycle 6 (CDC6) axis regulated through the phosphatidylinositide 3-kinases- (PI3K-) protein kinase B (AKT) signaling pathway controls the development of PCa. Methods. lncRNA/miRNA/mRNA associated with PCa was downloaded and analyzed by Gene Expression Omnibus. The expression and correlation of LINC01088/miR-22/CDC6 in PCa were analyzed and verified by RT-qPCR. Dual-luciferase was used to analyze the binding between miR-22 and LINC01088 or CDC6. Cell Counting Kit-8 and Transwell were used to analyze the effects of LINC01088/miR-22/CDC6 interactions on PCa cell viability or migration/invasion ability. Localization of LINC01088 in cells was analyzed by nuclear cytoplasmic separation. The effect of LINC01088/miR-22/CDC6 interaction on downstream PI3K/AKT signaling was analyzed by Western blot. Results. LINC01088 or CDC6 was upregulated in prostate tumor tissues or cells, whereas miR-22 was downregulated, miR-22 directly targets both LINC01088 and CDC6. si-LINC01088 inhibits the PCa process by suppressing the PI3K/AKT pathway. CDC6 reverses si-linc01088-mediated cell growth inhibition and reduction of PI3K and AKT protein levels. Conclusion. Our results demonstrate that the LINC01088/miR-22/CDC6 axis functions in PCa progression and provide a promising diagnostic and therapeutic target. |
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fullrecord | <record><control><sourceid>gale_doaj_</sourceid><recordid>TN_cdi_doaj_primary_oai_doaj_org_article_ce1f062c36194325b77bfa8c646964a0</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A759027348</galeid><doaj_id>oai_doaj_org_article_ce1f062c36194325b77bfa8c646964a0</doaj_id><sourcerecordid>A759027348</sourcerecordid><originalsourceid>FETCH-LOGICAL-c539t-2ec2983e632f0905dc2875ee8f49906a78ef975f3b0bb178ca0e9bac03c9bb253</originalsourceid><addsrcrecordid>eNp9ksuP0zAQxiMEYsvCjTOKxAUJsvX7cUJVeFVbQbVazpbjTlJXabzE6S7973FoWShCyAfb49989oy_LHuO0QXGnE8JInSqCZKYqQfZBDMhCqwEfphNkBak0JTjs-xJjBuEEGdMPc7OqOQIa0ommVvMP5cII6WmW39VEDIt35Uin333Mb-CZtfaAWK-7EMc0iovbeegH_dNDzH60OXVPp-5wd_awXdNPqwhX87p5XR2eZ0v7bC-s_un2aPathGeHefz7OuH99flp2Lx5eO8nC0Kx6keCgKOaEVBUFIjjfjKESU5gKqZ1khYqaDWkte0QlWFpXIWga6sQ9TpqiKcnmfzg-4q2I256f3W9nsTrDc_A6FvjO0H71owDnCNBHFUYM0o4ZWUVW2VE0xowSxKWm8PWje7agsrB93Q2_ZE9PSk82vThFuDEZWY6_E1r44Kffi2gziYrY8O2tZ2EHbREMUY0oRgldCXf6GbsOu71KuRoiIxiv-mGpsq8F0d0sVuFDUzyTUikrJR6-IfVBor2HoXOqh9ip8kvDkkuPTJsYf6vkiMzOgwMzrMHB2W8Bd_NuYe_mWpBLw-AGvfreyd_7_cD1ak0uk</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2843621885</pqid></control><display><type>article</type><title>LINC01088/miR-22/CDC6 Axis Regulates Prostate Cancer Progression by Activating the PI3K/AKT Pathway</title><source>PubMed Central Free</source><source>Wiley Online Library Open Access</source><source>Publicly Available Content Database</source><creator>Li, Jianwei ; Huang, Xinghua ; Chen, Haodong ; Gu, Caifu ; Ni, Binyu ; Zhou, Jianhua</creator><contributor>Pan, Jinghua ; Jinghua Pan</contributor><creatorcontrib>Li, Jianwei ; Huang, Xinghua ; Chen, Haodong ; Gu, Caifu ; Ni, Binyu ; Zhou, Jianhua ; Pan, Jinghua ; Jinghua Pan</creatorcontrib><description>Background. Prostate cancer (PCa) harms the male reproductive system, and lncRNA may play an important role in it. Here, we report that the LINC01088/microRNA- (miRNA/miR-) 22/cell division cycle 6 (CDC6) axis regulated through the phosphatidylinositide 3-kinases- (PI3K-) protein kinase B (AKT) signaling pathway controls the development of PCa. Methods. lncRNA/miRNA/mRNA associated with PCa was downloaded and analyzed by Gene Expression Omnibus. The