ArticleJournal of molecular cell biology2024
Single-cell analysis defines LGALS1+ fibroblasts that promote proliferation and migration of intrahepatic cholangiocarcinoma.
Article in Journal of molecular cell biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- Cuproptosis: potential new direction in liver-related diseases research and treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- An integrated single-cell lung cancer atlas reveals distinct fibroblast phenotypes between adenocarcinoma and squamous cell carcinomas.NPJ precision oncology · 2026Article
- Cancer‑associated fibroblasts: a pivotal regulator of tumor microenvironment in the context of radiotherapy.Cell communication and signaling : CCS · 2025Review
- Integrated analysis of single cell and spatial transcriptomics revealed a metastasis mechanism mediated by fatty acid metabolism in lymph nodes of head and neck cancer.Frontiers in immunology · 2025Article
- Review
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Authors and funding
10 authors.
Funding
Abstract
The incidence rate of intrahepatic cholangiocarcinoma (ICC), which has a poor prognosis, is rapidly increasing. To investigate the intratumor heterogeneity in ICC, we analyzed single-cell RNA sequencing data from the primary tumor and adjacent normal tissues of 14 treatment-naïve patients. We identified 10 major cell types, along with 45 subclusters of cells. Notably, we identified a fibroblast cluster, Fibroblast_LUM+, which was preferably enriched in tumor tissues and actively interacted with cholangiocytes. LGALS1 was verified as a marker gene of Fibroblast_LUM+, contributing to the malignant phenotype of ICC. Higher amount of LGALS1+ fibroblasts was associated with poorer overall survival of ICC patients. Mechanistically, LGALS1+ fibroblasts activated the proliferation and migration of tumor cells by upregulating the expression levels of CCR2, ADAM15, and β-integrin. Silencing LGALS1 in cancer-associated fibroblasts (CAFs) suppressed CAF-augmented tumor cell migration and invasion in vitro as well as tumor formation in vivo, suggesting that blockade of LGALS1 serves as a potential therapeutic approach for ICC. Taken together, our single-cell analysis provides insight into the interaction between malignant cells and specific subtypes of fibroblasts, which contributes to better understanding of the intratumor heterogeneity in ICC and the development of novel strategies for the treatment of ICC by targeting fibroblasts in the tumor microenvironment.
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