<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Sun Z</submitter><funding>Beijing Municipal Commission of Science and Technology</funding><pagination>7635-7647</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8974003</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(3)</volume><pubmed_abstract>The role of programmed cell death ligand 1 (PD-L1) in suppressing antitumor immune responses has been widely reported, and recent studies showed that PD-L1 also plays an important role in epithelial-mesenchymal transition (EMT), determination of tumor cell phenotypes, metastasis, and drug resistance. Long non-coding RNAs (lncRNAs) are involved in a variety of epigenetic regulatory processes. The tumorigenesis and development of most cancers cannot be studied separately from their regulation by lncRNAs. To explore the epigenetic regulation of PD-L1, we identified an lncRNA, LINC00244, which reduced PD-L1 expression and predicted good clinical outcomes in hepatocellular carcinoma (HCC). LINC00244 inhibited the proliferation, invasion, and metastasis of HCC by downregulating PD-L1 expression. In addition, low LINC00244 expression activated epithelial-mesenchymal transition (EMT) pathways and facilitated the rapid growth and metastasis of HCC cells. Thus, LINC00244 is a potential therapeutic target for HCC.</pubmed_abstract><journal>Bioengineered</journal><pubmed_title>LINC00244 suppresses cell growth and metastasis in hepatocellular carcinoma by downregulating programmed cell death ligand 1.</pubmed_title><pmcid>PMC8974003</pmcid><funding_grant_id>Z171100000417011</funding_grant_id><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Xue C</pubmed_authors><pubmed_authors>Du Y</pubmed_authors><pubmed_authors>Sun Z</pubmed_authors><pubmed_authors>Zhao H</pubmed_authors><pubmed_authors>Du N</pubmed_authors></additional><is_claimable>false</is_claimable><name>LINC00244 suppresses cell growth and metastasis in hepatocellular carcinoma by downregulating programmed cell death ligand 1.</name><description>The role of programmed cell death ligand 1 (PD-L1) in suppressing antitumor immune responses has been widely reported, and recent studies showed that PD-L1 also plays an important role in epithelial-mesenchymal transition (EMT), determination of tumor cell phenotypes, metastasis, and drug resistance. Long non-coding RNAs (lncRNAs) are involved in a variety of epigenetic regulatory processes. The tumorigenesis and development of most cancers cannot be studied separately from their regulation by lncRNAs. To explore the epigenetic regulation of PD-L1, we identified an lncRNA, LINC00244, which reduced PD-L1 expression and predicted good clinical outcomes in hepatocellular carcinoma (HCC). LINC00244 inhibited the proliferation, invasion, and metastasis of HCC by downregulating PD-L1 expression. In addition, low LINC00244 expression activated epithelial-mesenchymal transition (EMT) pathways and facilitated the rapid growth and metastasis of HCC cells. Thus, LINC00244 is a potential therapeutic target for HCC.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Mar</publication><modification>2025-04-19T21:49:31.294Z</modification><creation>2025-04-19T21:49:31.294Z</creation></dates><accession>S-EPMC8974003</accession><cross_references><pubmed>35266439</pubmed><doi>10.1080/21655979.2022.2050073</doi></cross_references></HashMap>