Evidence map›Paper›PMID 42178570›Full record

ArticleCell communication and signaling : CCS2026

A positive feedback loop between BACH1 and IL-1β promotes the progression of HPV-negative head and neck squamous cell carcinoma.

Zishanbai Zhang, Miao Wang, Wenjuan Wang, Minghui Zhao, Yiming Ding, Tingyao Ma, Zhaohan Zhang, Xilin Wang, Yuchen Xiang, Yaning Wang and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell communication and signaling : CCS, 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

15 authors.

Zishanbai Zhang *Department of Otolaryngology Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Key Laboratory of Otolaryngology Head and Neck Surgery, Ministry of Education, Capital Medical University, Dong Jiao Min Xiang Street, Beijing, China.
Miao Wang *Department of Otolaryngology Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Key Laboratory of Otolaryngology Head and Neck Surgery, Ministry of Education, Capital Medical University, Dong Jiao Min Xiang Street, Beijing, China.
Wenjuan WangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Laboratory for Clinical Medicine, Capital Medical University, 10 You'anmen Outer West 1 st Street, Beijing, 100069, China.
Minghui ZhaoDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Laboratory for Clinical Medicine, Capital Medical University, 10 You'anmen Outer West 1 st Street, Beijing, 100069, China.
Yiming DingDepartment of Otolaryngology Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Key Laboratory of Otolaryngology Head and Neck Surgery, Ministry of Education, Capital Medical University, Dong Jiao Min Xiang Street, Beijing, China.
Tingyao MaDepartment of Otolaryngology Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Key Laboratory of Otolaryngology Head and Neck Surgery, Ministry of Education, Capital Medical University, Dong Jiao Min Xiang Street, Beijing, China.
Zhaohan ZhangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Laboratory for Clinical Medicine, Capital Medical University, 10 You'anmen Outer West 1 st Street, Beijing, 100069, China.
Xilin WangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Laboratory for Clinical Medicine, Capital Medical University, 10 You'anmen Outer West 1 st Street, Beijing, 100069, China.
Yuchen XiangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Laboratory for Clinical Medicine, Capital Medical University, 10 You'anmen Outer West 1 st Street, Beijing, 100069, China.
Yaning WangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Laboratory for Clinical Medicine, Capital Medical University, 10 You'anmen Outer West 1 st Street, Beijing, 100069, China.
Wenying ZhongDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Laboratory for Clinical Medicine, Capital Medical University, 10 You'anmen Outer West 1 st Street, Beijing, 100069, China.
Zicheng WuDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Laboratory for Clinical Medicine, Capital Medical University, 10 You'anmen Outer West 1 st Street, Beijing, 100069, China.
Yiran MengDepartment of Otorhinolaryngology Head and Neck Surgery, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing, China.
Xiaohong ChenDepartment of Otolaryngology Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Key Laboratory of Otolaryngology Head and Neck Surgery, Ministry of Education, Capital Medical University, Dong Jiao Min Xiang Street, Beijing, China. trchxh@163.com.
Lin ShanDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Laboratory for Clinical Medicine, Capital Medical University, 10 You'anmen Outer West 1 st Street, Beijing, 100069, China. shanlin@ccmu.edu.cn.

Funding

"Ascending the Peak" Talent Training Program from the Beijing Hospital Management Center DFL20220201 to X.C.National Natural Science Foundation of China 82073122 to L.S.
6 · The paper itself

Abstract

Human papillomavirus (HPV)-negative head and neck squamous cell carcinoma (HNSCC) is associated with a poorer prognosis compared to its HPV-positive counterpart; however, the underlying regulatory molecular mechanisms driving its progression remain poorly understood. In this study, we identify BTB Domain and CNC Homolog 1 (BACH1) as a critical oncogenic regulator that is upregulated in HPV-negative HNSCC. We demonstrate that BACH1 promotes tumor progression by enhancing the proliferation and inhibiting apoptosis of cancer cells. Mechanistically, BACH1 is associated with the SWI/SNF chromatin remodeling complex and transcriptionally activates downstream target genes, including IL1B, thereby inducing a transcriptional reprogramming that promotes proliferation and resists apoptosis. Notably, BACH1-driven upregulation of interleukin-1β (IL-1β) establishes a positive feedback loop that sustains oncogenic signaling. Pharmacological disruption of this axis using the IL-1 receptor antagonist Anakinra significantly attenuates tumor growth in vitro and in vivo. Clinically, co-upregulation of BACH1, BRG1, and IL-1β is correlated with reduced overall survival in patients with HPV-negative HNSCC. Collectively, our findings characterize the BACH1-IL-1β signaling axis as a prognostic biomarker and highlight IL-1R blockade as a promising therapeutic strategy for the treatment of HPV-negative HNSCC.

Indexed as

Basic-Leucine Zipper Transcription FactorsDisease ProgressionFeedback, PhysiologicalHead and Neck NeoplasmsInterleukin-1betaSquamous Cell Carcinoma of Head and NeckAnimalsApoptosisCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHuman Papillomavirus VirusesHumansMiceTranscription FactorsBACH1 protein, humanBasic-Leucine Zipper Transcription FactorsInterleukin-1betaTranscription Factors

Identifiers

PMID42178570
PMCPMC13377829

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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.