expression and correlation of LINC01088/miR-22/CDC6 in PCa were analyzed and verified by RT-qPCR. Dual-luciferase was used to analyze the binding between miR-22 and LINC01088 or CDC6. Cell Counting Kit-8 and Transwell were used to analyze the effects of LINC01088/miR-22/CDC6 interactions on PCa cell viability or migration/invasion ability. Localization of LINC01088 in cells was analyzed by nuclear cytoplasmic separation. The effect of LINC01088/miR-22/CDC6 interaction on downstream PI3K/AKT signaling was analyzed by Western blot. Results. LINC01088 or CDC6 was upregulated in prostate tumor tissues or cells, whereas miR-22 was downregulated, miR-22 directly targets both LINC01088 and CDC6. si-LINC01088 inhibits the PCa process by suppressing the PI3K/AKT pathway. CDC6 reverses si-linc01088-mediated cell growth inhibition and reduction of PI3K and AKT protein levels. Conclusion. Our results demonstrate that the LINC01088/miR-22/CDC6 axis functions in PCa progression and provide a promising diagnostic and therapeutic target.</description><identifier>ISSN: 0962-9351</identifier><identifier>EISSN: 1466-1861</identifier><identifier>DOI: 10.1155/2023/9207148</identifier><identifier>PMID: 37501932</identifier><language>eng</language><publisher>United States: Hindawi</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Analysis ; Biomarkers ; Biopsy ; Cell division ; Cell migration ; Cell viability ; Gene expression ; Localization ; Medical prognosis ; MicroRNAs ; miRNA ; Non-coding RNA ; Prostate cancer ; Reproductive system ; Signal transduction ; Statistical analysis ; Statistical significance ; Survival analysis ; Therapeutic targets ; Tumorigenesis</subject><ispartof>Mediators of inflammation, 2023-07, Vol.2023, p.9207148-14</ispartof><rights>Copyright © 2023 Jianwei Li et al.</rights><rights>COPYRIGHT 2023 John Wiley & Sons, Inc.</rights><rights>Copyright © 2023 Jianwei Li et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2023 Jianwei Li et al. 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c539t-2ec2983e632f0905dc2875ee8f49906a78ef975f3b0bb178ca0e9bac03c9bb253</cites><orcidid>0009-0008-9627-6517</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2843621885/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2843621885?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37501932$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Pan, Jinghua</contributor><contributor>Jinghua Pan</contributor><creatorcontrib>Li, Jianwei</creatorcontrib><creatorcontrib>Huang, Xinghua</creatorcontrib><creatorcontrib>Chen, Haodong</creatorcontrib><creatorcontrib>Gu, Caifu</creatorcontrib><creatorcontrib>Ni, Binyu</creatorcontrib><creatorcontrib>Zhou, Jianhua</creatorcontrib><title>LINC01088/miR-22/CDC6 Axis Regulates Prostate Cancer Progression by Activating the PI3K/AKT Pathway</title><title>Mediators of inflammation</title><addtitle>Mediators Inflamm</addtitle><description>Background. Prostate cancer (PCa) harms the male reproductive system, and lncRNA may play an important role in it. Here, we report that the LINC01088/microRNA- (miRNA/miR-) 22/cell division cycle 6 (CDC6) axis regulated through the phosphatidylinositide 3-kinases- (PI3K-) protein kinase B (AKT) signaling pathway controls the development of PCa. Methods. lncRNA/miRNA/mRNA associated with PCa was downloaded and analyzed by Gene Expression Omnibus. The expression and correlation of LINC01088/miR-22/CDC6 in PCa were analyzed and verified by RT-qPCR. Dual-luciferase was used to analyze the binding between miR-22 and LINC01088 or CDC6. Cell