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miR-200b/200a/429 Cluster Stimulates Ovarian Cancer Development by Targeting ING5
Ovarian cancer is the second most common gynaecological malignancy, and microRNAs (miRNAs) play important role in the cancer development. Here, we found that the level of miR-200b/200a/429 was significantly increased in serum and tumor tissues of patients with stage-I ovarian cancer. Consistent with...
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Published in: | Journal of oncology 2020, Vol.2020 (2020), p.1-8 |
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description | Ovarian cancer is the second most common gynaecological malignancy, and microRNAs (miRNAs) play important role in the cancer development. Here, we found that the level of miR-200b/200a/429 was significantly increased in serum and tumor tissues of patients with stage-I ovarian cancer. Consistent with these results, we detected increased expression levels of miR-200b/200a/429 in ovarian cancer cell lines compared with the human nontumorigenic ovarian epithelial cell line T80. The overexpression of miR-200b/200a/429 in T80 cells stimulated proliferation and caused their growth in soft agar and tumor formation in nude mice. Furthermore, we determined that miR-200b/200a/429 targets inhibitor of growth family 5 (ING5) and that the overexpression of ING5 can block miR-200b/200a/429-induced T80 cell transformation and tumorigenesis. Our findings suggest that miR-200b/200a/429 may be a useful biomarker for the early detection of ovarian cancer and that miR-200b/200a/429 significantly contributes to ovarian cancer development through ING5. |
doi_str_mv | 10.1155/2020/3404059 |
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Here, we found that the level of miR-200b/200a/429 was significantly increased in serum and tumor tissues of patients with stage-I ovarian cancer. Consistent with these results, we detected increased expression levels of miR-200b/200a/429 in ovarian cancer cell lines compared with the human nontumorigenic ovarian epithelial cell line T80. The overexpression of miR-200b/200a/429 in T80 cells stimulated proliferation and caused their growth in soft agar and tumor formation in nude mice. Furthermore, we determined that miR-200b/200a/429 targets inhibitor of growth family 5 (ING5) and that the overexpression of ING5 can block miR-200b/200a/429-induced T80 cell transformation and tumorigenesis. Our findings suggest that miR-200b/200a/429 may be a useful biomarker for the early detection of ovarian cancer and that miR-200b/200a/429 significantly contributes to ovarian cancer development through ING5.</description><identifier>ISSN: 1687-8450</identifier><identifier>EISSN: 1687-8450</identifier><identifier>EISSN: 1687-8469</identifier><identifier>DOI: 10.1155/2020/3404059</identifier><identifier>PMID: 32377191</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Cancer ; Carboplatin ; Cell culture ; Cell growth ; Comparative analysis ; Development and progression ; Diagnosis ; Experiments ; Gene expression ; Metastasis ; MicroRNA ; MicroRNAs ; Ovarian cancer ; Patients ; Protein expression ; Proteins ; Tumorigenesis ; Tumors</subject><ispartof>Journal of oncology, 2020, Vol.2020 (2020), p.1-8</ispartof><rights>Copyright © 2020 Wei Guan et al.</rights><rights>COPYRIGHT 2020 John Wiley & Sons, Inc.</rights><rights>Copyright © 2020 Wei Guan et al. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Copyright © 2020 Wei Guan et al. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c565t-4ab28349b3520f525831fd1e08000416294fa99ebd45ebdfcedcd7ce9b9085b03</citedby><cites>FETCH-LOGICAL-c565t-4ab28349b3520f525831fd1e08000416294fa99ebd45ebdfcedcd7ce9b9085b03</cites><orcidid>0000-0003-4605-4015 ; 0000-0001-5491-7533</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2410718211/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2410718211?