ReviewHepatology (Baltimore, Md.)2011
Hepatic stellate cells: partners in crime for liver metastases?
Review in Hepatology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
112 citing papers in PubMed, 206 citations in OpenAlex.
- TUFT1 stabilizes TGF-β receptor II protein and facilitates activation of hepatic stellate cells into metastasis-promoting myofibroblasts.Cell death and differentiation · 2026Article
- Association between preoperative aspartate aminotransferase-to-platelet ratio index and prognosis in colorectal liver metastases: a systematic review and meta-analysis.Journal of gastrointestinal oncology · 2026Article
- A magnetic resonance imaging-guided drug delivery system for premetastatic niche theranostics and colorectal cancer liver metastasis intervention.Journal of nanobiotechnology · 2026Article
- Comprehensive analysis of non-tumor lung, liver, and kidney transcriptomes in canine metastatic osteosarcoma.Communications biology · 2026Article
- Deubiquitinase OTUD5 facilitates stiffness-induced hepatic stellate cell activation by stabilizing YAP.Molecular and cellular biochemistry · 2026Article
- Review
- A pH-sensitive peptide amphiphilic-based drug delivery system inhibits hepatocellular carcinoma growth by suppressing hepatic stellate cell activation.Materials today. Bio · 2025Article
- Cancer metastasis: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2025Review
- Colorectal cancer cells-derived exosomal miR-188-3p promotes liver metastasis by creating a pre-metastatic niche via activation of hepatic stellate cells.Journal of translational medicine · 2025Article
- The lncRNA MIR181A1HG in extracellular vesicles derived from highly metastatic colorectal cancer cells promotes liver metastasis by remodeling the extracellular matrix and recruiting myeloid-derived suppressor cells.Cell & bioscience · 2025Article
- Periostin-mediated NOTCH1 activation between tumor cells and HSCs crosstalk promotes liver metastasis of small cell lung cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- ATF3-mediated transactivation of CXCL14 in HSCs during liver fibrosis.Clinical and translational medicine · 2024Article
- CMTM6 mediates the Warburg effect and promotes the liver metastasis of colorectal cancer.Experimental & molecular medicine · 2024Article
- New Insights into the Exosome-Induced Migration of Uveal Melanoma Cells and the Pre-Metastatic Niche Formation in the Liver.Cancers · 2024Article
- Unveil Intrahepatic Cholangiocarcinoma Heterogeneity through the Lens of Omics and Multi-Omics Approaches.Cancers · 2024Review
- Linking fatty liver diseases to hepatocellular carcinoma by hepatic stellate cells.Journal of the National Cancer Center · 2024Review
- The diverse influences of relaxin-like peptide family on tumor progression: Potential opportunities and emerging challenges.Heliyon · 2024Review
- Emerging role of lipophagy in liver disorders.Molecular and cellular biochemistry · 2024Review
- Vessel co-option: a unique vascular-immune niche in liver cancer.Frontiers in oncology · 2024Review
- Netrin-1 feedforward mechanism promotes pancreatic cancer liver metastasis via hepatic stellate cell activation, retinoid, and ELF3 signaling.Cell reports · 2023Article
52 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
unlabelledHepatic stellate cells (HSCs) were recently postulated as a component of the prometastatic liver microenvironment, because they can transdifferentiate into highly proliferative and motile myofibroblasts that are implicated in the desmoplastic reaction and metastatic growth. This review focuses on bidirectional interactions between tumor cells and HSCs in the liver microenvironment and discusses mechanisms whereby tumor-derived factors activate HSCs, and in turn, activated HSCs promote metastatic growth. Bidirectional interactions between tumors and HSCs may function as an "amplification loop" to further enhance metastatic growth in the liver. The activation of HSCs is a complex process regulated by multiple factors such as transforming growth factor-β and platelet-derived growth factor signaling pathways, which may present as therapeutic targets in the prevention and treatment of liver metastases.
conclusionHSCs may present a new therapeutic target in the treatment of liver metastases. Targeting HSCs and/or myofibroblasts with transforming growth factor-β or platelet-derived growth factor antagonists in coordination with chemotherapy, radiotherapy, or surgery may prove to be effective at reducing liver metastases and increasing the survival benefit of patients by targeting both tumor cells and the tumor microenvironment.
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Registered trials
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.