Counting Kit-8 and Transwell were used to analyze the effects of LINC01088/miR-22/CDC6 interactions on PCa cell viability or migration/invasion ability. Localization of LINC01088 in cells was analyzed by nuclear cytoplasmic separation. The effect of LINC01088/miR-22/CDC6 interaction on downstream PI3K/AKT signaling was analyzed by Western blot. Results. LINC01088 or CDC6 was upregulated in prostate tumor tissues or cells, whereas miR-22 was downregulated, miR-22 directly targets both LINC01088 and CDC6. si-LINC01088 inhibits the PCa process by suppressing the PI3K/AKT pathway. CDC6 reverses si-linc01088-mediated cell growth inhibition and reduction of PI3K and AKT protein levels. Conclusion. Our results demonstrate that the LINC01088/miR-22/CDC6 axis functions in PCa progression and provide a promising diagnostic and therapeutic target.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Analysis</subject><subject>Biomarkers</subject><subject>Biopsy</subject><subject>Cell division</subject><subject>Cell migration</subject><subject>Cell viability</subject><subject>Gene expression</subject><subject>Localization</subject><subject>Medical prognosis</subject><subject>MicroRNAs</subject><subject>miRNA</subject><subject>Non-coding RNA</subject><subject>Prostate cancer</subject><subject>Reproductive system</subject><subject>Signal transduction</subject><subject>Statistical analysis</subject><subject>Statistical significance</subject><subject>Survival analysis</subject><subject>Therapeutic targets</subject><subject>Tumorigenesis</subject><issn>0962-9351</issn><issn>1466-1861</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNp9ksuP0zAQxiMEYsvCjTOKxAUJsvX7cUJVeFVbQbVazpbjTlJXabzE6S7973FoWShCyAfb49989oy_LHuO0QXGnE8JInSqCZKYqQfZBDMhCqwEfphNkBak0JTjs-xJjBuEEGdMPc7OqOQIa0ommVvMP5cII6WmW39VEDIt35Uin333Mb-CZtfaAWK-7EMc0iovbeegH_dNDzH60OXVPp-5wd_awXdNPqwhX87p5XR2eZ0v7bC-s_un2aPathGeHefz7OuH99flp2Lx5eO8nC0Kx6keCgKOaEVBUFIjjfjKESU5gKqZ1khYqaDWkte0QlWFpXIWga6sQ9TpqiKcnmfzg-4q2I256f3W9nsTrDc_A6FvjO0H71owDnCNBHFUYM0o4ZWUVW2VE0xowSxKWm8PWje7agsrB93Q2_ZE9PSk82vThFuDEZWY6_E1r44Kffi2gziYrY8O2tZ2EHbREMUY0oRgldCXf6GbsOu71KuRoiIxiv-mGpsq8F0d0sVuFDUzyTUikrJR6-IfVBor2HoXOqh9ip8kvDkkuPTJsYf6vkiMzOgwMzrMHB2W8Bd_NuYe_mWpBLw-AGvfreyd_7_cD1ak0uk</recordid><startdate>20230719</startdate><enddate>20230719</enddate><creator>Li, Jianwei</creator><creator>Huang, Xinghua</creator><creator>Chen, Haodong</creator><creator>Gu, Caifu</creator><creator>Ni, Binyu</creator><creator>Zhou, Jianhua</creator><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0009-0008-9627-6517</orcidid></search><sort><creationdate>20230719</creationdate><title>LINC01088/miR-22/CDC6 Axis Regulates Prostate Cancer Progression by Activating the PI3K/AKT Pathway</title><author>Li, Jianwei ; Huang, Xinghua ; Chen, Haodong ; Gu, Caifu ; Ni, Binyu ; Zhou, Jianhua</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c539t-2ec2983e632f0905dc2875ee8f49906a78ef975f3b0bb178ca0e9bac03c9bb253</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Analysis</topic><topic>Biomarkers</topic><topic>Biopsy</topic><topic>Cell division</topic><topic>Cell migration</topic><topic>Cell viability</topic><topic>Gene expression</topic><topic>Localization</topic><topic>Medical prognosis</topic><topic>MicroRNAs</topic><topic>miRNA</topic><topic>Non-coding RNA</topic><topic>Prostate cancer</topic><topic>Reproductive system</topic><topic>Signal transduction</topic><topic>Statistical analysis</topic><topic>Statistical significance</topic><topic>Survival analysis</topic><topic>Therapeutic