<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>21(6)</volume><submitter>Cai B</submitter><funding>funding</funding><pubmed_abstract>Nasopharyngeal carcinoma (NPC) has a low five-year survival rate, and its pathogenesis remains unclear. There is an urgent need to improve our understanding of the genetic regulation of NPC tumorigenesis and development. The role of miR-26a-5p in NPC growth regulation and the expression of its target, PTGS2, was analyzed. Quantitative Real-time PCR assay was used to detect miR-26a-5p and PTGS2 expression in human NPC tissues and cell lines. The RNA pull-down dual-luciferase reporter assay was used to determine the association between miR-26a-5p and PTGS2. The effects of miR-26a-5p and PTGS2 on NPC cell viability, proliferation, migration, and invasion were measured by CCK-8, BrdU, and Transwell assays. miR-26a-5p expression in NPC tissues and cell lines was significantly decreased. The overexpression of miR-26a-5p inhibited the viability, proliferation, migration, and invasion of NPC cells. miR-26a-5p bound to the 3-'untranslated region of PTGS2, thus reducing PTGS2 protein levels. miR-26a-5p inhibited NPC development by reducing the expression of its target PTGS2.</pubmed_abstract><journal>Cell cycle (Georgetown, Tex.)</journal><pagination>618-629</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8942422</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>miR-26a-5p suppresses nasopharyngeal carcinoma progression by inhibiting PTGS2 expression.</pubmed_title><pmcid>PMC8942422</pmcid><pubmed_authors>Cai B</pubmed_authors><pubmed_authors>Kan D</pubmed_authors><pubmed_authors>Qu X</pubmed_authors><pubmed_authors>Luo Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>miR-26a-5p suppresses nasopharyngeal carcinoma progression by inhibiting PTGS2 expression.</name><description>Nasopharyngeal carcinoma (NPC) has a low five-year survival rate, and its pathogenesis remains unclear. There is an urgent need to improve our understanding of the genetic regulation of NPC tumorigenesis and development. The role of miR-26a-5p in NPC growth regulation and the expression of its target, PTGS2, was analyzed. Quantitative Real-time PCR assay was used to detect miR-26a-5p and PTGS2 expression in human NPC tissues and cell lines. The RNA pull-down dual-luciferase reporter assay was used to determine the association between miR-26a-5p and PTGS2. The effects of miR-26a-5p and PTGS2 on NPC cell viability, proliferation, migration, and invasion were measured by CCK-8, BrdU, and Transwell assays. miR-26a-5p expression in NPC tissues and cell lines was significantly decreased. The overexpression of miR-26a-5p inhibited the viability, proliferation, migration, and invasion of NPC cells. miR-26a-5p bound to the 3-'untranslated region of PTGS2, thus reducing PTGS2 protein levels. miR-26a-5p inhibited NPC development by reducing the expression of its target PTGS2.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Mar-Mar</publication><modification>2026-06-19T03:17:32.584Z</modification><creation>2025-04-21T16:58:26.881Z</creation></dates><accession>S-EPMC8942422</accession><cross_references><pubmed>35073820</pubmed><doi>10.1080/15384101.2022.2030168</doi></cross_references></HashMap>