LINC00365 promotes colorectal cancer cell progression through the Wnt/β‐catenin signaling pathway
In the past decade, substantial evidence established that long noncoding RNAs are serious about mediating the evolution of malignancies. In previous studies, LINC00365, which has not been reported in colorectal cancer (CRC), was selected using the bioinformatics analysis in GSE109454 and GSE41655 da...
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| Veröffentlicht in: | Journal of cellular biochemistry 2020-02, Vol.121 (2), p.1260-1272 |
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| container_title | Journal of cellular biochemistry |
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| creator | Zhu, Yiping Bian, Yinzhu Zhang, Qun Hu, Jing Li, Li Yang, Mi Qian, Hanqing Yu, Lixia Liu, Baorui Qian, Xiaoping |
| description | In the past decade, substantial evidence established that long noncoding RNAs are serious about mediating the evolution of malignancies. In previous studies, LINC00365, which has not been reported in colorectal cancer (CRC), was selected using the bioinformatics analysis in GSE109454 and GSE41655 data sets. However, the function and mechanism of LINC00365 are still obscure. In our study, LINC00365 was found upregulated in CRC specimens and intimately connected with the prognosis of patients with CRC. In addition, LINC00365 overexpression enhances the cell abilities of proliferation, migration, and invasion in vitro. Meanwhile, mechanistic studies showed that LINC00365 might involve in CRC cell progression by mediating the Wnt/β‐catenin pathway. Furthermore, LINC00365 upregulation increased CDK1 protein expression. In conclusion, this study suggests that LINC00365 acts as a vital part in facilitating CRC progression and might play as a therapeutic target for patients with CRC.
In this study, we identified LINC00365 was upregulated in colorectal cancer (CRC) and it might promote CRC cell progression via Wnt/β‐catenin signaling pathway. Our study indicated that LINC00365 played a cruial role as an oncogenes and promoted tumor progression, and it might serve as a potential therapeutic target for CRC. |
| doi_str_mv | 10.1002/jcb.29359 |
| format | Article |
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In this study, we identified LINC00365 was upregulated in colorectal cancer (CRC) and it might promote CRC cell progression via Wnt/β‐catenin signaling pathway. Our study indicated that LINC00365 played a cruial role as an oncogenes and promoted tumor progression, and it might serve as a potential therapeutic target for CRC.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.29359</identifier><identifier>PMID: 31544991</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Animals ; Apoptosis ; beta Catenin - genetics ; beta Catenin - metabolism ; Bioinformatics ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Cancer ; cancer progression ; Catenin ; Cell migration ; Cell Proliferation ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - metabolism ; Colorectal Neoplasms - pathology ; Disease Progression ; Gene Expression Regulation, Neoplastic ; Humans ; LINC00365 ; Male ; Mice ; Mice, Nude ; Prognosis ; RNA, Long Noncoding - genetics ; Signal transduction ; Therapeutic applications ; Tumor Cells, Cultured ; Wnt protein ; Wnt/β‐catenin signaling ; Wnt1 Protein - genetics ; Wnt1 Protein - metabolism ; Xenograft Model Antitumor Assays</subject><ispartof>Journal of cellular biochemistry, 2020-02, Vol.121 (2), p.1260-1272</ispartof><rights>2019 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3539-cfbec4df8ca535e195142be2d0458c3d6ecfa5acadd47a3f405fcaf06c660263</citedby><cites>FETCH-LOGICAL-c3539-cfbec4df8ca535e195142be2d0458c3d6ecfa5acadd47a3f405fcaf06c660263</cites><orcidid>0000-0002-4738-1125</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcb.29359$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcb.29359$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31544991$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhu, Yiping</creatorcontrib><creatorcontrib>Bian, Yinzhu</creatorcontrib><creatorcontrib>Zhang, Qun</creatorcontrib><creatorcontrib>Hu, Jing</creatorcontrib><creatorcontrib>Li, Li</creatorcontrib><creatorcontrib>Yang, Mi</creatorcontrib><creatorcontrib>Qian, Hanqing</creatorcontrib><creatorcontrib>Yu, Lixia</creatorcontrib><creatorcontrib>Liu, Baorui</creatorcontrib><creatorcontrib>Qian, Xiaoping</creatorcontrib><title>LINC00365 promotes colorectal cancer cell progression through the Wnt/β‐catenin signaling pathway</title><title>Journal of cellular biochemistry</title><addtitle>J Cell Biochem</addtitle><description>In the past decade, substantial evidence established that long noncoding RNAs are serious about mediating the evolution of malignancies. In previous studies, LINC00365, which has not been reported in colorectal cancer (CRC), was selected using the bioinformatics analysis in GSE109454 and GSE41655 data sets. However, the function and mechanism of LINC00365 are still obscure. In our study, LINC00365 was found upregulated in CRC specimens and intimately connected with the prognosis of patients with CRC. In addition, LINC00365 overexpression enhances the cell abilities of proliferation, migration, and invasion in vitro. Meanwhile, mechanistic studies showed that LINC00365 might involve in CRC cell progression by mediating the Wnt/β‐catenin pathway. Furthermore, LINC00365 upregulation increased CDK1 protein expression. In conclusion, this study suggests that LINC00365 acts as a vital part in facilitating CRC progression and might play as a therapeutic target for patients with CRC.
