ArticleJournal of gastrointestinal oncology2023
Phosphatase regenerating liver 3 participates in Integrinβ1/FAK-Src/MAPK signaling pathway and contributes to the regulation of malignant behaviors in hepatocellular carcinoma cells.
Article in Journal of gastrointestinal oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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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
4 citing papers in PubMed, 5 citations in OpenAlex.
- Polydopamine-Coated Surfaces Promote Adhesion, Migration, Proliferation, Chemoresistance, Stemness, and Epithelial-Mesenchymal Transition of Human Prostate Cancer Cell Lines In Vitro via Integrin αInternational journal of molecular sciences · 2026Article
- PRL-3: unveiling a new horizon in cancer therapy.Acta pharmacologica Sinica · 2025Review
- Protein Tyrosine Phosphatase PRL-3: A Key Player in Cancer Signaling.Biomolecules · 2024Review
- A Potential miR-1246-5p-H3K27ac-NOL12 Regulatory Axis and Its Putative Tumour-Promoting Function in Hepatocellular Carcinoma.IET systems biologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Hepatocellular carcinoma (HCC) is the leading cause of mortality worldwide. Phosphatase regenerating liver 3 (PRL-3) was associated with cancer metastasis. However, the significance of PRL-3 in the prognosis of HCC remains elusive. The aim of this study was to elucidate the role of PRL-3 in HCC metastasis and its prognosis. Methods: The expressions of PRL-3 in cancer tissues isolated from 114 HCC patients, who underwent curative hepatectomy from May to November in 2008, were analyzed by immunohistochemistry, and its prognostic significance was evaluated. Thereafter, the migration, invasion, and metastatic alterations in MHCC97H cells with PRL-3 overexpression or knockdown were explored and compared with the tumor size and lung metastasis in orthotopic HCC model of nude mice derived from MHCC97H cells with PRL-3 overexpression or knockdown. The underlying mechanism involving PRL-3-mediated effect on HCC migration, invasion, and metastasis was further examined. Results: Univariate and multivariate analysis demonstrated PRL-3 overexpression was an independent prognostic factor for poor overall survival (OS) and progression-free survival (PFS) of the HCC patients. Increased PRL-3 expression in MHCC97H cells was in accordance with the enhanced metastasis potential. PRL-3 knockdown inhibited the migration, invasiveness, and clone forming ability in MHCC97H cells, whereas PRL-3 overexpression reverted the above behavior. The growth of xenograft tumor in the liver was suppressed, and the lung metastasis in nude mice was inhibited by PRL-3 downregulation. The knockdown of PRL-3 could downregulate the expressions of Integrinβ1 and p-Src (Tyr416), p-Erk (Thr202/Tyr204) activation, and reduce MMP9 expression. Both MEK1/2 inhibitor (U0126) and Src inhibitor could repress PRL-3-induced invasiveness and migration in MHCC97H cells. Conclusions: PRL-3 was significantly overexpressed and an independent prognostic factor to predict the death of HCC patients. Mechanically, PRL-3 plays a critical role in HCC invasive and metastasis via Integrinβ1/FAK-Src/RasMAPK signaling. Validation of PRL-3 as a clinical prediction marker in HCC warrants further research.
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