Comprehensive pan-cancer analysis of FSCN1 as a marker for prognosis and immunity

Our plain-English summary of Comprehensive pan-cancer analysis of FSCN1 as a marker for prognosis and immunity, by R. Xu, W. Xu, C. Dong, et al (Discover Oncology, 2026).

The study

• Authors: R. Xu, W. Xu, C. Dong, G. Qiang
• Journal: Discover Oncology
• Published: 2026;17(1)
• Read it: PubMed · Publisher · Free full text

Abstract

BACKGROUND: Fascin actin-bundling protein 1 (FSCN1), a member of actin cytoskeletal protein family genes, plays critical roles in cell migration, motility, adhesion, and other cellular interactions. It has shown its ascending importance in tumors of multiple systems, including the nervous system, respiratory system, digestive system and urinary system. Nevertheless, no systematic pan-cancer analysis has been carried out to investigate its function in diagnosis, prognosis, and immunological prediction. METHODS: We used UCSC Xena, The Cancer Genome Atlas (TCGA), Genotype Tissue Expression Project (GTEx), Human Protein Atlas (HPA), cBioPortal, STRING, Cancer single-cell state Atlas (CancerSEA), Genomics of Drug Sensitivity in Cancer (GDSC) and Xiantao Academic analysis tool websites and databases for the extraction of pan-cancer data on FSCN1. We adopted bioinformatics methods to explore the potential role of FSCN1 in pan-cancer, including analysis of the correlation between FSCN1 and clinicopathologic features, prognosis, genetic alteration, immune, DNA methylation, single cell function and drug sensitivity. Furthermore, a protein–protein interaction network was drawn, and gene set enrichment analysis was conducted to explore the functions of FSCN1. Finally, we validated the effects of FSCN1 on cell proliferation and apoptosis through experiments. RESULTS: The findings of the comprehensive pan-cancer analysis revealed that FSCN1 was highly expressed in most cancers, except in acute myeloid leukemia, prostate adenocarcinoma and thyroid carcinoma, and it has a certain diagnostic and prognosis value in many cancers. Furthermore, FSCN1 expression was found to correlate with immune cell infiltration, immune checkpoint (ICP) genes expression, DNA methylation and drug sensitivity in a variety of cancers. In addition, we discovered that FSCN1 participated in the proliferation and DNA repair at the single-cell level. Besides, Gene function enrichment analyses revealed that genes that were co-expressed with FSCN1 were enriched within the actin filament regulation pathways. CCK-8 assay and flow cytometry apoptosis assay results indicated that FSCN1 knockdown inhibited proliferation and induced apoptosis in mesothelioma (MESO). CONCLUSION: FSCN1 is a prospective marker for the diagnosis, prognosis, immunology, chemotherapy, and small molecular drugs targeted for pan-cancer treatment.

In plain English

This study did not examine asbestos exposure. It analyzed public cancer databases, mainly The Cancer Genome Atlas (33 cancer types), and tested a mesothelioma cell line in the lab. The authors studied FSCN1, a gene for a protein involved in cell movement. In combined TCGA and GTEx data, FSCN1 expression was higher in tumors than in normal tissue in 24 cancer types and lower in three. Patients were split into high and low FSCN1 groups at the median. In mesothelioma, the high-FSCN1 group had worse overall and disease-specific survival (both p less than 0.001) and a worse progression-free interval (p = 0.016). Hazard ratios appear in the text only as greater than 1. In the lab, two of three molecules used to reduce FSCN1 in NCI-H2452 mesothelioma cells slowed cell growth and increased cell death. The third had no statistically significant effect on growth. The authors concluded that FSCN1 is a prospective marker across cancers. They noted that their results rest mainly on bioinformatic analyses, that combining databases could cause systematic bias, and that further prospective studies are required.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Bioinformatics (computer) analysis of public cancer and normal-tissue databases, with laboratory cell-line experiments in mesothelioma cells
• Who was studied: Tumor and normal-tissue data covering 33 cancer types from The Cancer Genome Atlas (TCGA) and the GTEx database. The genetic alteration analysis covered 10,953 TCGA patients. The laboratory work used the mesothelioma cell line NCI-H2452. A healthy mesothelial cell line, MET-5A, is listed in the methods.
• Exposure: No asbestos or fiber exposure was studied. The factor studied was FSCN1 gene expression: patients were split into high and low groups at the median. In the lab, FSCN1 was reduced in mesothelioma cells using three siRNAs and compared with a scrambled control.
• Main results:
  • In combined TCGA and GTEx data, FSCN1 expression was significantly higher in tumors than in normal tissue in 24 cancer types. It was lower in three cancer types (LAML, PRAD and THCA).
  • In mesothelioma (MESO), among other cancers, FSCN1 expression was lower in patients with lymph node metastasis than in patients without it.
  • In mesothelioma, FSCN1 expression was associated with overall survival (p less than 0.001, hazard ratio greater than 1). Low expression was associated with better overall survival.
  • In mesothelioma, high FSCN1 expression was associated with poor disease-specific survival (p less than 0.001, hazard ratio greater than 1).
  • In mesothelioma, high FSCN1 expression was associated with a poor progression-free interval (p = 0.016, hazard ratio greater than 1).
  • In multivariate analysis, high FSCN1 expression remained a poor prognostic factor for progression-free interval in ACC, COAD, MESO, PAAD and TGCT.
  • Across 10,953 TCGA patients, 209 (2%) had an FSCN1 gene alteration.
  • In NCI-H2452 mesothelioma cells, reducing FSCN1 lowered cell growth with si-FSCN1 #1 (p = 0.0006) and si-FSCN1 #2 (p = 0.0002).
  • The third siRNA (si-FSCN1 #3) had no statistically significant effect on cell growth.
  • Reducing FSCN1 increased cell death (apoptosis) in NCI-H2452 cells with si-FSCN1 #1 (p less than 0.0001) and si-FSCN1 #2 (p = 0.0036).
• The authors' conclusion: The authors concluded that FSCN1 is a prospective marker for diagnosis, prognosis, immunology and drug treatment across cancers. They added that further prospective studies are required to confirm its diagnostic and prognostic value.
• Limitations the authors state:
  • The results were based on bioinformatic analyses. FSCN1's biological functions were confirmed only by cell-growth and flow cytometry tests in mesothelioma cells, and other experimental studies are needed.
  • It remains unclear how FSCN1 regulates the immune response, and further study is needed.
  • Combining several databases could lead to systematic bias.

Topics

Medical terms in this study, explained in our Lexicon: Prognosis, Apoptosis, Adenocarcinoma, Carcinoma, Mesothelioma, Chemotherapy.

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