LEF1 Enhances the Progression of Colonic Adenocarcinoma via Remodeling the Cell Motility Associated Structures
Lymphoid enhancer-binding factor 1 (LEF1) is a key transcription factor mediating the Wnt signaling pathway. LEF1 is a regulator that is closely associated with tumor malignancy and is usually upregulated in cancers, including colonic adenocarcinoma. The underlying molecular mechanisms of LEF1 regul...
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| Veröffentlicht in: | International journal of molecular sciences 2021-10, Vol.22 (19), p.10870 |
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| creator | Xiao, Li Zhang, Caixia Li, Xinyao Jia, Chenshuang Chen, Lirong Yuan, Yue Gao, Qian Lu, Zheng Feng, Yang Zhao, Ruixia Zhao, Xuewei Cheng, Sinan Shu, Zhan Xu, Jie Duan, Wei Nie, Guochao Hou, Yingchun |
| description | Lymphoid enhancer-binding factor 1 (LEF1) is a key transcription factor mediating the Wnt signaling pathway. LEF1 is a regulator that is closely associated with tumor malignancy and is usually upregulated in cancers, including colonic adenocarcinoma. The underlying molecular mechanisms of LEF1 regulation for colonic adenocarcinoma progression remain unknown. To explore it, the LEF1 expression in caco2 cells was inhibited using an shRNA approach. The results showed that downregulation of LEF1 inhibited the malignancy and motility associated microstructures, such as polymerization of F-actin, β-tubulin, and Lamin B1 in caco2 cells. LEF1 inhibition suppressed the expression of epithelial/endothelial-mesenchymal transition (EMT) relevant genes. Overall, the current results demonstrated that LEF1 plays a pivotal role in maintaining the malignancy of colonic adenocarcinoma by remodeling motility correlated microstructures and suppressing the expression of EMT-relevant genes. Our study provided evidence of the roles LEF1 played in colonic adenocarcinoma progression, and suggest LEF1 as a potential target for colonic adenocarcinoma therapy. |
| doi_str_mv | 10.3390/ijms221910870 |
| format | Article |
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LEF1 is a regulator that is closely associated with tumor malignancy and is usually upregulated in cancers, including colonic adenocarcinoma. The underlying molecular mechanisms of LEF1 regulation for colonic adenocarcinoma progression remain unknown. To explore it, the LEF1 expression in caco2 cells was inhibited using an shRNA approach. The results showed that downregulation of LEF1 inhibited the malignancy and motility associated microstructures, such as polymerization of F-actin, β-tubulin, and Lamin B1 in caco2 cells. LEF1 inhibition suppressed the expression of epithelial/endothelial-mesenchymal transition (EMT) relevant genes. Overall, the current results demonstrated that LEF1 plays a pivotal role in maintaining the malignancy of colonic adenocarcinoma by remodeling motility correlated microstructures and suppressing the expression of EMT-relevant genes. Our study provided evidence of the roles LEF1 played in colonic adenocarcinoma progression, and suggest LEF1 as a potential target for colonic adenocarcinoma therapy.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms221910870</identifier><identifier>PMID: 34639214</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>Actin ; Adenocarcinoma ; Apoptosis ; Cancer ; Cell division ; Cell growth ; Colorectal cancer ; DNA damage ; Gene expression ; Genes ; Malignancy ; Mesenchyme ; Metastasis ; Microstructure ; Molecular modelling ; Morphology ; Motility ; Polymerization ; Proteins ; RNA polymerase ; Signal transduction ; Transcription factors ; Tubulin ; Tumors ; Wnt protein</subject><ispartof>International journal of molecular sciences, 2021-10, Vol.22 (19), p.10870</ispartof><rights>2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 by the authors. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c392t-eec1f5d14dc21550871b95093b908489505633fa77a1678a903c71d11eaf2fe53</citedby><cites>FETCH-LOGICAL-c392t-eec1f5d14dc21550871b95093b908489505633fa77a1678a903c71d11eaf2fe53</cites><orcidid>0000-0002-1147-3562 ; 0000-0001-8563-0607</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/PMC8509209/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8509209/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27915,27916,53782,53784</link.rule.ids></links><search><creatorcontrib>Xiao, Li</creatorcontrib><creatorcontrib>Zhang, Caixia</creatorcontrib><creatorcontrib>Li, Xinyao</creatorcontrib><creatorcontrib>Jia, Chenshuang</creatorcontrib><creatorcontrib>Chen, Lirong</creatorcontrib><creatorcontrib>Yuan, Yue</creatorcontrib><creatorcontrib>Gao, Qian</creatorcontrib><creatorcontrib>Lu, Zheng</creatorcontrib><creatorcontrib>Feng, Yang</creatorcontrib><creatorcontrib>Zhao, Ruixia</creatorcontrib><creatorcontrib>Zhao, Xuewei</creatorcontrib><creatorcontrib>Cheng, Sinan</creatorcontrib><creatorcontrib>Shu, Zhan</creatorcontrib><creatorcontrib>Xu, Jie</creatorcontrib><creatorcontrib>Duan, Wei</creatorcontrib><creatorcontrib>Nie, Guochao</creatorcontrib><creatorcontrib>Hou, Yingchun</creatorcontrib><title>LEF1 Enhances the Progression of Colonic Adenocarcinoma via Remodeling the Cell Motility Associated Structures</title><title>International