Evidence map›Paper›PMID 34101624›Full record

ArticleThe Journal of clinical investigation2021

FOXA1 overexpression suppresses interferon signaling and immune response in cancer.

Yundong He, Liguo Wang, Ting Wei, Yu-Tian Xiao, Haoyue Sheng, Hengchuan Su, Daniel P Hollern, Xiaoling Zhang, Jian Ma, Simeng Wen and 19 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 2 pooled it
5.5field-weighted citation impact, top 3% of its field
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

66 citing papers in PubMed, 2 syntheses or guidelines pooled it, 86 citations in OpenAlex.

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6 more citing papers are in PubMed but not listed here.

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

29 authors at 7 institutions in 2 countries.

Yundong HeDepartment of Biochemistry and Molecular Biology.
Liguo WangDivision of Computational Biology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota, USA.
Ting WeiDivision of Computational Biology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota, USA.
Yu-Tian XiaoDepartment of Urology, Shanghai Changhai Hospital, Shanghai, China.
Haoyue ShengDepartment of Biochemistry and Molecular Biology.
Hengchuan SuDepartment of Urology, Fudan University Shanghai Cancer Center, Shanghai, China.
Daniel P HollernLineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina, USA.
Xiaoling ZhangKey Laboratory of Organ Regeneration and Transplantation of the Ministry of Education, Institute of Immunology, The First Hospital of Jinlin University, Changchun, Jilin, China.
Jian MaDepartment of Biochemistry and Molecular Biology.
Simeng WenDepartment of Biochemistry and Molecular Biology.
Hongyan XieDepartment of Biochemistry and Molecular Biology.
Yuqian YanDepartment of Biochemistry and Molecular Biology.
Yunqian PanDepartment of Biochemistry and Molecular Biology.
Xiaonan HouDepartment of Oncology.
Xiaojia TangDivision of Computational Biology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota, USA.
Vera J SumanDivision of Computational Biology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota, USA.
Jodi M CarterDepartment of Laboratory Medicine and Pathology, and.
Richard WeinshilboumDepartment of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic College of Medicine and Science, Rochester, Minnesota, USA.
Liewei WangDepartment of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic College of Medicine and Science, Rochester, Minnesota, USA.
Krishna R KalariDivision of Computational Biology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota, USA.
Saravut J WerohaDepartment of Oncology.
Alan H BryceDivision of Hematology and Oncology, Department of Internal Medicine, Mayo Clinic College of Medicine and Science, Phoenix, Arizona, USA.
Judy C BougheyDepartment of Surgery.
Haidong DongDepartment of Urology, and.
Charles M PerouLineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina, USA.
Dingwei YeDepartment of Urology, Fudan University Shanghai Cancer Center, Shanghai, China.
Matthew P GoetzDepartment of Oncology.
Shancheng RenDepartment of Urology, Shanghai Changhai Hospital, Shanghai, China.
Haojie HuangDepartment of Biochemistry and Molecular Biology.
Mayo Clinic · USShanghai Medical College of Fudan University · CNSecond Military Medical University · CNUniversity of North Carolina at Chapel Hill · USEmory University Hospital · USJilin University · CNMayo Clinic in Arizona · US

Funding

Women's Cancer ProgramP30CA015083 · NCI · MAYO CLINIC ROCHESTER · PI AKHILESH PANDEY · 1985 to 2026
$151.3M
The Role of CHFR in Tumorigenesis and Paclitaxel-Sensitivity in Breast CancerP50CA116201 · NCI · MAYO CLINIC ROCHESTER · PI Fergus Joseph Couch · 2005 to 2026
$49.9M
Role of proinflammatory cytokine-induced AR degradation in castration-resistant prostate cancerR01CA130908 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI HUANG, HAOJIE · 2010 to 2021
$3.5M
Mechanism and role of aberrant AR activity in castration-resistant prostate cancerR01CA203849 · NCI · MAYO CLINIC ROCHESTER · PI HUANG, HAOJIE · 2018 to 2022
$1.8M
NCI NIH HHS N01 CA015083NCI NIH HHS P30 CA015083NCI NIH HHS P50 CA116201NCI NIH HHS R01 CA130908NCI NIH HHS R01 CA203849
6 · The paper itself

Abstract

Androgen receptor-positive prostate cancer (PCa) and estrogen receptor-positive luminal breast cancer (BCa) are generally less responsive to immunotherapy compared with certain tumor types such as melanoma. However, the underlying mechanisms are not fully elucidated. In this study, we found that FOXA1 overexpression inversely correlated with interferon (IFN) signature and antigen presentation gene expression in PCa and BCa patients. FOXA1 bound the STAT2 DNA-binding domain and suppressed STAT2 DNA-binding activity, IFN signaling gene expression, and cancer immune response independently of the transactivation activity of FOXA1 and its mutations detected in PCa and BCa. Increased FOXA1 expression promoted cancer immuno- and chemotherapy resistance in mice and PCa and BCa patients. These findings were also validated in bladder cancer expressing high levels of FOXA1. FOXA1 overexpression could be a prognostic factor to predict therapy resistance and a viable target to sensitize luminal PCa, BCa, and bladder cancer to immuno- and chemotherapy.

Indexed as

AnimalsFemaleGene Expression Regulation, NeoplasticHepatocyte Nuclear Factor 3-alphaHumansInterferonsMaleMiceNeoplasm ProteinsNeoplasmsSignal TransductionFOXA1 protein, humanFoxa1 protein, mouseHepatocyte Nuclear Factor 3-alphaInterferonsNeoplasm ProteinsCancerCancer immunotherapyCell BiologyMolecular biologyTherapeutics

Identifiers

PMID34101624
PMCPMC8279591
OpenAlexW3167766609

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.