Evidence map›Paper›PMID 34348789›Full record

ArticleCell & bioscience2021

FOXD1 promotes EMT and cell stemness of oral squamous cell carcinoma by transcriptional activation of SNAI2.

Yang Chen, Weilian Liang, Ke Liu, Zhengjun Shang

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. ITGA5 is overexpressed and promotes tumor progression through SNAI2 in OSCC.Frontiers in cell and developmental biology · 2026
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  10. Heliyon · 2023
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  11. The IL-17 family in diseases: from bench to bedside.Signal transduction and targeted therapy · 2023
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  19. Cancers · 2022
    Article
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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

4 authors at 1 institution in 1 country.

Yang Chen *The State Key Laboratory Breeding Base of Basic Science of Stomatology, Hubei Province and Key Laboratory of Oral Biomedicine (Wuhan University), Ministry of Education (Hubei-MOST KLOS & KLOBM), Wuhan, China.
Weilian Liang *The State Key Laboratory Breeding Base of Basic Science of Stomatology, Hubei Province and Key Laboratory of Oral Biomedicine (Wuhan University), Ministry of Education (Hubei-MOST KLOS & KLOBM), Wuhan, China.
Ke LiuDepartment of Oral and Maxillofacial-Head and Neck Oncology, School and Hospital of Stomatology, Wuhan University, 237 Luoyu Road, Hongshan District, Wuhan, 430079, China. liuke.1999@whu.edu.cn.
Zhengjun ShangDepartment of Oral and Maxillofacial-Head and Neck Oncology, School and Hospital of Stomatology, Wuhan University, 237 Luoyu Road, Hongshan District, Wuhan, 430079, China. shangzhengjun@whu.edu.cn.ORCID http://orcid.org/0000-0002-4884-8129
Wuhan University · CN

Funding

National Natural Science Foundation of China 81972547
6 · The paper itself

Abstract

backgroundEpithelial-mesenchymal transition (EMT) and cell stemness are implicated in the initiation and progression of oral squamous cell carcinoma (OSCC). Revealing the intrinsic regulatory mechanism may provide effective therapeutic targets for OSCC.

resultsIn this study, we found that Forkhead box D1 (FOXD1) was upregulated in OSCC compared with normal samples. Patients with a higher FOXD1 expression had a poorer overall survival and disease-free survival. Immunohistochemical staining results showed that FOXD1 expression was related to the clinical stage and relapse status of OSCC patients. When FOXD1 expression was knocked down in CAL27 and SCC25 cells, the migration, invasion, colony formation, sphere formation, and proliferation abilities decreased. Moreover, EMT and stemness-related markers changed remarkably, which indicated that the EMT process and cell stemness were inhibited. Conversely, overexpression of FOXD1 promoted EMT and cell stemness. Further study demonstrated that FOXD1 could bind to the promoter region and activate the transcription of SNAI2. In turn, the elevated SNAI2 affected EMT and cell stemness. An in vivo study showed that FOXD1-overexpressing CAL27 cells possessed a stronger tumorigenic ability.

conclusionsOur findings revealed a novel mechanism in regulating EMT and cell stemness and proposed FOXD1 as a potential marker for the diagnosis and treatment of OSCC.

Indexed as

EMTFOXD1OSCCSNAI2STEMNESS

Identifiers

PMID34348789
PMCPMC8335989
OpenAlexW3191620640

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.