<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>19</volume><submitter>Yu GJ</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>LncRNAs may exert a regulatory effect in tumorigenesis. Although the expression of lncRNA &lt;i>HOTAIR&lt;/i> has been confirmed to be notably elevated in the tissues of CSCC, its biological mechanism in CSCC is still unknown.&lt;h4>Methods&lt;/h4>&lt;i>HOTAIR&lt;/i> expression level in CSCC cell lines was monitored via qRT-PCR. Then CCK-8 assay, Transwell assay and EdU assay were adopted to detect cell migration and proliferation. Meanwhile, through bioinformatics analysis and luciferase reporter gene detection, a new target of &lt;i>HOTAIR&lt;/i> was identified. Additionally, Western blotting and RIP analysis were adopted to discuss the possible mechanism.&lt;h4>Results&lt;/h4>&lt;i>HOTAIR&lt;/i> expression in CSCC cell lines exhibited an obvious elevation. Cell function analysis revealed that &lt;i>HOTAIR&lt;</pubmed_abstract><journal>Cancer cell international</journal><pagination>270</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6805682</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Long non-coding RNA HOTAIR functions as a competitive endogenous RNA to regulate PRAF2 expression by sponging miR-326 in cutaneous squamous cell carcinoma.</pubmed_title><pmcid>PMC6805682</pmcid><pubmed_authors>Zhang DW</pubmed_authors><pubmed_authors>Yu GJ</pubmed_authors><pubmed_authors>Sun Y</pubmed_authors><pubmed_authors>Zhang P</pubmed_authors></additional><is_claimable>false</is_claimable><name>Long non-coding RNA HOTAIR functions as a competitive endogenous RNA to regulate PRAF2 expression by sponging miR-326 in cutaneous squamous cell carcinoma.</name><description>&lt;h4>Background&lt;/h4>LncRNAs may exert a regulatory effect in tumorigenesis. Although the expression of lncRNA &lt;i>HOTAIR&lt;/i> has been confirmed to be notably elevated in the tissues of CSCC, its biological mechanism in CSCC is still unknown.&lt;h4>Methods&lt;/h4>&lt;i>HOTAIR&lt;/i> expression level in CSCC cell lines was monitored via qRT-PCR. Then CCK-8 assay, Transwell assay and EdU assay were adopted to detect cell migration and proliferation. Meanwhile, through bioinformatics analysis and luciferase reporter gene detection, a new target of &lt;i>HOTAIR&lt;/i> was identified. Additionally, Western blotting and RIP analysis were adopted to discuss the possible mechanism.&lt;h4>Results&lt;/h4>&lt;i>HOTAIR&lt;/i> expression in CSCC cell lines exhibited an obvious elevation. Cell function analysis revealed that &lt;i>HOTAIR&lt;</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019</publication><modification>2025-06-01T01:14:48.001Z</modification><creation>2025-06-01T01:14:48.001Z</creation></dates><accession>S-EPMC6805682</accession><cross_references><pubmed>31649487</pubmed><doi>10.1186/s12935-019-0992-x</doi></cross_references></HashMap>