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Study on the Molecular Mechanism of Salidroside@T-exo Inducing Breast Cancer Immune Microenvironment Remodeling and Reversing Acquired Resistance to Immunotherapy by Regulating the PI3K/AKT/mTOR Signaling Pathway

ABSTRACT: To elucidate how Salidroside-loaded, oligopeptide-modified tumor exosomes (Salidroside@T-exo) rewire the PI3K/AKT/mTOR axis to remodel the immune microenvironment (IME) and reverse acquired PD-1 resistance in breast cancer

ORGANISM(S): Mus Musculus

SUBMITTER: Jun Qian

PROVIDER: PXD070218 | iProX | Mon Nov 03 00:00:00 GMT 2025

REPOSITORIES: iProX

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The Application of Salidroside@T-exo Regulated by the PI3K/AKT/mTOR Pathway in the Remodeling of the Immune Microenvironment in Breast Cancer

Project description:Breast cancer (Breast Cancer, BC) patients often face the issue of acquired resistance during PD-1 immunotherapy, which significantly limits the efficacy and durability of treatment. Research indicates that the tumor immune microenvironment is closely linked to the development of resistance. To address this challenge, this study aims to regulate the PI3K/AKT/mTOR signaling pathway by using Salidroside-loaded oligopeptide-modified tumor stem cell-derived exosomes (Salidroside@T-exo), thereby reshaping the immune microenvironment of breast cancer and reversing PD-1 immunotherapy resistance. We modified the oligopeptide TMTP1 onto the surface of tumor stem cell exosomes and introduced Salidroside via electroporation to prepare Salidroside@T-exo. The experiment involved in vitro construction of a MA782/5s-8101 PD-1-resistant cell model, combined with high-throughput sequencing, proteomics, and metabolomics analyses, to investigate the effects of Salidroside@T-exo on tumor cell proliferation, metabolism, and the immune microenvironment. The results demonstrated that Salidroside@T-exo significantly inhibited the activity of the PI3K/AKT/mTOR signaling pathway, enhanced T cell proliferation and tumor cell-killing capacity, reshaped the immune microenvironment, and successfully reversed PD-1 resistance. Our study provides an innovative therapeutic strategy for breast cancer, which may help improve the efficacy of immunotherapy.

2025-11-04 | PXD070267 |

Comparative study of a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor in MCL

Project description:Phosphatidylinositol-3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway activation contributes to mantle cell lymphoma (MCL) pathogenesis and drug resistance. However, the use of mTOR inhibitors as single agents have shown limited clinical efficacy in relation with drug activation of feedback loops. Selective PI3K inhibition or dual PI3K/mTOR catalytic inhibition are different therapeutic approaches developed to achieve effective pathway blockage. Here, we evaluated the antitumor activity of a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor in primary MCL cells. We found that dual PI3K/mTOR inhibitor modulated angiogenesis, tumor invasiveness and cytokine signaling compared to a mTOR inhibitor and a pan-PI3K inhibitor in MCL. We used microarrays to compare the effect of these three compounds in MCL and identified distinct classes of down-regulated genes modulated by each compound. Global RNA expression in primary cells from two MCL patients treated with a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor for 8 hours

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Comparative study of a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor in MCL

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SUM52PE treated with PI3K-mTOR inhibitors

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Metastasis and Survival of Breast Cancer Stem Cells Mediated by Cytoskeleton Remodeling and PI3K/mTOR Signaling transcription factors

Project description:Cancer metastasis is a fetal problem that claims life of over 90% of cancer patients. It is hypothesized that cancer stem cells (CSCs) mediate cancer metastasis and such cells are often resistant to chemotherapy. Studying BRCA1 associated cancers, we found that CSCs form fillopodia and protrusions enriching for active forms of ezrin/radixin/moesin proteins and they have a much higher potential to metastasize than non-CSCs. Microarray analysis indicated that many pathways related to cell adhesion, extracellular matrix and cytoskeleton were differentially regulated in CSCs. Although inhibition of cytoskeleton remodeling by cisplatin treatment retarded CSC motility and cancer metastasis, drug resistant cancers eventually emerge containing markedly increased number of CSCs. This event is at least partially attributed to the activation of PI3K/mTOR signaling, and can be significantly inhibited by the treatment of rapamycin. These results provide strong evidence that cytoskeletal rearrangement and PI3K/mTOR signaling play a distinct role in mediating CSC mobility and viability, and blocking of both pathways in CSCs synergistically inhibits primary and metastatic cancer growth in BRCA1 associated tumors. The sorted subpopulations based upon CD24, CD29 expression were used in the microarray analysis that was performed with 3 independent biologic sample sets.

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SUM52PE treated with PI3K-mTOR inhibitors

Project description:PI3K/mTOR inhibition alters gene transcription signatures involved in metabolism and cell cycle control in the human breast cancer cell line, SUM52PE

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Trial of MEK Inhibitor and PI3K/mTOR Inhibitor in Subjects With Locally Advanced or Metastatic Solid Tumors

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TLR-mediated type I IFN induction in pDCs requires the rapamycin-sensitive PI3K-mTOR-p70S6K pathway

Project description:Robust type I interferon (IFN-alpha/beta) production in plasmacytoid dendritic cells (pDCs) is critical for anti-viral immunity. Here we demonstrated a role for the mammalian target of rapamycin (mTOR) pathway in regulating interferon production by pDCs. Inhibition of mTOR or the ‘downstream’ mediators of mTOR p70S6K1,2 kinases during pDC activation via Toll-like receptor 9 (TLR9) blocked the interaction of TLR9 with the adaptor MyD88 and the subsequent activation of interferon response factor 7 (IRF7), resulting in impaired IFN-alpha production. Microarray analysis confirmed that inhibition of mTOR by the immunosuppressive drug rapamycin suppressed anti-viral and anti-inflammatory gene expression. Consistent with this, targeting rapamycin-encapsulated microparticles to antigen-presenting cells in vivo resulted in a diminution of IFN-alpha production in response to CpG DNA or the yellow fever vaccine virus strain 17D. Thus, mTOR signaling plays a critical role in TLR-mediated IFN-alpha responses by pDCs. CpGA is a TLR9 agonist. pDCs were isolated from mouse spleen or human PBMC. The effect of rapamycin on pDCs IFN-alpha production as induced by TLR ligands was studied. The mechanism of rapamycin effect was dissected in RAW cell line.

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