ArticleAging cell2023
Spatial resolution of cellular senescence dynamics in human colorectal liver metastasis.
Article in Aging cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 34 citations in OpenAlex.
- Characterization of SPP1 + macrophages and their correlation with resistance to neoadjuvant chemotherapy in colorectal cancer liver metastasis.Molecular biomedicine · 2026Article
- ViMST: vision transformer-based dual modality multi-task graph contrastive network for spatial transcriptomics microenvironments investigation.BMC biology · 2026Article
- APOC1⁺IFI30⁺ TAMs orchestrate colorectal cancer liver metastasis by coupling cholesterol biosynthesis with secretion of immunosuppressive factors.Cellular and molecular life sciences : CMLS · 2026Article
- scTACL: a multitask topology-aware contrastive learning approach for single-cell transcriptomics analysis.Bioinformatics (Oxford, England) · 2026Article
- SpaNiche: spatial niche analysis to explore colocalization patterns and cellular interactions in spatial transcriptomics data.Genome biology · 2026Article
- Senescence-driven molecular subtyping in pancreatic cancer: a multi-omics framework for precision medicine.BMC cancer · 2025Article
- SLGCA: spatial cross-level graph contrastive autoencoder for multislice spatial domain identification and microenvironment exploration.Briefings in bioinformatics · 2025Article
- SURF: A Self-Supervised Deep Learning Method for Reference-Free Deconvolution in Spatial Transcriptomics.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- SMTdb: A Comprehensive Spatial Meta-Transcriptome Resource in Cancer.Molecular biology and evolution · 2025Article
- Article
- A visual-omics foundation model to bridge histopathology with spatial transcriptomics.Nature methods · 2025Article
- stClinic dissects clinically relevant niches by integrating spatial multi-slice multi-omics data in dynamic graphs.Nature communications · 2025Article
- Article
- Prognostic impact of a senescence gene signature in multiple myeloma.GeroScience · 2025Article
- Immune therapeutic strategies for the senescent tumor microenvironment.British journal of cancer · 2025Review
- Glycolysis-Driven Immune Evasion in Microsatellite Instability-High Colorectal Cancer: An Integrated Single-Cell and Spatial Transcriptomics Study.OncoTargets and therapy · 2025Article
- Unveiling the Power of Mitochondrial Fission and Fusion: A Five- Gene Signature for Personalized Prognosis in Gastric Cancer.Current medicinal chemistry · 2025Article
- Cellular senescence in colorectal cancer: its occurrence, effect and therapy.Frontiers in oncology · 2025Review
- Editorial for Special Issue "Cellular Senescence: Recent Cellular Advances and Discoveries".Biomedicines · 2024Article
- STimage-1K4M: A histopathology image-gene expression dataset for spatial transcriptomics.Advances in neural information processing systems · 2024Article
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatic metastasis is a clinical challenge for colorectal cancer (CRC). Senescent cancer cells accumulate in CRC favoring tumor dissemination. Whether this mechanism progresses also in metastasis is unexplored. Here, we integrated spatial transcriptomics, 3D-microscopy, and multicellular transcriptomics to study the role of cellular senescence in human colorectal liver metastasis (CRLM). We discovered two distinct senescent metastatic cancer cell (SMCC) subtypes, transcriptionally located at the opposite pole of epithelial (e) to mesenchymal (m) transition. SMCCs differ in chemotherapy susceptibility, biological program, and prognostic roles. Mechanistically, epithelial (e)SMCC initiation relies on nucleolar stress, whereby c-myc dependent oncogene hyperactivation induces ribosomal RPL11 accumulation and DNA damage response. In a 2D pre-clinical model, we demonstrated that RPL11 co-localized with HDM2, a p53-specific ubiquitin ligase, leading to senescence activation in (e)SMCCs. On the contrary, mesenchymal (m)SMCCs undergo TGFβ paracrine activation of NOX4-p15 effectors. SMCCs display opposing effects also in the immune regulation of neighboring cells, establishing an immunosuppressive environment or leading to an active immune workflow. Both SMCC signatures are predictive biomarkers whose unbalanced ratio determined the clinical outcome in CRLM and CRC patients. Altogether, we provide a comprehensive new understanding of the role of SMCCs in CRLM and highlight their potential as new therapeutic targets to limit CRLM progression.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.