<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yi B</submitter><funding>Breast Cancer Research Foundation</funding><funding>U.S. Department of Health &amp;amp; Human Services | NIH | National Cancer Institute</funding><funding>NCI NIH HHS</funding><funding>Alabama</funding><pagination>268-279</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8781987</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>41(2)</volume><pubmed_abstract>MicroRNA-3662 (miR-3662) is minimally expressed in normal human tissues but is highly expressed in all types of cancers, including breast cancer. As determined with The Cancer Genome Atlas dataset, miR-3662 expression is higher in triple-negative breast cancers (TNBCs) and African American breast cancers than in other breast cancer types. However, the functional role of miR-3662 remains a topic of debate. Here, we found that inhibition or knockout of endogenous, mature miR-3662 in TNBC cells suppresses proliferation and migration in vitro and tumor growth and metastasis in vivo. Functional analysis revealed that, for TNBC cells, knockout of miR-3662 reduces the activation of Wnt/β-catenin signaling. Furthermore, using CRISPR-mediated miR-3662 activation and repression, dual-luciferase assa</pubmed_abstract><journal>Oncogene</journal><pubmed_title>CRISPR interference and activation of the microRNA-3662-HBP1 axis control progression of triple-negative breast cancer.</pubmed_title><pmcid>PMC8781987</pmcid><funding_grant_id>R56 CA223077</funding_grant_id><funding_grant_id>CA223077</funding_grant_id><funding_grant_id>R01 CA242917</funding_grant_id><funding_grant_id>R01 CA238273</funding_grant_id><funding_grant_id>CA242917</funding_grant_id><funding_grant_id>P30 CA013148</funding_grant_id><funding_grant_id>CA238273</funding_grant_id><pubmed_authors>Liu Z</pubmed_authors><pubmed_authors>Stringer-Reasor E</pubmed_authors><pubmed_authors>Wang S</pubmed_authors><pubmed_authors>Bae S</pubmed_authors><pubmed_authors>Wei S</pubmed_authors><pubmed_authors>Yi B</pubmed_authors><pubmed_authors>Liu R</pubmed_authors><pubmed_authors>Wang X</pubmed_authors><pubmed_authors>Zhang C</pubmed_authors><pubmed_authors>Li M</pubmed_authors><pubmed_authors>Gao S</pubmed_authors><pubmed_authors>Wang L</pubmed_authors></additional><is_claimable>false</is_claimable><name>CRISPR interference and activation of the microRNA-3662-HBP1 axis control progression of triple-negative breast cancer.</name><description>MicroRNA-3662 (miR-3662) is minimally expressed in normal human tissues but is highly expressed in all types of cancers, including breast cancer. As determined with The Cancer Genome Atlas dataset, miR-3662 expression is higher in triple-negative breast cancers (TNBCs) and African American breast cancers than in other breast cancer types. However, the functional role of miR-3662 remains a topic of debate. Here, we found that inhibition or knockout of endogenous, mature miR-3662 in TNBC cells suppresses proliferation and migration in vitro and tumor growth and metastasis in vivo. Functional analysis revealed that, for TNBC cells, knockout of miR-3662 reduces the activation of Wnt/β-catenin signaling. Furthermore, using CRISPR-mediated miR-3662 activation and repression, dual-luciferase assa</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jan</publication><modification>2026-05-10T02:11:15.142Z</modification><creation>2024-11-09T18:56:31.185Z</creation></dates><accession>S-EPMC8781987</accession><cross_references><pubmed>34728806</pubmed><doi>10.1038/s41388-021-02089-6</doi></cross_references></HashMap>