MicroRNA 101 Attenuated NSCLC Proliferation through IDH2/HIFα Axis Suppression in the Warburg Effect
Lung cancer is the most diagnosed and deadly cancer in China. MicroRNAs are small noncoding RNA gene products that exhibit multifunctional regulation in cancer cell progressions. MiR-101 loss was illustrated in about 29% of lung cancer patients, and sophisticated mechanisms of miR-101 regulation in...
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| Veröffentlicht in: | Oxidative medicine and cellular longevity 2022-10, Vol.2022, p.1-12 |
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| container_title | Oxidative medicine and cellular longevity |
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| creator | Han, Le Zhang, Yili Zhao, Bin Yue, Jianren Chen, Zhenghong Lei, Guangyan Huang, Chen Chen, Wenjuan |
| description | Lung cancer is the most diagnosed and deadly cancer in China. MicroRNAs are small noncoding RNA gene products that exhibit multifunctional regulation in cancer cell progressions. MiR-101 loss was illustrated in about 29% of lung cancer patients, and sophisticated mechanisms of miR-101 regulation in NSCLC are eager to be disclosed. Here, using specimens from NSCLC patients and Dural-luciferase reporter assay, we got a clue that miR-101 correlated with IDH2. MiR-101 overexpression and IDH2 deficiency both suppressed NSCLC tumor growth in mice. Moreover, in NSCLC, miR-101 suppressed IDH2 expression levels, further increased α-KG concentration, and finally inhibited the Warburg effect under hypoxic conditions through downregulating HIF1α expression by promoting HIF1α hydroxylation and degradation. In conclusion, miR-101 attenuated the Warburg effect and NSCLC proliferation through IDH2/HIF1α pathway. |
| doi_str_mv | 10.1155/2022/4938811 |
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MicroRNAs are small noncoding RNA gene products that exhibit multifunctional regulation in cancer cell progressions. MiR-101 loss was illustrated in about 29% of lung cancer patients, and sophisticated mechanisms of miR-101 regulation in NSCLC are eager to be disclosed. Here, using specimens from NSCLC patients and Dural-luciferase reporter assay, we got a clue that miR-101 correlated with IDH2. MiR-101 overexpression and IDH2 deficiency both suppressed NSCLC tumor growth in mice. Moreover, in NSCLC, miR-101 suppressed IDH2 expression levels, further increased α-KG concentration, and finally inhibited the Warburg effect under hypoxic conditions through downregulating HIF1α expression by promoting HIF1α hydroxylation and degradation. In conclusion, miR-101 attenuated the Warburg effect and NSCLC proliferation through IDH2/HIF1α pathway.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2022/4938811</identifier><language>eng</language><publisher>New York: Hindawi</publisher><subject>Angiogenesis ; Cell cycle ; Cell growth ; DNA methylation ; Laboratory animals ; Liver cancer ; Lung cancer ; Medical prognosis ; Medical research ; MicroRNAs ; Patients ; Surgery</subject><ispartof>Oxidative medicine and cellular longevity, 2022-10, Vol.2022, p.1-12</ispartof><rights>Copyright © 2022 Le Han et al.</rights><rights>Copyright © 2022 Le Han 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 © 2022 Le Han et al. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c425t-ec6ed955cd97fa1d06dedf1a7cf82ea6e10617d15129636eaeeae8386d42f50e3</citedby><cites>FETCH-LOGICAL-c425t-ec6ed955cd97fa1d06dedf1a7cf82ea6e10617d15129636eaeeae8386d42f50e3</cites><orcidid>0000-0002-0519-6634 ; 0000-0002-6217-6672 ; 0000-0002-0683-0502</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9596240/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9596240/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53769,53771</link.rule.ids></links><search><contributor>Roy, Subhadeep</contributor><contributor>Subhadeep Roy</contributor><creatorcontrib>Han, Le</creatorcontrib><creatorcontrib>Zhang, Yili</creatorcontrib><creatorcontrib>Zhao, Bin</creatorcontrib><creatorcontrib>Yue, Jianren</creatorcontrib><creatorcontrib>Chen, Zhenghong</creatorcontrib><creatorcontrib>Lei, Guangyan</creatorcontrib><creatorcontrib>Huang, Chen</creatorcontrib><creatorcontrib>Chen, Wenjuan</creatorcontrib><title>MicroRNA 