<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>6(19)</volume><submitter>Tan Y</submitter><pubmed_abstract>Cancer treatment alters microRNA (miRNA) expression, revealing potential therapeutic targets (oncotarget). Here we treated pancreatic cancer (ASPC-1) cells with either recombinant human endostatin (rh-endostatin) or gemcitabine. Then high-throughput sequencing assay was performed to screen for altered miRNAs. Both treatments decreased levels of MiR-19a. We found that miR-19a stimulated cell proliferation, migration, invasion in vitro and tumor growth in vivo. High levels of miR-19a correlated with poor prognosis in patients. Ras homolog family member B (RHOB) was identified as a direct target of miR-19a. Furthermore, RHOB was down-regulated in human pancreatic cancer samples. Restoration of RHOB induced apoptosis, inhibited proliferation and migration of ASPC-1 cells. SP-1 was identified as an upstream transcription factor of miR-19a gene, promoting miR-19a transcription. Rh-endostatin decreased miR-19a expression by down-regulating SP-1. These findings suggest that miR-19a is a potential therapeutic target in pancreatic cancer.</pubmed_abstract><journal>Oncotarget</journal><pagination>17391-403</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4627316</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Sp1-driven up-regulation of miR-19a decreases RHOB and promotes pancreatic cancer.</pubmed_title><pmcid>PMC4627316</pmcid><pubmed_authors>Zou H</pubmed_authors><pubmed_authors>Fang J</pubmed_authors><pubmed_authors>Li D</pubmed_authors><pubmed_authors>Liang Y</pubmed_authors><pubmed_authors>Zhang H</pubmed_authors><pubmed_authors>Sun C</pubmed_authors><pubmed_authors>Fu W</pubmed_authors><pubmed_authors>Zheng W</pubmed_authors><pubmed_authors>Yang X</pubmed_authors><pubmed_authors>Yin H</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Cao W</pubmed_authors><pubmed_authors>Tan Y</pubmed_authors><pubmed_authors>Zeng J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Sp1-driven up-regulation of miR-19a decreases RHOB and promotes pancreatic cancer.</name><description>Cancer treatment alters microRNA (miRNA) expression, revealing potential therapeutic targets (oncotarget). Here we treated pancreatic cancer (ASPC-1) cells with either recombinant human endostatin (rh-endostatin) or gemcitabine. Then high-throughput sequencing assay was performed to screen for altered miRNAs. Both treatments decreased levels of MiR-19a. We found that miR-19a stimulated cell proliferation, migration, invasion in vitro and tumor growth in vivo. High levels of miR-19a correlated with poor prognosis in patients. Ras homolog family member B (RHOB) was identified as a direct target of miR-19a. Furthermore, RHOB was down-regulated in human pancreatic cancer samples. Restoration of RHOB induced apoptosis, inhibited proliferation and migration of ASPC-1 cells. SP-1 was identified as an upstream transcription factor of miR-19a gene, promoting miR-19a transcription. Rh-endostatin decreased miR-19a expression by down-regulating SP-1. These findings suggest that miR-19a is a potential therapeutic target in pancreatic cancer.</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015 Jul</publication><modification>2024-11-15T13:35:15.805Z</modification><creation>2019-03-27T02:01:05Z</creation></dates><accession>S-EPMC4627316</accession><cross_references><pubmed>26041879</pubmed><doi>10.18632/oncotarget.3975</doi></cross_references></HashMap>