<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE186238" accession="SRP342313">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP342313</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA773061</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE186238</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>PRMT7 knockdown in Jurkat-Cas9  and Molt-4 T-ALL cell line</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Transcriptome Analysis"/>
      <STUDY_ABSTRACT>T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy with only few established prognostic biomarkers.In this study, we examined the expression of protein arginine methyltransferases across hematological malignancies and discovered high levels of PRMT7 mRNA in T-ALL, particularly in the mature subtypes of T-ALL. High PRMT7 was associated with decreased event-free and overall survival in two independent patient cohorts. Genetic deletion of PRMT7 by CRISPR-Cas9 significantly decreased the colony-forming capacity of the cells and negatively impacted cell viability. In the knockout cells, alterations were seen in the monomethyl arginine levels in proteins associated with RNA processing. These results suggest that PRMT7 plays an active role in T-ALL pathogenesis. Overall design: mRNA expression profiler were generated from four different Jurkat Cas9 PRMT7 knockdown and two Molt-4 derived PRMT7 knockout cell lines, three replicates per cell line (knockdown made using CRISRP-Cas9 technology)</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE186238</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
    <STUDY_LINKS>
      <STUDY_LINK>
        <XREF_LINK>
          <DB>pubmed</DB>
          <ID>35565298</ID>
        </XREF_LINK>
      </STUDY_LINK>
    </STUDY_LINKS>
  </STUDY>
</STUDY_SET>
