Evidence map›Paper›PMID 38413558›Full record

ArticleCell death discovery2024

IGF-1-mediated FOXC1 overexpression induces stem-like properties through upregulating CBX7 and IGF-1R in esophageal squamous cell carcinoma.

Hao Wu, Zhao-Xing Li, Kang Fang, Zi-Ying Zhao, Ming-Chuang Sun, An-Qi Feng, Zhu-Yun Leng, Ze-Hua Zhang, Yuan Chu, Li Zhang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

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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

12 authors at 2 institutions in 1 country.

Hao Wu *Endoscopy Center, Department of Gastroenterology, Shanghai East Hospital, School of Medicine, Tongji University, 200120, Shanghai, China.
Zhao-Xing Li *Endoscopy Center, Department of Gastroenterology, Shanghai East Hospital, School of Medicine, Tongji University, 200120, Shanghai, China.
Kang FangEndoscopy Center, Department of Gastroenterology, Shanghai East Hospital, School of Medicine, Tongji University, 200120, Shanghai, China.
Zi-Ying ZhaoEndoscopy Center, Department of Gastroenterology, Shanghai East Hospital, School of Medicine, Tongji University, 200120, Shanghai, China.
Ming-Chuang SunEndoscopy Center, Department of Gastroenterology, Shanghai East Hospital, School of Medicine, Tongji University, 200120, Shanghai, China.
An-Qi FengEndoscopy Center, Department of Gastroenterology, Shanghai East Hospital, School of Medicine, Tongji University, 200120, Shanghai, China.
Zhu-Yun LengEndoscopy Center, Department of Gastroenterology, Shanghai East Hospital, School of Medicine, Tongji University, 200120, Shanghai, China.
Ze-Hua ZhangEndoscopy Center, Department of Gastroenterology, Shanghai East Hospital, School of Medicine, Tongji University, 200120, Shanghai, China.
Yuan ChuEndoscopy Center, Department of Gastroenterology, Shanghai East Hospital, School of Medicine, Tongji University, 200120, Shanghai, China.
Li ZhangDepartment of Pathology, Shanghai East Hospital, School of Medicine, Tongji 8 University, 200120, Shanghai, China.
Tao ChenEndoscopy Center, Department of Gastroenterology, Shanghai East Hospital, School of Medicine, Tongji University, 200120, Shanghai, China. chentao@tongji.edu.cn.ORCID http://orcid.org/0000-0002-8016-9732
Mei-Dong XuEndoscopy Center, Department of Gastroenterology, Shanghai East Hospital, School of Medicine, Tongji University, 200120, Shanghai, China. 1800512@tongji.edu.cn.ORCID http://orcid.org/0000-0002-7219-5826
Shanghai East Hospital · CNTongji University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82072684 and 82073224
6 · The paper itself

Abstract

Substantial evidence attests to the pivotal role of cancer stem cells (CSC) in both tumorigenesis and drug resistance. A member of the forkhead box (FOX) family, FOXC1, assumes significance in embryonic development and organogenesis. Furthermore, FOXC1 functions as an overexpressed transcription factor in various tumors, fostering proliferation, enhancing migratory capabilities, and promoting drug resistance, while maintaining stem-cell-like properties. Despite these implications, scant attention has been devoted to its role in esophageal squamous cell carcinoma. Our investigation revealed a pronounced upregulation of FOXC1 expression in ESCC, correlating with a poor prognosis. The downregulation of FOXC1 demonstrated inhibitory effects on ESCC tumorigenesis, proliferation, and tolerance to chemotherapeutic agents, concurrently reducing the levels of stemness-related markers CD133 and CD44. Further studies validated that FOXC1 induces ESCC stemness by transactivating CBX7 and IGF-1R. Additionally, IGF-1 activated the PI3K/AKT/NF-κB and MEK/ERK/NF-κB pathways through its binding to IGF-1R, thereby augmenting FOXC1 expression. Conversely, suppressing FOXC1 impeded ESCC stemness induced by IGF-1. The presence of a positive feedback loop, denoted by IGF-1-FOXC1-IGF-1R, suggests the potential of FOXC1 as a prognostic biomarker for ESCC. Taken together, targeting the IGF-1-FOXC1-IGF-1R axis emerges as a promising approach for anti-CSC therapy in ESCC.

Identifiers

PMID38413558
PMCPMC10899262
OpenAlexW4392200454

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.