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,4024,25753,27923,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32377191$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Izadpanah, Reza</contributor><contributor>Reza Izadpanah</contributor><creatorcontrib>Zou, Hua</creatorcontrib><creatorcontrib>Lee, Jin-Won</creatorcontrib><creatorcontrib>Chun, Wan Joo</creatorcontrib><creatorcontrib>Huang, Ping</creatorcontrib><creatorcontrib>Cui, Huiling</creatorcontrib><creatorcontrib>Guan, Wei</creatorcontrib><creatorcontrib>Kim, Heasung</creatorcontrib><title>miR-200b/200a/429 Cluster Stimulates Ovarian Cancer Development by Targeting ING5</title><title>Journal of oncology</title><addtitle>J Oncol</addtitle><description>Ovarian cancer is the second most common gynaecological malignancy, and microRNAs (miRNAs) play important role in the cancer development. 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Our findings suggest that miR-200b/200a/429 may be a useful biomarker for the early detection of ovarian cancer and that miR-200b/200a/429 significantly contributes to ovarian cancer development through ING5.</description><subject>Cancer</subject><subject>Carboplatin</subject><subject>Cell culture</subject><subject>Cell growth</subject><subject>Comparative analysis</subject><subject>Development and progression</subject><subject>Diagnosis</subject><subject>Experiments</subject><subject>Gene expression</subject><subject>Metastasis</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>Ovarian cancer</subject><subject>Patients</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><issn>1687-8450</issn><issn>1687-8450</issn><issn>1687-8469</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNqNkU1v1DAURa0K1JbCrmsUiU0lSOf5K7E3laoBSqWKCmjXlpO8TF0lztROBvXf42GGMrDqxrb0jo7f1SXkmMIppVLOGDCYcQECpN4jh7RQZa6EhBc77wPyKsZ7gEKALvbJAWe8LKmmh-Rb777nDKBKHrAzwXQ276Y4Ysh-jK6fOjtizK5XNjjrs7n1dZp8xBV2w7JHP2bVY3ZjwwJH5xfZ5dcL-Zq8bG0X8c32PiK3nz_dzL_kV9cXl_Pzq7yWhRxzYSumuNAVlwxayaTitG0oggIAQQumRWu1xqoRMh1tjU3dlDXqSoOSFfAjcrbxLqeqT8O0TLCdWQbX2_BoBuvMvxPv7sxiWJkUnHOgSXCyFYThYcI4mt7FGrvOehymaBjXWvFSiTX67j_0fpiCT_EMExRKqhjdoRa2Q-N8O6R_67XUnBeslLoofrs-bKg6DDEGbJ9WpmDWjZp1o2bbaMLf7sZ8gv9UmID3G-DO-cb-dM_UYWKwtX9pqpTSmv8CRsqunQ</recordid><startdate>2020</startdate><enddate>2020</enddate><creator>Zou, Hua</creator><creator>Lee, Jin-Won</creator><creator>Chun, Wan Joo</creator><creator>Huang, Ping</creator><creator>Cui, Huiling</creator><creator>Guan, Wei</creator><creator>Kim, Heasung</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</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>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>NAPCQ</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-4605-4015</orcidid><orcidid>https://orcid.org/0000-0001-5491-7533</orcidid></search><sort><creationdate>2020</creationdate><title>miR-200b/200a/429 Cluster Stimulates Ovarian Cancer Development by Targeting ING5</title><author>Zou, Hua ; 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Here, we found that the level of miR-200b/200a/429 was significantly increased in serum and tumor tissues of patients with stage-I ovarian cancer. Consistent with these results, we detected increased expression levels of miR-200b/200a/429 in ovarian cancer cell lines compared with the human nontumorigenic ovarian epithelial cell line T80. The overexpression of miR-200b/200a/429 in T80 cells stimulated proliferation and caused their growth in soft agar and tumor formation in nude mice. Furthermore, we determined that miR-200b/200a/429 targets inhibitor of growth family 5 (ING5) and that the overexpression of ING5 can block miR-200b/200a/429-induced T80 cell transformation and tumorigenesis. Our findings suggest that miR-200b/200a/429 may be a useful biomarker for the early detection of ovarian cancer and that miR-200b/200a/429 significantly contributes to ovarian cancer development through ING5.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>32377191</pmid><doi>10.1155/2020/3404059</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0003-4605-4015</orcidid><orcidid>https://orcid.org/0000-0001-5491-7533</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Cancer Carboplatin Cell culture Cell growth Comparative analysis Development and progression Diagnosis Experiments Gene expression Metastasis MicroRNA MicroRNAs Ovarian cancer Patients Protein expression Proteins Tumorigenesis Tumors |
title | miR-200b/200a/429 Cluster Stimulates Ovarian Cancer Development by Targeting ING5 |
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