Evidence map›Paper›PMID 41203834›Full record

ArticleBritish journal of cancer2026

Profilin-2 promotes tumour aggressiveness in oral squamous cell carcinoma via HDAC1 modulation: implications for EMT and targeted therapy.

Li-Han Lin, Kuo-Wei Chang, Hui-Wen Cheng, Chung-Ji Liu

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Article in British journal of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Li-Han LinDepartment of Medical Research, MacKay Memorial Hospital, Taipei, Taiwan.
Kuo-Wei ChangInstitute of Oral Biology, School of Dentistry, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Hui-Wen ChengDepartment of Medical Research, MacKay Memorial Hospital, Taipei, Taiwan.
Chung-Ji LiuDepartment of Medical Research, MacKay Memorial Hospital, Taipei, Taiwan. cjliu@mmh.org.tw.ORCID http://orcid.org/0000-0002-0385-869X

Funding

Mackay Memorial Hospital (MMH-E-105-12 and MMH-E-108-12Ministry of Science and Technology, Taiwan (Ministry of Science and Technology of Taiwan) MOST 108-2314-B-195 -002 -MY2, 110-2314-B-195 -015 -MY3,
6 · The paper itself

Abstract

backgroundProfilin-2 (PFN2) is implicated in cancer metastasis, yet its significance in oral squamous cell carcinoma (OSCC) is unclear.

methodsWe quantified PFN2 mRNA and protein in 236 OSCC tumours using qRT-PCR and immunohistochemistry, correlating findings with clinicopathology and survival. Gain- and loss-of-function studies were performed in OSCC cell lines and xenograft mice. RNA sequencing with gene-set enrichment, subcellular fractionation, and immunofluorescence delineated PFN2-dependent pathways. Sensitivity to the histone deacetylase (HDAC) inhibitor SAHA was assessed in vitro.

resultsHigh PFN2 expression correlated with lymph-node metastasis, stage IV disease, and poorer overall and disease-free survival (p < 0.01). PFN2 increased proliferation, invasion, and epithelial-mesenchymal transition (EMT) in vitro, and accelerated primary tumour growth plus cervical/lung metastasis in vivo; knockout produced opposite effects. Transcriptomics revealed enrichment of EMT, E2F, G2/M, and hypoxia signatures, with a 44% overlap with HDAC1 targets. PFN2 shifted HDAC1 to the cytoplasm and downregulated NuRD partners MBD3/MTA1 without altering total HDAC1. PFN2-driven EMT was independent of β-catenin nuclear entry. PFN2 overexpression sensitized cells to SAHA, enhancing G2/M arrest, apoptosis, and invasion blockade.

conclusionsPFN2 is an oncogenic driver that promotes OSCC progression through HDAC1-dependent transcriptional reprogramming. PFN2 may serve as a prognostic biomarker and predictor of response to HDAC-targeted therapy.

Indexed as

Carcinoma, Squamous CellHistone Deacetylase 1Mouth NeoplasmsProfilinsSquamous Cell Carcinoma of Head and NeckAnimalsCell Line, TumorCell ProliferationEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHistone Deacetylase InhibitorsHumansMaleMiceMiddle AgedHDAC1 protein, humanHistone Deacetylase 1Histone Deacetylase InhibitorsPFN2 protein, humanProfilinsVorinostat

Identifiers

PMID41203834
PMCPMC12819395

What Socratic holds

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Registered trials

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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 Socratic graph.