<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE172156" accession="SRP314971">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP314971</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA722247</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE172156</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>S1PR1 Overexpression cells activates endogenous complement signaling and inflammasome to induce tumor metastasis in mice</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Transcriptome Analysis"/>
      <STUDY_ABSTRACT>Cancer metastasis remains one of the major causes of cancer deaths. The molecular mechanisms of pro-survival lipid signaling activation in inducing cancer cell migration and metastasis are largely unknown. Here, our RNA seq data showed that S1PR1 overexpression B16 melanoma cells injected in C57BL/6 mice via tail vein, activates endogenous complement signaling and inflammasome to induce tumor lung metastasis. Overall design: C57BL/6 mice (Wildtype) and C3 knockout mice, were injected with S1PR1 overexpression B16 melanoma cell lines, via tail vein. Empty vector was injected in wildtype mice as control. After 21-30 days, mice were euthanized and lung extracted and stored in RNA stabilizer solution (ThermoFisher Scientific, cat# AM7022), until ready to use. Total RNA from mice lungs were isolated and sent for RNA sequencing.</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE172156</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
    <STUDY_LINKS>
      <STUDY_LINK>
        <XREF_LINK>
          <DB>pubmed</DB>
          <ID>36476873</ID>
        </XREF_LINK>
      </STUDY_LINK>
    </STUDY_LINKS>
  </STUDY>
</STUDY_SET>