targets</topic><topic>Tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Jianwei</creatorcontrib><creatorcontrib>Huang, Xinghua</creatorcontrib><creatorcontrib>Chen, Haodong</creatorcontrib><creatorcontrib>Gu, Caifu</creatorcontrib><creatorcontrib>Ni, Binyu</creatorcontrib><creatorcontrib>Zhou, Jianhua</creatorcontrib><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep (ProQuest)</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest research library</collection><collection>ProQuest Biological Science Journals</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</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 Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Mediators of inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Jianwei</au><au>Huang, Xinghua</au><au>Chen, Haodong</au><au>Gu, Caifu</au><au>Ni, Binyu</au><au>Zhou, Jianhua</au><au>Pan, Jinghua</au><au>Jinghua Pan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>LINC01088/miR-22/CDC6 Axis Regulates Prostate Cancer Progression by Activating the PI3K/AKT Pathway</atitle><jtitle>Mediators of inflammation</jtitle><addtitle>Mediators Inflamm</addtitle><date>2023-07-19</date><risdate>2023</risdate><volume>2023</volume><spage>9207148</spage><epage>14</epage><pages>9207148-14</pages><issn>0962-9351</issn><eissn>1466-1861</eissn><abstract>Background. Prostate cancer (PCa) harms the male reproductive system, and lncRNA may play an important role in it. Here, we report that the LINC01088/microRNA- (miRNA/miR-) 22/cell division cycle 6 (CDC6) axis regulated through the phosphatidylinositide 3-kinases- (PI3K-) protein kinase B (AKT) signaling pathway controls the development of PCa. Methods. lncRNA/miRNA/mRNA associated with PCa was downloaded and analyzed by Gene Expression Omnibus. The expression and correlation of LINC01088/miR-22/CDC6 in PCa were analyzed and verified by RT-qPCR. Dual-luciferase was used to analyze the binding between miR-22 and LINC01088 or CDC6. Cell Counting Kit-8 and Transwell were used to analyze the effects of LINC01088/miR-22/CDC6 interactions on PCa cell viability or migration/invasion ability. Localization of LINC01088 in cells was analyzed by nuclear cytoplasmic separation. The effect of LINC01088/miR-22/CDC6 interaction on downstream PI3K/AKT signaling was analyzed by Western blot. Results. LINC01088 or CDC6 was upregulated in prostate tumor tissues or cells, whereas miR-22 was downregulated, miR-22 directly targets both LINC01088 and CDC6. si-LINC01088 inhibits the PCa process by suppressing the PI3K/AKT pathway. CDC6 reverses si-linc01088-mediated cell growth inhibition and reduction of PI3K and AKT protein levels. Conclusion. Our results demonstrate that the LINC01088/miR-22/CDC6 axis functions in PCa progression and provide a promising diagnostic and therapeutic target.</abstract><cop>United States</cop><pub>Hindawi</pub><pmid>37501932</pmid><doi>10.1155/2023/9207148</doi><tpages>14</tpages><orcidid>https://orcid.org/0009-0008-9627-6517</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | 1-Phosphatidylinositol 3-kinase AKT protein Analysis Biomarkers Biopsy Cell division Cell migration Cell viability Gene expression Localization Medical prognosis MicroRNAs miRNA Non-coding RNA Prostate cancer Reproductive system Signal transduction Statistical analysis Statistical significance Survival analysis Therapeutic targets Tumorigenesis |
title | LINC01088/miR-22/CDC6 Axis Regulates Prostate Cancer Progression by Activating the PI3K/AKT Pathway |
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