ArticleTranslational oncology2019
Targeting PIM Kinases Affects Maintenance of CD133 Tumor Cell Population in Hepatoblastoma.
Article in Translational oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 52 citations in OpenAlex.
- Macrophage PIM1 Drives Atherosclerosis by Enhancing Foam Cell Formation Via CD36.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Pediatric Hepatoblastoma: From Developmental Molecular Mechanisms to Innovative Therapeutic Strategies.Cancers · 2026Review
- Targeted silencing of SOCS1 by DNMT1 promotes stemness of human liver cancer stem-like cells.Cancer cell international · 2024Article
- Inhibition of PIM Kinases Promotes Neuroblastoma Cell Differentiation to a Neuronal Phenotype.Journal of pediatric surgery · 2023Article
- The Role of PIM Kinases in Pediatric Solid Tumors.Cancers · 2022Review
- Metastatic human hepatoblastoma cells exhibit enhanced tumorigenicity, invasiveness and a stem cell-like phenotype.Journal of pediatric surgery · 2022Article
- CRISPR/Cas9-mediated knockout of PIM3 suppresses tumorigenesis and cancer cell stemness in human hepatoblastoma cells.Cancer gene therapy · 2022Article
- Therapeutically viable generation of neurons with antisense oligonucleotide suppression of PTB.Nature neuroscience · 2021Article
- PIM447 inhibits oncogenesis and potentiates cisplatin effects in hepatoblastoma.Journal of pediatric surgery · 2021Article
- PIM kinases mediate resistance to cisplatin chemotherapy in hepatoblastoma.Scientific reports · 2021Article
- Protein kinase PIM2: A simple PIM family kinase with complex functions in cancer metabolism and therapeutics.Journal of Cancer · 2021Review
- Targeting protein palmitoylation decreases palmitate‑induced sphere formation of human liver cancer cells.Molecular medicine reports · 2020Article
- Association of CMYC polymorphisms with hepatoblastoma risk.Translational cancer research · 2020Article
- Wnt/β-catenin signaling as a useful therapeutic target in hepatoblastoma.Bioscience reports · 2019Review
- The Emerging Roles of Cancer Stem Cells and Wnt/Beta-Catenin Signaling in Hepatoblastoma.Cancers · 2019Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Hepatoblastoma is the most common primary liver tumor in children, but treatment has not changed significantly in the past 20 years. We have previously demonstrated that Proviral Integration site for Moloney murine leukemia (PIM) kinases promote tumorigenesis in hepatoblastoma. Stem cell-like cancer cells (SCLCCs) are a subset of cells thought to be responsible for chemoresistance, metastasis, relapse, and recurrence. The aim of this study was to identify SCLCCs in hepatoblastoma and determine the role of PIM kinases in SCLCCs. Hepatoblastoma cells were separated into CD133-enriched and CD133-depleted populations and the frequency of SCLCCs was assessed. CD133 expression was determined in the presence or absence of the PIM inhibitor, AZD1208. The effects of AZD1208 on proliferation, apoptosis, and motility were assessed in vitro and the effect of AZD1208 on tumor growth was examined in vivo. We identified CD133 as a marker for SCLCCs in hepatoblastoma and showed that PIM kinases promote a SCLCC phenotype. PIM kinase inhibition with AZD1208 decreased proliferation, migration, and invasion and increased apoptosis in both SCLCCs and non-SCLCCs in a long-term passaged hepatoblastoma cell line and patient-derived xenograft. Additionally, tumor growth in mice implanted with hepatoblastoma SCLCCs was decreased with PIM inhibition such that 57% of the tumors regressed. These findings identify CD133 as a marker for SCLCCs in hepatoblastoma and provide evidence that inhibition of PIM kinases decreases stemness and tumorigenicity of SCLCCs in hepatoblastoma, making them potential therapeutic targets for the treatment of hepatoblastoma.
Identifiers
What OpenQuestion holds
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.