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Use of integrated spatial transcriptomics and histopathological analysis in adamantinomatous craniopharyngiomas to identify stromal cells as a new cellular source of leukemia inhibitory factor

  • 01Department of Neurosurgery, Sanbo Brain Hospital of Capital Medical University, Beijing, China.
Journal of Neurosurgery +

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August 1, 2025

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August 1, 2025

View abstract on PubMed

Summary

This summary is machine-generated.

Leukemia inhibitory factor (LIF) is overexpressed in adamantinomatous craniopharyngioma (ACP) and originates from tumor stroma. Targeting LIF and stromal cells may offer new therapeutic strategies for ACP.

Area Of Science

  • Neuro-oncology
  • Molecular Biology
  • Cancer Stem Cell Research

Background

  • Adamantinomatous craniopharyngioma (ACP) is a common sellar region tumor with frequent recurrence and poor prognosis after resection.
  • Leukemia inhibitory factor (LIF) is a key regulator of stem cell self-renewal, but its role in ACP remains unclear.

Purpose Of The Study

  • To investigate the spatial distribution, cell of origin, and biological functions of LIF in ACP.
  • To explore the therapeutic potential of targeting LIF and its associated pathways in ACP.

Main Methods

  • Single-cell sequencing and spatial transcriptome analysis to identify LIF and LIF receptor (LIFR) transcriptional sites.
  • Immunohistochemistry and immunofluorescence to determine LIF and LIFR distribution.
  • Analysis of gene expression, stemness markers (CD44, β-catenin), PI3K-AKT pathway activation, and correlation with imaging and prognosis.

Main Results

  • LIF is overexpressed in ACP and originates from tumor stromal cells (interstitial region, palisade epithelium, stellate reticulum), while LIFR is mainly produced by tumor cell clusters.
  • LIF binding to LIFR may activate the PI3K-AKT signaling pathway, and LIF expression is enriched in stem cell marker-positive clusters (CD44, β-catenin).
  • Higher LIF expression is observed in cystic ACP tumors compared to solid tumors, correlating with a trend toward poorer prognosis.

Conclusions

  • LIF in ACP predominantly originates from the tumor microenvironment's stromal cells.
  • Tumor stromal cells represent a novel cellular and molecular target for developing new ACP therapies.

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