<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Li T</submitter><funding>Guangzhou Science &amp;amp; Technology Plan Project</funding><funding>National Basic Research Program of China</funding><funding>Guangdong Provincial Natural Science Foundation of China</funding><funding>Presidents fund of Nanfang Hospital</funding><funding>National Natural Science Foundation of China</funding><funding>Guangdong Provincial medical scientific research Foundation of China</funding><funding>Key Program of National Natural Science Foundation of Guangdong, China</funding><funding>Guangzhou Science &amp; Technology Plan Project</funding><pagination>238</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6156870</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>37(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Aberrant activation of Wnt/β-catenin signaling pathway is considered to be an important issue in progression and metastasis of various human cancers, especially in colorectal cancer (CRC). MiR-452 could activate of Wnt/β-catenin signaling. But the mechanism remains unclear.&lt;h4>Methods&lt;/h4>The expression of miR-452 in CRC and normal tissues was detected by real-time quantitative PCR. The effect of miR-452 on CRC growth and invasion was conducted by functional experiments in vitro and in vivo. Bioinformatics and cell luciferase function studies verified the direct regulation of miR-452 on the 3'-UTR of the GSK3β, which leads to the activation of Wnt/β-catenin signaling.&lt;h4>Results&lt;/h4>MiR-452 was upregulated in CRC compared with normal tissues and was correlated with clini</pubmed_abstract><journal>Journal of experimental &amp; clinical cancer research : CR</journal><pubmed_title>MiR-452 promotes an aggressive colorectal cancer phenotype by regulating a Wnt/β-catenin positive feedback loop.</pubmed_title><pmcid>PMC6156870</pmcid><funding_grant_id>2010B031500012</funding_grant_id><funding_grant_id>2015C009</funding_grant_id><funding_grant_id>No. 2017A030313707, 2016A030310394, 2017A030313463, 2017A030313643, 2017A030313583, 2017A030310081, 2017A030310117, 2017C1034229, 2016A030310394, 2016A030310392, 2016A030310395, 2015A030306048, 2014A030310134</funding_grant_id><funding_grant_id>National Natural Science Foundation of China</funding_grant_id><funding_grant_id>201300000056</funding_grant_id><funding_grant_id>973 program, 2015CB554002</funding_grant_id><funding_grant_id>A2016218</funding_grant_id><pubmed_authors>He H</pubmed_authors><pubmed_authors>Yang M</pubmed_authors><pubmed_authors>Zhou W</pubmed_authors><pubmed_authors>Liu T</pubmed_authors><pubmed_authors>Ye Y</pubmed_authors><pubmed_authors>Jiao H</pubmed_authors><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Deng D</pubmed_authors><pubmed_authors>Ding Y</pubmed_authors><pubmed_authors>Zhu J</pubmed_authors><pubmed_authors>Li T</pubmed_authors><pubmed_authors>Wang S</pubmed_authors><pubmed_authors>Zheng L</pubmed_authors><pubmed_authors>Lai Q</pubmed_authors><pubmed_authors>Jian X</pubmed_authors></additional><is_claimable>false</is_claimable><name>MiR-452 promotes an aggressive colorectal cancer phenotype by regulating a Wnt/β-catenin positive feedback loop.</name><description>&lt;h4>Background&lt;/h4>Aberrant activation of Wnt/β-catenin signaling pathway is considered to be an important issue in progression and metastasis of various human cancers, especially in colorectal cancer (CRC). MiR-452 could activate of Wnt/β-catenin signaling. But the mechanism remains unclear.&lt;h4>Methods&lt;/h4>The expression of miR-452 in CRC and normal tissues was detected by real-time quantitative PCR. The effect of miR-452 on CRC growth and invasion was conducted by functional experiments in vitro and in vivo. Bioinformatics and cell luciferase function studies verified the direct regulation of miR-452 on the 3'-UTR of the GSK3β, which leads to the activation of Wnt/β-catenin signaling.&lt;h4>Results&lt;/h4>MiR-452 was upregulated in CRC compared with normal tissues and was correlated with clini</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Sep</publication><modification>2025-04-04T11:20:51.854Z</modification><creation>2019-03-26T23:57:33Z</creation></dates><accession>S-EPMC6156870</accession><cross_references><pubmed>30253791</pubmed><doi>10.1186/s13046-018-0879-z</doi></cross_references></HashMap>