<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Huang X</submitter><funding>Sichuan Science and Technology Program</funding><pagination>4153-4165</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8973590</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(2)</volume><pubmed_abstract>LncRNA down syndrome cell adhesion molecule antisense 1 (DSCAM-AS1) plays an important role in tumor progression, but its function in pancreatic cancer is unknown. DSCAM-AS1 level was evaluated by &lt;i>in situ&lt;/i> hybridization (ISH) assay and qRT-PCR. DSCAM-AS1 was knocked down in pancreatic cancer cells, and its impacts on cell proliferation, invasion, and migration were detected. The binding relationship among DSCAM-AS1, miR-136-5p, and pre-B-cell leukemia homeobox 3 (PBX3) was investigated by bioinformatic analysis and luciferase reporter assay. An &lt;i>in vivo&lt;/i> animal model was constructed to determine the role of DSCAM-AS1 in tumor growth. Our results showed that DSCAM-AS1 was elevated in tumor tissues of pancreatic cancer patients and cell lines. DSCAM-AS1 knockdown efficiently inhibited PANC-1 cell proliferation, migration, and invasion and suppressed tumor growth. DSCAM-AS1 could promote PBX3 expression by sponging miR-136-5p, and its function in pancreatic cancer was partially mediated by the miR-136-5p/PBX3 axis. Overall, DSCAM-AS1 knockdown inhibits pancreatic cancer progression by modulating the miR-136-5p/PBX3 axis.</pubmed_abstract><journal>Bioengineered</journal><pubmed_title>Long non-coding RNA DSCAM-AS1 promotes pancreatic cancer progression via regulating the miR-136-5p/PBX3 axis.</pubmed_title><pmcid>PMC8973590</pmcid><funding_grant_id>2021YFS0234</funding_grant_id><pubmed_authors>Yue C</pubmed_authors><pubmed_authors>Li Z</pubmed_authors><pubmed_authors>Lu H</pubmed_authors><pubmed_authors>Hu W</pubmed_authors><pubmed_authors>Huang X</pubmed_authors><pubmed_authors>Hou S</pubmed_authors><pubmed_authors>Wang Z</pubmed_authors></additional><is_claimable>false</is_claimable><name>Long non-coding RNA DSCAM-AS1 promotes pancreatic cancer progression via regulating the miR-136-5p/PBX3 axis.</name><description>LncRNA down syndrome cell adhesion molecule antisense 1 (DSCAM-AS1) plays an important role in tumor progression, but its function in pancreatic cancer is unknown. DSCAM-AS1 level was evaluated by &lt;i>in situ&lt;/i> hybridization (ISH) assay and qRT-PCR. DSCAM-AS1 was knocked down in pancreatic cancer cells, and its impacts on cell proliferation, invasion, and migration were detected. The binding relationship among DSCAM-AS1, miR-136-5p, and pre-B-cell leukemia homeobox 3 (PBX3) was investigated by bioinformatic analysis and luciferase reporter assay. An &lt;i>in vivo&lt;/i> animal model was constructed to determine the role of DSCAM-AS1 in tumor growth. Our results showed that DSCAM-AS1 was elevated in tumor tissues of pancreatic cancer patients and cell lines. DSCAM-AS1 knockdown efficiently inhibited PANC-1 cell proliferation, migration, and invasion and suppressed tumor growth. DSCAM-AS1 could promote PBX3 expression by sponging miR-136-5p, and its function in pancreatic cancer was partially mediated by the miR-136-5p/PBX3 axis. Overall, DSCAM-AS1 knockdown inhibits pancreatic cancer progression by modulating the miR-136-5p/PBX3 axis.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Feb</publication><modification>2025-04-04T19:10:03.936Z</modification><creation>2025-04-04T19:10:03.936Z</creation></dates><accession>S-EPMC8973590</accession><cross_references><pubmed>35142595</pubmed><doi>10.1080/21655979.2021.2016326</doi></cross_references></HashMap>