journal of molecular sciences</title><description>Lymphoid enhancer-binding factor 1 (LEF1) is a key transcription factor mediating the Wnt signaling pathway. LEF1 is a regulator that is closely associated with tumor malignancy and is usually upregulated in cancers, including colonic adenocarcinoma. The underlying molecular mechanisms of LEF1 regulation for colonic adenocarcinoma progression remain unknown. To explore it, the LEF1 expression in caco2 cells was inhibited using an shRNA approach. The results showed that downregulation of LEF1 inhibited the malignancy and motility associated microstructures, such as polymerization of F-actin, β-tubulin, and Lamin B1 in caco2 cells. LEF1 inhibition suppressed the expression of epithelial/endothelial-mesenchymal transition (EMT) relevant genes. Overall, the current results demonstrated that LEF1 plays a pivotal role in maintaining the malignancy of colonic adenocarcinoma by remodeling motility correlated microstructures and suppressing the expression of EMT-relevant genes. Our study provided evidence of the roles LEF1 played in colonic adenocarcinoma progression, and suggest LEF1 as a potential target for colonic adenocarcinoma therapy.</description><subject>Actin</subject><subject>Adenocarcinoma</subject><subject>Apoptosis</subject><subject>Cancer</subject><subject>Cell division</subject><subject>Cell growth</subject><subject>Colorectal cancer</subject><subject>DNA damage</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Malignancy</subject><subject>Mesenchyme</subject><subject>Metastasis</subject><subject>Microstructure</subject><subject>Molecular modelling</subject><subject>Morphology</subject><subject>Motility</subject><subject>Polymerization</subject><subject>Proteins</subject><subject>RNA polymerase</subject><subject>Signal transduction</subject><subject>Transcription factors</subject><subject>Tubulin</subject><subject>Tumors</subject><subject>Wnt protein</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkc1rGzEQxUVpSFI3x94FvfSyiUbaD-lSMMZJCi4NaXsWsnbWltmVUkkbyH9f5YOS9DQD85s37zGEfAJ2LoRiF-4wJc5BAZMde0dOoea8Yqzt3r_qT8iHlA6MccEbdUxORN0KxaE-JX6zvgS69nvjLSaa90hvYthFTMkFT8NAV2EM3lm67NEHa6J1PkyG3jtDb3EKPY7O754WVziO9HvIbnT5gS5TCtaZjD39meNs81xEP5KjwYwJz17qgvy-XP9aXVebH1ffVstNZYuvXCFaGJoe6t5yaJoSDbaqYUpsFZO1LG3TCjGYrjPQdtIoJmwHPQCagQ_YiAX5-qx7N28n7C36HM2o76KbTHzQwTj9duLdXu_CvZblCi-HFuTLi0AMf2ZMWU8u2RLQeAxz0ryRILmEti3o5__QQ5ijL_GeKAZMSVGo6pmyMaQUcfhnBph-_KR-80nxF5IvkHw</recordid><startdate>20211008</startdate><enddate>20211008</enddate><creator>Xiao, Li</creator><creator>Zhang, Caixia</creator><creator>Li, Xinyao</creator><creator>Jia, Chenshuang</creator><creator>Chen, Lirong</creator><creator>Yuan, Yue</creator><creator>Gao, Qian</creator><creator>Lu, Zheng</creator><creator>Feng, Yang</creator><creator>Zhao, Ruixia</creator><creator>Zhao, Xuewei</creator><creator>Cheng, Sinan</creator><creator>Shu, Zhan</creator><creator>Xu, Jie</creator><creator>Duan, Wei</creator><creator>Nie, Guochao</creator><creator>Hou, Yingchun</creator><general>MDPI AG</general><general>MDPI</general><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/0000-0002-1147-3562</orcidid><orcidid>https://orcid.org/0000-0001-8563-0607</orcidid></search><sort><creationdate>20211008</creationdate><title>LEF1 Enhances the Progression of Colonic Adenocarcinoma via Remodeling the Cell Motility Associated Structures</title><author>Xiao, Li ; 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LEF1 is a regulator that is closely associated with tumor malignancy and is usually upregulated in cancers, including colonic adenocarcinoma. The underlying molecular mechanisms of LEF1 regulation for colonic adenocarcinoma progression remain unknown. To explore it, the LEF1 expression in caco2 cells was inhibited using an shRNA approach. The results showed that downregulation of LEF1 inhibited the malignancy and motility associated microstructures, such as polymerization of F-actin, β-tubulin, and Lamin B1 in caco2 cells. LEF1 inhibition suppressed the expression of epithelial/endothelial-mesenchymal transition (EMT) relevant genes. Overall, the current results demonstrated that LEF1 plays a pivotal role in maintaining the malignancy of colonic adenocarcinoma by remodeling motility correlated microstructures and suppressing the expression of EMT-relevant genes. Our study provided evidence of the roles LEF1 played in colonic adenocarcinoma progression, and suggest LEF1 as a potential target for colonic adenocarcinoma therapy.</abstract><cop>Basel</cop><pub>MDPI AG</pub><pmid>34639214</pmid><doi>10.3390/ijms221910870</doi><orcidid>https://orcid.org/0000-0002-1147-3562</orcidid><orcidid>https://orcid.org/0000-0001-8563-0607</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Actin Adenocarcinoma Apoptosis Cancer Cell division Cell growth Colorectal cancer DNA damage Gene expression Genes Malignancy Mesenchyme Metastasis Microstructure Molecular modelling Morphology Motility Polymerization Proteins RNA polymerase Signal transduction Transcription factors Tubulin Tumors Wnt protein |
| title | LEF1 Enhances the Progression of Colonic Adenocarcinoma via Remodeling the Cell Motility Associated Structures |
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