ArticleOncotarget2015
Knockdown of CD44 inhibits the invasion and metastasis of hepatocellular carcinoma both in vitro and in vivo by reversing epithelial-mesenchymal transition.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- Quantitative assessment of CD44 genetic variants and cancer susceptibility in Asians: a meta-analysis.Oncotarget · 2016Pooled it
- CD44 knockdown and TGF‑β inhibition modulate cell proliferation and invasion in claudin‑low breast cancer cells.Oncology reports · 2026Article
- CD44 and phosphorylated ERK1/2 coexpression predicts distant metastasis in colorectal cancer based on a study of 1137 Saudi patients.Scientific reports · 2025Article
- The Role of the Fox Gene in Breast Cancer Progression.International journal of molecular sciences · 2025Review
- Transforming Growth Factor-β Modulates Cancer Stem Cell Traits on CD44 Subpopulations in Hepatocellular Carcinoma.Journal of cellular biochemistry · 2025Article
- Cancer stem cells in hepatocellular carcinoma: therapy resistance and emerging treatments.Frontiers in immunology · 2025Review
- Review
- Emodin is a Potential Drug Targeting CD44-positive Hepatocellular Cancer.Current cancer drug targets · 2024Article
- Identification of a gene set that maintains tumorigenicity of the hepatocellular carcinoma cell line Li-7.Human cell · 2023Article
- Photothermal Attenuation of Cancer Cell Stemness, Chemoresistance, and Migration Using CD44-Targeted MoSNano letters · 2023Article
- Cellular and Molecular Biology of Cancer Stem Cells of Hepatocellular Carcinoma.International journal of molecular sciences · 2023Review
- Proteolysis of CD44 at the cell surface controls a downstream protease network.Frontiers in molecular biosciences · 2023Article
- CD44 Promotes Breast Cancer Metastasis through AKT-Mediated Downregulation of Nuclear FOXA2.Biomedicines · 2022Article
- Hemimycale Arabica Induced Non-Cytotoxic Anti-Migratory Activity in Hepatocellular Carcinoma In Vitro.Asian Pacific journal of cancer prevention : APJCP · 2022Article
- Mechanism of cancer stemness maintenance in human liver cancer.Cell death & disease · 2022Review
- Hyaluronated and PEGylated Liposomes as a Potential Drug-Delivery Strategy to Specifically Target Liver Cancer and Inflammatory Cells.Molecules (Basel, Switzerland) · 2022Article
- Article
- Cancer and stem cells.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- Immunotherapy against programmed death-1/programmed death ligand 1 in hepatocellular carcinoma: Importance of molecular variations, cellular heterogeneity, and cancer stem cells.World journal of stem cells · 2021Review
- Interplay of autophagy and cancer stem cells in hepatocellular carcinoma.Molecular biology reports · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mounting evidence has shown that induction of epithelial-mesenchymal transition (EMT) contributes to the the expression of CSC (cancer stem cell) markers. However, whether and how CSC markers could be involved in regulating EMT has rarely been reported. CD44, being one of the most commonly used CSC markers in hepatocellular carcinoma (HCC), has been demonstrated to act as a multidomain, transmembrane platform that serves to integrate a wide variety of extracellular signals. Therefore, we determined to seek whether CD44 is necessary for the EMT process in HCC. First, we noticed that CD44 expression was associated with the mesenchymal phenotype in HCC cell lines, and knocking down CD44 with lentivirus-mediated shRNA in HCC cell lines resulted in the mesenchymal-epithelial-transition (MET) and the subsequent impaired migration and invasion in vitro. Moreover, in a metastatic mice model established by tail vein injection of luciferase labelled MHCC97-H cells, we confirmed that CD44 knockdown resulted in the decreased metastasis of HCC cells. Furthermore, we found that the induction of MET by CD44 inhibition might be achieved, at least in part, by repressing the ERK/Snail pathway.
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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.