<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE186555" accession="SRP343136">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP343136</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA774507</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE186555</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>Anti-cnacer effects of ginsenoside Rh2 with doxorubicin from breast tumor bearing mice</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Transcriptome Analysis"/>
      <STUDY_ABSTRACT>The FDA approved drug Doxorubicin provokes copious irreversible cardiotoxicity and even increases the risk of heart failure. Considering the multiple and interacted molecular pathways in cancer, there is a big possibility that tumors are simultaneously sensitive to different drugs. This makes achievable to study the combinations of drug, having the virtues of less toxicity, higher efficacy and potentially antagonizing drug resistance in cancer therapy. In the present study, we addressed the synergistic effects of ginsenoside Rh2 on doxorubicin-treated breast cancer bearing mice. We showed that Rh2 significantly enhanced the anti-cancer effects of doxorubicin and greatly attenuated the cardiotoxicity. Transcriptomic changes can clearly distinguish the chemotherapeutic groups and non-treated control groups. Transcriptomic analysis domestrated that Rh2 protection involved in multiple vital pathways including cellular stress, apoptosis and inflammation. Overall design: Examination of pontential anti-cancer effects of ginsenoside Rh2 by analyzing transcriptomes changes between doxorubicin treated samples with or without ginsenoside Rh2 and vehicle samples.</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE186555</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
  </STUDY>
</STUDY_SET>
