ArticleBMC cancer2024
FERMT1 promotes cell migration and invasion in non-small cell lung cancer via regulating PKP3-mediated activation of p38 MAPK signaling.
Article in BMC cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Construction and validation of a model based on necroptosis-related genes for predicting glioma prognosis.Discover oncology · 2026Article
- FCRLB-mediated dual control of tumor metabolism and macrophage polarization promotes lung cancer malignancy.Journal of translational medicine · 2026Article
- Article
- Induction of necroptosis in lung adenocarcinoma by miR‑10b‑5p through modulation of the PKP3/RIPK3/MLKL cascade.Oncology reports · 2025Article
- The mechanism of high mobility group box-1 in the proliferation and macrophage polarization in esophageal squamous cell carcinoma cells.European journal of medical research · 2025Article
- Kindlin-1 promotes gastric cancer cell motility through the Wnt/β-catenin signaling pathway.Scientific reports · 2025Article
- A Prognostic Riskscore Model Related toInternational journal of genomics · 2025Article
- Identification of a novelFrontiers in pediatrics · 2024Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundFermitin family member 1 (FERMT1) is highly expressed in many tumors and acts as an oncogene. Nonetheless, the precise function of FERMT1 in non-small cell lung cancer (NSCLC) has not been clearly elucidated.
methodsBioinformatics software predicted the FERMT1 expression in NSCLC. Transwell assays facilitated the detection of NSCLC cell migration and invasion. Western blotting techniques were employed to detect the protein levels regulated by FERMT1.
resultsFERMT1 exhibited high expression levels in NSCLC and was linked to the patients' poor prognosis, as determined by a variety of bioinformatics predictions combined with experimental verification. FERMT1 promoted the migration and invasion of NSCLC and regulated epithelial to mesenchymal transition (EMT) -related markers. Further studies showed that FERMT1 could up-regulate the expression level of plakophilin 3(PKP3). Further research has indicated that FERMT1 can promote cell migration and invasion via up-regulating PKP3 expression. By exploring downstream signaling pathways, we found that FERMT1 has the capability to activate the p38 mitogen-activated protein kinases (p38 MAPK) signaling pathway, and knocking down PKP3 can counteract the activation induced by FERMT1 overexpression.
conclusionsFERMT1 was highly expressed in NSCLC and can activate the p38 MAPK signaling pathway through up-regulation of PKP3, thus promoting the invasion and migration of NSCLC.
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Registered trials
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