In this study, we identified LINC00365 was upregulated in colorectal cancer (CRC) and it might promote CRC cell progression via Wnt/β‐catenin signaling pathway. Our study indicated that LINC00365 played a cruial role as an oncogenes and promoted tumor progression, and it might serve as a potential therapeutic target for CRC.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>beta Catenin - genetics</subject><subject>beta Catenin - metabolism</subject><subject>Bioinformatics</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Cancer</subject><subject>cancer progression</subject><subject>Catenin</subject><subject>Cell migration</subject><subject>Cell Proliferation</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - metabolism</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Disease Progression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>LINC00365</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Prognosis</subject><subject>RNA, Long Noncoding - genetics</subject><subject>Signal transduction</subject><subject>Therapeutic applications</subject><subject>Tumor Cells, Cultured</subject><subject>Wnt protein</subject><subject>Wnt/β‐catenin signaling</subject><subject>Wnt1 Protein - genetics</subject><subject>Wnt1 Protein - metabolism</subject><subject>Xenograft Model Antitumor Assays</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10DtOw0AUBdARAkH4FGwAWaKBwmS-dqaEiE9QBA0SpTV5fk4cOZ4wYytKxxJYCwthEayECQkUSFSveEdXV5eQY0YvGKW8O4XRBddC6S3SYVSnsUyk3CYdmgoac8H4Htn3fkop1VrwXbInmJJSa9Yh-XDw0KdUJCqaOzuzDfoIbGUdQmOqCEwN6CLAqlr9xw69L20dNRNn2_EkXIye66b78f75-gamwbqsI1-Oa1OV9Tiam2ayMMtDslOYyuPR5h6Qp5vrp_5dPHy8HfQvhzEIJXQMxQhB5kUPjBIKmVZM8hHynErVA5EnCIVRBkyey9SIQlJVgCloAklCeSIOyNk6NjR9adE32az0q-qmRtv6jHOdMC7Tngr09A-d2taF1kEJnopU90Qa1PlagbPeOyyyuStnxi0zRrPV8llYPvtePtiTTWI7mmH-K3-mDqC7BouywuX_Sdl9_2od-QUuNI8m</recordid><startdate>202002</startdate><enddate>202002</enddate><creator>Zhu, Yiping</creator><creator>Bian, Yinzhu</creator><creator>Zhang, Qun</creator><creator>Hu, Jing</creator><creator>Li, Li</creator><creator>Yang, Mi</creator><creator>Qian, Hanqing</creator><creator>Yu, Lixia</creator><creator>Liu, Baorui</creator><creator>Qian, Xiaoping</creator><general>Wiley Subscription Services, Inc</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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4738-1125</orcidid></search><sort><creationdate>202002</creationdate><title>LINC00365 promotes colorectal cancer cell progression through the Wnt/β‐catenin signaling pathway</title><author>Zhu, Yiping ; 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In previous studies, LINC00365, which has not been reported in colorectal cancer (CRC), was selected using the bioinformatics analysis in GSE109454 and GSE41655 data sets. However, the function and mechanism of LINC00365 are still obscure. In our study, LINC00365 was found upregulated in CRC specimens and intimately connected with the prognosis of patients with CRC. In addition, LINC00365 overexpression enhances the cell abilities of proliferation, migration, and invasion in vitro. Meanwhile, mechanistic studies showed that LINC00365 might involve in CRC cell progression by mediating the Wnt/β‐catenin pathway. Furthermore, LINC00365 upregulation increased CDK1 protein expression. In conclusion, this study suggests that LINC00365 acts as a vital part in facilitating CRC progression and might play as a therapeutic target for patients with CRC.
In this study, we identified LINC00365 was upregulated in colorectal cancer (CRC) and it might promote CRC cell progression via Wnt/β‐catenin signaling pathway. Our study indicated that LINC00365 played a cruial role as an oncogenes and promoted tumor progression, and it might serve as a potential therapeutic target for CRC.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>31544991</pmid><doi>10.1002/jcb.29359</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-4738-1125</orcidid></addata></record> |
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| subjects | Animals Apoptosis beta Catenin - genetics beta Catenin - metabolism Bioinformatics Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Cancer cancer progression Catenin Cell migration Cell Proliferation Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - genetics Colorectal Neoplasms - metabolism Colorectal Neoplasms - pathology Disease Progression Gene Expression Regulation, Neoplastic Humans LINC00365 Male Mice Mice, Nude Prognosis RNA, Long Noncoding - genetics Signal transduction Therapeutic applications Tumor Cells, Cultured Wnt protein Wnt/β‐catenin signaling Wnt1 Protein - genetics Wnt1 Protein - metabolism Xenograft Model Antitumor Assays |
| title | LINC00365 promotes colorectal cancer cell progression through the Wnt/β‐catenin signaling pathway |
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