101 Attenuated NSCLC Proliferation through IDH2/HIFα Axis Suppression in the Warburg Effect</title><title>Oxidative medicine and cellular longevity</title><description>Lung cancer is the most diagnosed and deadly cancer in China. MicroRNAs are small noncoding RNA gene products that exhibit multifunctional regulation in cancer cell progressions. MiR-101 loss was illustrated in about 29% of lung cancer patients, and sophisticated mechanisms of miR-101 regulation in NSCLC are eager to be disclosed. Here, using specimens from NSCLC patients and Dural-luciferase reporter assay, we got a clue that miR-101 correlated with IDH2. MiR-101 overexpression and IDH2 deficiency both suppressed NSCLC tumor growth in mice. Moreover, in NSCLC, miR-101 suppressed IDH2 expression levels, further increased α-KG concentration, and finally inhibited the Warburg effect under hypoxic conditions through downregulating HIF1α expression by promoting HIF1α hydroxylation and degradation. In conclusion, miR-101 attenuated the Warburg effect and NSCLC proliferation through IDH2/HIF1α pathway.</description><subject>Angiogenesis</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>DNA methylation</subject><subject>Laboratory animals</subject><subject>Liver cancer</subject><subject>Lung cancer</subject><subject>Medical prognosis</subject><subject>Medical research</subject><subject>MicroRNAs</subject><subject>Patients</subject><subject>Surgery</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp90d9KHDEUBvChKNQ_vesDBLwR7Lo5mUlmciMsW-0urLbUll6GODnZjcxO1iTT6mP1RXwmZ91F0AshkEB-fOTky7LPQE8BOB8yytiwkHlVAXzI9kAWbEClLHZezpR-zPZjvKVU5KyAvQwvXR38z6sRAQpklBK2nU5oyNX1eDYmP4JvnMWgk_MtSYvgu_mCTL9O2HAyvXj8T0b3LpLrbrUKGOPauDVD8keHmy7Mybm1WKfDbNfqJuKn7X6Q_b44_zWeDGbfv03Ho9mgLhhPA6wFGsl5bWRpNRgqDBoLuqxtxVALBCqgNMCBSZEL1NivKq-EKZjlFPOD7GyTu-pulmhqbFPQjVoFt9ThQXnt1Oub1i3U3P9VkkvBCtoHHG8Dgr_rMCa1dLHGptEt-i4qVuY0BygZ7-nRG3rru9D24z0r4KKgVa--bFT_yzEGtC-PAarWpal1aWpbWs9PNnzhWqP_uff1E_6vlu4</recordid><startdate>20221018</startdate><enddate>20221018</enddate><creator>Han, Le</creator><creator>Zhang, Yili</creator><creator>Zhao, Bin</creator><creator>Yue, Jianren</creator><creator>Chen, Zhenghong</creator><creator>Lei, Guangyan</creator><creator>Huang, Chen</creator><creator>Chen, Wenjuan</creator><general>Hindawi</general><general>Hindawi Limited</general><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-0519-6634</orcidid><orcidid>https://orcid.org/0000-0002-6217-6672</orcidid><orcidid>https://orcid.org/0000-0002-0683-0502</orcidid></search><sort><creationdate>20221018</creationdate><title>MicroRNA 101 Attenuated NSCLC Proliferation through IDH2/HIFα Axis Suppression in the Warburg Effect</title><author>Han, Le ; 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MicroRNAs are small noncoding RNA gene products that exhibit multifunctional regulation in cancer cell progressions. MiR-101 loss was illustrated in about 29% of lung cancer patients, and sophisticated mechanisms of miR-101 regulation in NSCLC are eager to be disclosed. Here, using specimens from NSCLC patients and Dural-luciferase reporter assay, we got a clue that miR-101 correlated with IDH2. MiR-101 overexpression and IDH2 deficiency both suppressed NSCLC tumor growth in mice. Moreover, in NSCLC, miR-101 suppressed IDH2 expression levels, further increased α-KG concentration, and finally inhibited the Warburg effect under hypoxic conditions through downregulating HIF1α expression by promoting HIF1α hydroxylation and degradation. 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| source | Wiley-Blackwell Open Access Titles; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection; PubMed Central Open Access |
| subjects | Angiogenesis Cell cycle Cell growth DNA methylation Laboratory animals Liver cancer Lung cancer Medical prognosis Medical research MicroRNAs Patients Surgery |
| title | MicroRNA 101 Attenuated NSCLC Proliferation through IDH2/HIFα Axis Suppression in the Warburg Effect |
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