Evidence map›Paper›PMID 41683623›Full record

ArticleInternational journal of molecular sciences2026

FOXA1 in Ovarian Cancer: A Potential Therapeutic Target to Enhance Immunotherapy Efficacy.

Taewan Kim, Jaesung Ryu, Hyejeong Kong, Beamjun Park, Kwangseock Kim, Eunjung Yang, Taesung Ahn, Seob Jeon

Abstract read
In one paragraph

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

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Taewan KimFuture Innovation Medical Research Center, Soonchunhyang University Cheonan Hospital, Cheonan 31151, Republic of Korea.ORCID 0000-0003-1455-2343
Jaesung RyuDepartment of Medical Life Science, Soonchunhyang University, Asan 31538, Republic of Korea.ORCID 0000-0002-8650-3092
Hyejeong KongDepartment of Medical Life Science, Soonchunhyang University, Asan 31538, Republic of Korea.ORCID 0000-0002-3512-8472
Beamjun ParkDepartment of Medical Life Science, Soonchunhyang University, Asan 31538, Republic of Korea.ORCID 0009-0003-6561-4361
Kwangseock KimFuture Innovation Medical Research Center, Soonchunhyang University Cheonan Hospital, Cheonan 31151, Republic of Korea.ORCID 0000-0002-3329-1225
Eunjung YangDepartment of Gynecology, College of Medicine, Soonchunhyang University Cheonan Hospital, Cheonan 31151, Republic of Korea.ORCID 0000-0001-9826-3519
Taesung AhnDepartment of Colorectal Surgery, College of Medicine, Soonchunhyang University Cheonan Hospital, Cheonan 31151, Republic of Korea.ORCID 0000-0001-5617-0365
Seob JeonDepartment of Gynecology, College of Medicine, Soonchunhyang University Cheonan Hospital, Cheonan 31151, Republic of Korea.ORCID 0000-0001-5230-1997

Funding

Ministry of Trade, Industry & Energy (MOTIE, Korea). RS-2024-00400101Soonchunhyang University Research Fund 2025-0043
6 · The paper itself

Abstract

This study aimed to elucidate the oncogenic role of FOXA1(forkhead box A1) in ovarian cancer and to evaluate its potential as both a therapeutic target and a diagnostic biomarker. We further investigated whether FOXA1 inhibition could enhance responsiveness to immune checkpoint blockade and overcome chemoresistance. A total of seventy-six ovarian tissue samples were analyzed, including nine normal, thirty-four benign, and thirty-three malignant specimens. IHC (immunohistochemistry) staining was performed to assess FOXA1 expression and its correlation with tumor stage. Functional studies were conducted using FOXA1 siRNA in SK-OV3 and HEYA8 cell lines. Changes in cell proliferation, migration, invasion, and wound-healing ability were evaluated following FOXA1 silencing. Quantitative RT-PCR was used to measure the expression of FOXA1 and EMT (epithelial-mesenchymal transition)-related genes. The effects of FOXA1 inhibition on sensitivity to carboplatin and the immune checkpoint inhibitor atezolizumab were also examined. IHC analysis revealed significant differences in FOXA1 expression among normal, benign, and malignant tissues, with levels correlating with tumor stage. FOXA1 silencing significantly reduced proliferation and decreased migration and invasion by 60-80%, accompanied by marked downregulation of EMT-related genes. Moreover, FOXA1 inhibition enhanced atezolizumab responsiveness and reduced carboplatin resistance in ovarian cancer cells. In summary, FOXA1 acts as an oncogenic driver in ovarian cancer, promoting proliferation, invasion, and EMT activation. Its overexpression correlates with disease progression, supporting its potential as a biomarker and therapeutic target. Targeting FOXA1 could enhance immunotherapy efficacy and help overcome chemoresistance in ovarian cancer.

Indexed as

Hepatocyte Nuclear Factor 3-alphaImmunotherapyOvarian NeoplasmsBiomarkers, TumorCell Line, TumorCell MovementCell ProliferationDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansBiomarkers, TumorFOXA1 protein, humanHepatocyte Nuclear Factor 3-alphabiomarkerchemoresistanceforkhead box A1FOXA1immune checkpoint inhibitoroncogeneovarian cancer

Identifiers

PMID41683623
PMCPMC12897294

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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 OpenQuestion graph.