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Transcriptome analysis of tumor tissues dervied from lung cancer patients

ABSTRACT: The prognosis of non-small cell lung cancer (NSCLC) with leptomeningeal metastases (LM) is dismal. The regulators of LM progression remain elusive, thus impeding effective clinical intervention. Here, we performed transcriptome analysis of the molecular features of tumor tissues dervied from leptomeningeal-metastatic lung cancer patients. In patients with NSCLC, FUS downregulation and CD36 or SYP upregulation were associated with aggressive LM progression. CD36-mediated fatty acid metabolism and NED signature are crucial for LM progression in NSCLC, highlighting CD36 as a potential LM biomarker and a promising therapeutic target for LM treatment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE337540 | GEO | 2026/07/05

REPOSITORIES: GEO

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Transcriptome analysis of leptomeningeal-metastatic cancer cells and FUS-deficient cancer cells

Project description:The prognosis of non-small cell lung cancer (NSCLC) with leptomeningeal metastases (LM) is dismal. The regulators of LM progression remain elusive, thus impeding effective clinical intervention. Here, we performed in vivo genome-wide CRISPR-based screens and discovered that Fused in sarcoma (FUS) ablation promoted LM in both PC9 and A549 cell lines. FUS repressed CD36 expression by directly interacting with and destabilizing PPARA mRNA. CD36 augmented fatty acid uptake and oxidative phosphorylation in NSCLC cells. Matrix metallopeptidase 2 (MMP2) was upregulated through CD36-mediated fatty acid metabolism, which enabled NSCLC cells to disrupt the endothelial barrier. FUS-deficient NSCLC cells increased the expression of neuroendocrine differentiation (NED) related markers, including SRY-box transcription factor 2 (SOX2), microtubule associated protein 2 (MAP2), enolase 2 (NSE) and synaptophysin (SYP), exhibited neurite-like extensions, and expanded robustly in cerebrospinal fluid-supplemented medium through a CD36-dependent manner. Mechanistically, fatty acid uptake increased acetyl-CoA and H3K27ac modifications to promote the expression of NED signature genes and MMP2 in NSCLC cells. Genetic or pharmacological inhibition of CD36, or inhibition of NED signature in NSCLC cells hindered LM and prolonged survival in mice. In patients with NSCLC, FUS downregulation and CD36 or SYP upregulation were associated with aggressive LM progression. Thus, CD36-mediated fatty acid metabolism and NED signature are crucial for LM progression in NSCLC, highlighting CD36 as a potential LM biomarker and a promising therapeutic target for LM treatment.

2026-07-05 | GSE336920 | GEO

PAR-CLIP-sequencing of PC9 lung cancer cells to identify FUS bingind sites

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RNA profiling of CSF resident macrophages and monocyte-macrophages from leptomeningeal metastasis mice

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Single-cell atlas of mouse leptomeningeal immune cells

Project description:Metastasis to the cerebrospinal fluid (CSF)-filled leptomeninges, or leptomeningeal metastasis (LM), represents a fatal complication of cancer. Proteomic and transcriptomic analyses of human CSF reveal a substantial inflammatory infiltrate in LM. We find the solute and immune composition of CSF in the setting of LM changes dramatically, with notable enrichment in IFN-gamma signaling. To investigate the mechanistic relationships between immune cell signaling and cancer cells within the leptomeninges, we developed syngeneic lung, breast, and melanoma LM mouse models. We find that transgenic host mice, lacking IFN-gamma or its receptor, fail to control LM growth. Overexpression of Ifng through a targeted AAV system controls cancer cell growth independent of adaptive immunity. Instead, leptomeningeal IFN-gamma actively recruits and activates peripheral myeloid cells, generating a diverse spectrum of dendritic cell subsets. These migratory, CCR7+ dendritic cells orchestrate the influx, proliferation, and cytotoxic action of natural killer cells to control cancer cell growth in the leptomeninges. This work uncovers leptomeningeal-specific IFN-gamma signaling and suggests a novel immune-therapeutic approach against tumors within this space.

