ArticleDiagnostic pathology2024
PKM2 promotes lymphatic metastasis of hypopharyngeal carcinoma via regulating epithelial-mesenchymal transition: an experimental research.
Article in Diagnostic pathology, 2024. 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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Who cites it
4 citing papers in PubMed, 3 citations in OpenAlex.
- PKM2-Mediated Glycolytic Reprogramming in Thyroid Cancer: Mechanistic Insights and Therapeutic Potential.Molecules (Basel, Switzerland) · 2026Review
- Lymph Node Metastasis in Head and Neck Squamous Cell Carcinoma: Evolving Prognostic Markers, Molecular Insights, and Implications for Precision Staging.Diagnostics (Basel, Switzerland) · 2026Review
- Metastatic Hypopharyngeal Carcinoma Involving the Stomach: A Case Report and Literature Review.Cureus · 2026Article
- ITGB6 promotes tumor recurrence and metastasis by mediating the resistance of daughter cells of PGCCs to anoikis : ITGB6 promotes tumor recurrence and metastasis via Anoikis resistance.Scientific reports · 2025Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundPatients with hypopharyngeal carcinoma (HPC) have a poor prognosis mainly because of lymphatic metastasis. This research aimed to determine the PKM2 role in lymphatic metastasis in HPC and the underlying molecular mechanism contributing to this phenomenon.
methodsPKM2 in HPC was studied for its expression and its likelihood of overall survival using TCGA dataset. Western blotting, qRT-PCR, and IHC were employed to confirm PKM2 expression. Methods including gain- and loss-of-function were used to examine the PKM2 role in HPC metastasis in vitro and in vivo. In vitro and in vivo studies also confirmed lymphatic metastasis's mechanism.
resultsProminent PKM2 overexpression was seen in patients with lymphatic metastasis of HPC, and there was an inherent relationship between a high PKM2 level and poor prognosis. In vitro research showed that knocking down PKM2 decreased tumor cell invasion, migration, and proliferation while promoting apoptosis and inhibiting epithelial-mesenchymal transition, but overexpressing PKM2 had the reverse effect. Animal studies suggested that PKM2 may facilitate tumor development and lymphatic metastasis.
conclusionsOur findings suggest that PKM2 may be a tumor's promoter gene of lymphatic metastasis, which may promote lymphatic metastasis of HPC by regulating epithelial-mesenchymal transition. PKM2 may be a biomarker of metastatic potential, ultimately providing a basis for exploring new therapeutic targets.
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