<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>38(1)</volume><submitter>Li Y</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Multiple myeloma remains a virtually incurable hematologic malignancy, which is featured with the aberrant growth of malignant plasma cells.&lt;h4>Aims&lt;/h4>To elucidate the functions of miR-19a-3p in multiple myeloma.&lt;h4>Study design&lt;/h4>Cell study.&lt;h4>Methods&lt;/h4>Cell counting kit-8 assay was performed to detect cell viability, and flow cytometry was conducted to detect cell apoptosis. Bioinformatics analysis predicted miR-19a-3p-associated biological function, pathway, core regulatory network, and target genes. Luciferase reporter assay verified the target sequence of miR-19a-3p regulating FBXO32.&lt;h4>Results&lt;/h4>miR-19a-3p is upregulated in multiple myeloma cells (p&lt;0.01) and patients with multiple myeloma (p&lt;0.001). Overexpressed miR-19a-3p significantly increased cell viability (p&lt;0.05) and inhibited cell apoptosis (p&lt;0.01). FBXO32 is a target gene of miR-19a-3p (p&lt;0.01). Moreover, FBXO32 is downregulated in MM, and it significantly decreased cell viability (p&lt;0.05) and promoted cell apoptosis (p&lt;0.01). FBXO32 significantly rescued the influence of miR-19a-3p-inhibiting cell apoptosis (p&lt;0.05).&lt;h4>Conclusion&lt;/h4>miR-19a-3p promoted cell proliferation and inhibited cell apoptosis by degrading the target FBXO32 mRNA in multiple myeloma.</pubmed_abstract><journal>Balkan medical journal</journal><pagination>43-49</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8909224</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>miR-19a-3p Functions as an Oncogene by Regulating FBXO32 Expression in Multiple Myeloma.</pubmed_title><pmcid>PMC8909224</pmcid><pubmed_authors>Xue W</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Zhang D</pubmed_authors><pubmed_authors>Ma Y</pubmed_authors><pubmed_authors>Meng Y</pubmed_authors><pubmed_authors>Gao S</pubmed_authors></additional><is_claimable>false</is_claimable><name>miR-19a-3p Functions as an Oncogene by Regulating FBXO32 Expression in Multiple Myeloma.</name><description>&lt;h4>Background&lt;/h4>Multiple myeloma remains a virtually incurable hematologic malignancy, which is featured with the aberrant growth of malignant plasma cells.&lt;h4>Aims&lt;/h4>To elucidate the functions of miR-19a-3p in multiple myeloma.&lt;h4>Study design&lt;/h4>Cell study.&lt;h4>Methods&lt;/h4>Cell counting kit-8 assay was performed to detect cell viability, and flow cytometry was conducted to detect cell apoptosis. Bioinformatics analysis predicted miR-19a-3p-associated biological function, pathway, core regulatory network, and target genes. Luciferase reporter assay verified the target sequence of miR-19a-3p regulating FBXO32.&lt;h4>Results&lt;/h4>miR-19a-3p is upregulated in multiple myeloma cells (p&lt;0.01) and patients with multiple myeloma (p&lt;0.001). Overexpressed miR-19a-3p significantly increased cell viability (p&lt;0.05) and inhibited cell apoptosis (p&lt;0.01). FBXO32 is a target gene of miR-19a-3p (p&lt;0.01). Moreover, FBXO32 is downregulated in MM, and it significantly decreased cell viability (p&lt;0.05) and promoted cell apoptosis (p&lt;0.01). FBXO32 significantly rescued the influence of miR-19a-3p-inhibiting cell apoptosis (p&lt;0.05).&lt;h4>Conclusion&lt;/h4>miR-19a-3p promoted cell proliferation and inhibited cell apoptosis by degrading the target FBXO32 mRNA in multiple myeloma.</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Jan</publication><modification>2025-04-18T12:16:58.68Z</modification><creation>2025-04-06T21:51:00.461Z</creation></dates><accession>S-EPMC8909224</accession><cross_references><pubmed>32975519</pubmed><doi>10.4274/balkanmedj.galenos.2020.2020.3.121</doi></cross_references></HashMap>