DOI: 10.5061/dryad.djh9w0w82
title: Myeloid PTEN loss affects the therapeutic response by promoting stress granule assembly and impairing phagocytosis by macrophages in breast cancer

description: Breast cancer (BRCA) has become the most common type of cancer in
 women. Improving the therapeutic response remains a challenge.
 Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is a
 classic tumour suppressor with emerging new functions discovered in recent
 years, and myeloid PTEN loss has been reported to impair antitumour
 immunity. In this study, we revealed a novel mechanism by which myeloid
 PTEN potentially affects antitumour immunity in BRCA. We detected
 accelerated stress granule (SG) assembly under oxidative
 stress in PTEN-deficient bone marrow-derived macrophages
 (BMDMs) through the EGR1-promoted upregulation
 of TIAL1 transcription. PI3K/AKT/mTOR (PAM)
 pathway activation also promoted SG formation. ATP
 consumption during SG assembly in BMDMs impaired the phagocytic ability of
 4T1 cells, potentially contributing to the disruption of antitumour
 immunity. In a BRCA neoadjuvant cohort, we observed a poorer response in
 myeloid PTENlow patients with G3BP1 aggregating as SGs in CD68+
 cells, a finding that was consistent with the observation in our study
 that PTEN-deficient macrophages tended to more readily assemble SGs with
 impaired phagocytosis. Our results revealed the unconventional impact of
 SGs on BMDMs and might provide new perspectives on drug resistance and
 therapeutic strategies for the treatment of BRCA patients.
description: Here we submitted the original data of Detailed information,
 including the patient number, MP grade, and MOD of specific targets which 
 is summarized in Supplementary Table 2; the screened transcription factors
 among the DEGs between
 <em>Pten</em><sup>f/f</sup> and
 <em>Pten</em><sup>mko </sup>BMDMs as Supplementary
 Table 3; the jVenn results of 6 potential transcription factors of TIAL1
 as Supplementary Table 4 and the potential binding sites of TIAL1 using
 JASPAR software as Supplementary Table 5.
description: # Myeloid PTEN loss affects the therapeutic response by promoting stress
 granule assembly and impairing phagocytosis by macrophages in breast
 cancer ([https://doi.org/10.5061/dryad.djh9w0w82
 ](https://doi.org/10.5061/dryad.djh9w0w82)) This is the resource data of
 Supplementary table 2,3,4,5.  *(N/A)*: Not Applicable. Empty cells which
 have no data to display or there's no specific value for the cell. ##
 Description of the data and file structure **Supplementary Table 2**. is a
 summarization of detailed information, including the patient number, MP
 grade, and MOD of specific targets. *No*: serial number of specimens *H*:
 high *L*: low n: number of specimens **Supplementary Table 3** was the
 results of  all the transcription factors screened out from the DEGs
 between *Pten*f/f and *Pten*mko BMDMs. *TF:* transcription factors
 *DEGs*：differentially expressed genes **Supplementary Table 4** was the
 results of  the identified 6 potential TFs of TIAL1 among Supplementary
 Table 3 in BMDMs which were predicted using ChEA software and the ChIP-X
 database. *TF:* transcription factors *DEGs*：differentially expressed
 genes *DEGs-TF*：the transcription factors screened out of the
 differentially expressed genes *TIAL1-TF*：the predicted transcription
 factors of TIAL1 DEGs-TF|TIAL1-TF（p）: the potential transcription factors
 of TIAL1 in macrophages **Supplementary Table 5** was the prediction
 results of potential binding sites of TILA1 using JASPAR software.