<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE124407" accession="SRP174544">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP174544</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA511965</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE124407</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>BACH1 alters the expression of EMT-related genes to promote metastasis in pancreatic cancer [RNA-seq]</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Transcriptome Analysis"/>
      <STUDY_ABSTRACT>BTB and CNC homology 1 (BACH1) has been implicated in RAS-driven tumor formation. We focused on the role of BACH1 in Pancreatic ductal adenocarcinoma (PDAC), more than 90% of which have KRAS mutation. BACH1  directly or indirectly repressed the expression of genes for epithelial cell adhesion in AsPC-1 cells and SW1990. Knockdown and overexpression of BACH1 in PDAC cell lines indicated that BACH1 promoted cell migration and invasion in part by reducing E-cadherin expression. Overall design: Search of BACH1 target genes in pancreatic cancer cells</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE124407</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
    <STUDY_LINKS>
      <STUDY_LINK>
        <XREF_LINK>
          <DB>pubmed</DB>
          <ID>31919242</ID>
        </XREF_LINK>
      </STUDY_LINK>
      <STUDY_LINK>
        <XREF_LINK>
          <DB>pubmed</DB>
          <ID>37094356</ID>
        </XREF_LINK>
      </STUDY_LINK>
    </STUDY_LINKS>
    <STUDY_ATTRIBUTES>
      <STUDY_ATTRIBUTE>
        <TAG>parent_bioproject</TAG>
        <VALUE>PRJNA511961</VALUE>
      </STUDY_ATTRIBUTE>
    </STUDY_ATTRIBUTES>
  </STUDY>
</STUDY_SET>
