<HashMap><database>biostudies-literature</database><scores><citationCount>0</citationCount><reanalysisCount>0</reanalysisCount><viewCount>53</viewCount><searchCount>0</searchCount></scores><additional><omics_type>Unknown</omics_type><volume>12(7)</volume><submitter>Li HZ</submitter><pubmed_abstract>The current study was aimed at exploring the potential roles and possible mechanisms of miR-10a-5p in osteoarthritis (OA). We performed RT-qPCR, Western blot, CCK8, EdU Assay, and flow cytometry assay to clarify the roles of miR-10a-5p in OA. Furthermore, the whole transcriptome sequencing together with integrated bioinformatics analyses were conducted to elucidate the underlying mechanisms of miR-10a-5p involving in OA. Our results demonstrated that miR-10a-5p was upregulated in OA and acted as a significant contributing factor for OA. A large number of circRNAs, lncRNAs, miRNAs, and mRNAs were identified by overexpressing miR-10a-5p. Functional enrichment analyses indicated that these differentially-expressed genes were enriched in some important terms including PPAR signaling pathway, PI3K-Akt signaling pathway, and p53 signaling pathway. A total of 42 hub genes were identified in the protein-protein interaction network including SERPINA1, TTR, APOA1, and A2M. Also, we constructed the network regulatory interactions across coding and noncoding RNAs triggered by miR-10a-5p, which revealed the powerful regulating effects of miR-10a-5p. Moreover, we found that HOXA3 acted as the targeted genes of miR-10a-5p and miR-10a-5p contributed to the progression of OA by suppressing HOXA3 expression. Our findings shed insight on regulatory mechanisms of miR-10a-5p, which might provide novel therapeutic targets for OA.</pubmed_abstract><journal>Aging</journal><pagination>5948-5976</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7185093</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Overexpression of miR-10a-5p facilitates the progression of osteoarthritis.</pubmed_title><pmcid>PMC7185093</pmcid><pubmed_authors>Wang DW</pubmed_authors><pubmed_authors>Lu HD</pubmed_authors><pubmed_authors>Lin YM</pubmed_authors><pubmed_authors>Su ZZ</pubmed_authors><pubmed_authors>Li HZ</pubmed_authors><pubmed_authors>Xu XH</pubmed_authors><pubmed_authors>Lin N</pubmed_authors><view_count>53</view_count></additional><is_claimable>false</is_claimable><name>Overexpression of miR-10a-5p facilitates the progression of osteoarthritis.</name><description>The current study was aimed at exploring the potential roles and possible mechanisms of miR-10a-5p in osteoarthritis (OA). We performed RT-qPCR, Western blot, CCK8, EdU Assay, and flow cytometry assay to clarify the roles of miR-10a-5p in OA. Furthermore, the whole transcriptome sequencing together with integrated bioinformatics analyses were conducted to elucidate the underlying mechanisms of miR-10a-5p involving in OA. Our results demonstrated that miR-10a-5p was upregulated in OA and acted as a significant contributing factor for OA. A large number of circRNAs, lncRNAs, miRNAs, and mRNAs were identified by overexpressing miR-10a-5p. Functional enrichment analyses indicated that these differentially-expressed genes were enriched in some important terms including PPAR signaling pathway, PI3K-Akt signaling pathway, and p53 signaling pathway. A total of 42 hub genes were identified in the protein-protein interaction network including SERPINA1, TTR, APOA1, and A2M. Also, we constructed the network regulatory interactions across coding and noncoding RNAs triggered by miR-10a-5p, which revealed the powerful regulating effects of miR-10a-5p. Moreover, we found that HOXA3 acted as the targeted genes of miR-10a-5p and miR-10a-5p contributed to the progression of OA by suppressing HOXA3 expression. Our findings shed insight on regulatory mechanisms of miR-10a-5p, which might provide novel therapeutic targets for OA.</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Apr</publication><modification>2021-02-19T09:07:12Z</modification><creation>2020-05-22T18:56:36Z</creation></dates><accession>S-EPMC7185093</accession><cross_references><pubmed>32283545</pubmed><doi>10.18632/aging.102989</doi></cross_references></HashMap>