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LIF induced tumor plasticity establishes an immunosuppressive myeloid niche in LKB1 mutant lung cancer [sgLif_CITEseq]

ABSTRACT: Single Cell RNA-seq analysis (5' CITE-seq) of immune Cells from Murine Lkb1 mutant KP Lung Tumors with deletion of Lif or Lifr (Figure 3 and Figure 4)

ORGANISM(S): Mus musculus

PROVIDER: GSE322633 | GEO | 2026/03/07

REPOSITORIES: GEO

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LIF induced tumor plasticity establishes an immunosuppressive myeloid niche in LKB1 mutant lung cancer [antiLif_CITEseq]

Project description:Single Cell RNA-seq analysis (5' CITE-seq) of immune Cells from Murine Lkb1 mutant KP Lung Tumors with deletion of Lif or Lifr (Figure 3)

2026-03-07 | GSE322634 | GEO

LIF induced tumor plasticity establishes an immunosuppressive myeloid niche in LKB1 mutant lung cancer [10x_scRNAseq]

Project description:Single Cell RNA-seq analysis (3' 10x) of immune Cells from Murine Lkb1 wildtype or mutant KP Lung Tumors (Figure 1A, 1B, 1C)

2026-03-07 | GSE322632 | GEO

LIF induced tumor plasticity establishes an immunosuppressive myeloid niche in LKB1 mutant lung cancer [RNA-seq]

Project description:Bulk RNA-seq of sorted Lkb1 wildtype (sgNeo) and Lkb1 mutant (sgLkb1) tumor cells

2026-03-07 | GSE322570 | GEO

LIF induced tumor plasticity establishes an immunosuppressive myeloid niche in LKB1 mutant lung cancer [antiLif_CITEseq]

Project description:LIF induced tumor plasticity establishes an immunosuppressive myeloid niche in LKB1 mutant lung cancer [antiLif_CITEseq]

| PRJNA1430761 | ENA

LIF induced tumor plasticity establishes an immunosuppressive myeloid niche in LKB1 mutant lung cancer [10x_scRNAseq]

Project description:LIF induced tumor plasticity establishes an immunosuppressive myeloid niche in LKB1 mutant lung cancer [10x_scRNAseq]

| PRJNA1430762 | ENA

LIF induced tumor plasticity establishes an immunosuppressive myeloid niche in LKB1 mutant lung cancer [sgLif_CITEseq]

Project description:LIF induced tumor plasticity establishes an immunosuppressive myeloid niche in LKB1 mutant lung cancer [sgLif_CITEseq]

| PRJNA1430764 | ENA

LIF induced tumor plasticity establishes an immunosuppressive myeloid niche in LKB1 mutant lung cancer [RNA-seq]

Project description:LIF induced tumor plasticity establishes an immunosuppressive myeloid niche in LKB1 mutant lung cancer [RNA-seq]

| PRJNA1430561 | ENA

Oncostatin M (OSM) and Leukemia Inhibitory factor (LIF) treatment of osteoblasts via LIF and OSM receptors

Project description:Oncostatin M (OSM) and Leukemia Inhibitory Factor (LIF) signal within cells via the gp130 (Il6st) coreceptor bound either to the LIF receptor (LIFR) or the oncostatin M receptor (OSMR), but whether murine OSM can act through both receptors is controversial. Both LIF and OSM stimulate bone formation, inhibit adipocyte differentiation, and promote osteoclast differentiation, but our earlier work suggested this may depend on the receptor subtype used. This project aimed to identify those gene targets regulated by murine OSM via OSMR and LIFR by using wild type and OSMR null primary osteoblasts. Cells were differentiated to their most mature state (i.e. osteocytes) because the only prior target gene known to be regulated by murine OSM via the LIFR was an osteocyte-specific gene, sclerostin.

2016-08-17 | GSE83418 | GEO

Epithelial LIF signaling limits apoptosis and lung injury during bacterial pneumonia

Project description:During bacterial pneumonia, alveolar epithelial cells are critical for maintaining gas exchange and providing antimicrobial as well as pro-immune properties. We previously demonstrated that leukemia inhibitory factor (LIF), an IL-6 family cytokine, is produced by type II alveolar epithelial cells (ATII) and is critical for tissue protection during bacterial pneumonia. However, the target cells and mechanisms of LIF-mediated protection remain unknown. Here, we demonstrate that antibody-induced LIF blockade remodels the lung epithelial transcriptome in association with increased apoptosis. Based on these data, we performed pneumonia studies using a novel mouse model in which LIFR (the unique receptor for LIF) is absent in lung epithelium. While LIFR was detected on the surface of epithelial cells, its absence only minimally contributed to tissue protection during pneumonia. Single-cell RNA-sequencing (scRNAseq) was conducted to identify adult murine lung cell types most prominently expressing LIFR, revealing endothelial cells, mesenchymal cells, and ATIIs as major sources of LIFR. Sequencing data indicated that ATII cells were significantly impacted as a result of pneumonia, with additional differences observed in response to LIF neutralization, including but not limited to gene programs related to cell death, injury, and inflammation. Overall, our data suggest that LIF signaling on epithelial cells alters responses in this cell type during pneumonia. However, our results also suggest separate and perhaps more prominent roles of LIFR in other cell types, such as endothelial cells or mesenchymal cells, which provide grounds for future investigation.

2022-02-17 | GSE179764 | GEO

Super-enhancer driven LIF/LIFR-STAT3-SOX2 regulatory feedback loop promotes cancer stemness in head and neck squamous cell carcinoma (ChIP-seq)

Project description:Super-enhancers (SEs) have been recognized as key epigenetic regulators underlying cancer stemness and malignant traits by aberrant transcriptional control and promising therapeutic targets against human cancers. However, the SE landscape and their roles during head and neck squamous cell carcinoma (HNSCC) development especially in cancer stem cells (CSCs) maintenance remain underexplored yet. Here, we identified leukemia inhibitory factor (LIF)-SE as a representative oncogenic SE to activate LIF transcription in HNSCC. LIF secreted from cancer cells and cancer-associated fibroblasts promotes cancer stemness by driving SOX2 transcription in an autocrine or paracrine manner, respectively. Mechanistically, enhancer elements E1, 2, 4 within LIF-SE recruited SOX2/SMAD3/BRD4/EP300 to facilitate LIF transcription; LIF activated downstream LIFR-STAT3 signaling to drive SOX2 transcription, thus forming a previously unknown regulatory feedback loop (LIF-SE-LIF/LIFR-STAT3-SOX2) to maintain LIF overexpression and CSCs stemness. Clinically, increased LIF abundance in clinical samples correlated with malignant clinicopathological features and patient prognosis; higher LIF concentrations in presurgical plasma were negatively associated with patient survival and dramatically diminished following cancer eradication. Therapeutically, pharmacological targeting LIF-SE-LIF/LIFR-STAT3 significantly impaired tumor growth and reduced CSC subpopulations in HNSCC xenograft and PDX models. Our findings reveal a hitherto uncharacterized LIF-SE-mediated auto-regulatory loop in regulating HNSCC stemness and highlight LIF as a novel non-invasive biomarker and potential therapeutic target for HNSCC.

2024-11-06 | GSE274995 | GEO

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