<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="BioProject" alias="PRJNA508505" accession="SRP172550">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP172550</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA508505</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>Alternative Poly-A site usage in Glioblastoma cell line</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Other"/>
      <STUDY_ABSTRACT>Alternative polyadenylation (APA) has emerged as a prevalent feature associated with cancer development and progression. The advantage of APA to tumor progression is to induce oncogenes through 3'UTR shortening, and to inactivate tumor suppressor genes via the re-routing of microRNA competition. We previously identified the Cleavage and Polyadenylation Factor Nudt21 as a master APA regulator whose expression levels directly impact the tumorigenecity of glioblastoma (GBM) in vitro and in vivo. This data set is Poly-A site usage upon knockdown of Nudt21 in the human derived GBM LN229 cell line.</STUDY_ABSTRACT>
    </DESCRIPTOR>
  </STUDY>
</STUDY_SET>