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Phenotypic states of leptomeningeal metastasis

Project description:Leptomeningeal metastasis (LM), or spread of cancer cells into the cerebrospinal fluid, is characterized by a rapid onset of debilitating neurological symptoms and markedly bleak prognosis. The lack of reproducible in vitro and in vivo models has prevented development of novel, LM-specific therapies. Although LM allows for longitudinal sampling of floating cancer cells with a spinal tap, attempts to culture patient-derived leptomeningeal cancer cells have not been successful. We therefore employ leptomeningeal derivatives of human breast and lung cancer cell lines that reproduce both floating and adherent phenotypes of human LM in vivo and in vitro. We introduce a trypsin/EDTA-based fractionation method to reliably separate the two cell subsets and demonstrate that in vitro cultured floating cells have decreased proliferation rate, lower ATP content, and are enriched in distinct metabolic signatures. Long-term fractionation and transcriptomic analysis suggest a high degree plasticity between the two phenotypes in vitro. Floating cells colonize mouse leptomeninges more rapidly and associate with shortened survival. In addition, patients harboring LM diagnosed with CSF disease alone succumbed to the disease earlier than patients with adherent (MRI-positive) disease. Together, these data support mechanistic evidence of a metabolic adaptation that allows cancer cells to thrive in their natural environment but leads to death in vitro.

2020-01-21 | GSE137020 | GEO

Transcriptome analysis of tumor tissues dervied from lung cancer patients

Project description:Transcriptome analysis of tumor tissues dervied from lung cancer patients

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Genome-wide binding profiles of nuclear FGFR1 in Control and Schizophrenia hiPSC-dervied NPC [ChIP-seq]

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Genome-wide transcriptome profiles in Control and Schizophrenia hiPSC-dervied NPC [RNA-seq]

Project description:We Report the genome-wide RNA expression levels in control and schizophrenia hiPSC dervied NPC treated with neuronal media for 2 days. In total about 15,000 gene expression were detected in all samples, of which 1349 were dysregualted.

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Genome-wide microRNA transcriptome profiles in Control and Schizophrenia hiPSC-dervied NPC [miRNA-seq]

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2017-06-01 | GSE92875 | GEO

Gene expression profile at single cell level of cerebrospinal fluid (CSF) cells from lung adenocarcinoma leptomeningeal metastases patients (LUAD LM)

Project description:Lung adenocarcinoma (LUAD)-derived leptomeningeal metastases (LM) represent a predominant subtype among all LM cases. Nevertheless, the cerebrospinal fluid (CSF) profile of LUAD-LM patients remains poorly characterized and reliable CSF diagnostic biomarkers for LUAD-LM have yet to be established. Using single-cell RNA sequencing data of CSF cells from six LUAD-LM patients, we drew a systematic transcriptomic atlas of the CSF cellular landscape. Our analysis revealed that LUAD-LM reprograms CSF into an immunosuppressive state, marked by the emergence of pro-tumoral LGMN-SELENOPhigh macrophages and proliferating CSF circulating tumor cells (CSF-CTC). Cell-cell communication analysis showed that CSF-CTC reinforces immunosuppression by co-inhibitory checkpoint axis NECTIN2_TIGIT axis with the CD8+T/NK cells, and via CD47_SIRPA axis with antigen-presenting cells. Furthermore, we identified the single-cell transcriptomic difference between CSF-CTC and tumor cells of parenchymal brain metastases (PBM). Notably, Trophoblast cell surface antigen 2 (TROP2) levels in CSF were significantly elevated in LUAD-LM patients versus both normal controls (NC) and LUAD patients without LM (Non-LM). It showed strong diagnostic accuracy for distinguishing LUAD LM from Non-LM or NC, and PBM did not influence the CSF TROP2 level. Collectively, our findings advance the understanding of LUAD-LM pathogenesis and highlight the potential of CSF TROP2 as a diagnostic biomarker for LM.

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