ArticleCell death discovery2025
Targeting the FOXA1/BMI1 axis to overcome chemoresistance and suppress tumor progression in nasopharyngeal carcinoma.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
The trial behind it
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
2 citing papers in PubMed.
- FOXA1 drives chemoresistance through activating Wnt pathway in small cell lung cancer.Translational lung cancer research · 2026Article
- ALKBH5 promotes the progression of cisplatin-resistant oral squamous cell carcinoma by regulating FOXA1 expression via mDaru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Nasopharyngeal carcinoma (NPC) is a highly aggressive head and neck cancer characterized by a complex etiology and a propensity for metastasis. The current study explores the intricate relationship between Forkhead Box A1 (FOXA1) and B-cell-specific Moloney murine leukemia virus integration site 1 (BMI1) in the cancer progression and chemoresistance of NPC. Our research identified a significant downregulation of FOXA1 in NPC tissues and cell lines, which correlates with advanced clinical stages and poor differentiation, underscoring its potential role as a tumor suppressor. Functional assays demonstrated that the silencing of FOXA1 significantly enhanced the proliferation, migration, and invasive capabilities of NPC cells in vitro. Furthermore, the deficiency of FOXA1 was associated with a diminished sensitivity to cisplatin, as evidenced by increased cell viability, reduced apoptosis, and impaired cell cycle arrest upon drug exposure. Mechanistic studies revealed BMI1 as a critical downstream target of FOXA1. We observed a negative correlation between the expression levels of FOXA1 and BMI1 in NPC tissues. FOXA1 was shown to bind directly to the BMI1 promoter, effectively dampening its transcriptional activity. Rescue experiments indicated that the downregulation of BMI1 could partially reverse the malignant phenotypes induced by FOXA1 silencing, both in vitro and in vivo. Importantly, the knockdown of BMI1 significantly increased the chemosensitivity of FOXA1-depleted NPC cells to cisplatin, effectively counteracting the drug resistance associated with FOXA1 suppression. These findings highlight the pivotal role of FOXA1 in NPC development and progression and suggest that its loss leads to the upregulation of BMI1 and the acquisition of cisplatin resistance. Our study provides novel insights into the molecular mechanisms underlying the malignancy and chemoresistance of NPC and proposes that targeting the FOXA1/BMI1 axis could offer a promising therapeutic strategy for the treatment of this devastating disease.
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Registered trials
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 OpenQuestion graph.