Evidence map›Paper›PMID 38355684›Full record

ArticleCell death & disease2024

SALL4 promotes cancer stem-like cell phenotype and radioresistance in oral squamous cell carcinomas via methyltransferase-like 3-mediated m6A modification.

Junhong Huang, Huan Li, Zihui Yang, Rong Liu, Yahui Li, Yating Hu, Shengnan Zhao, Xiang Gao, Xinjie Yang, Jianhua Wei

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

18 citing papers in PubMed, 19 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

10 authors at 2 institutions in 1 country.

Junhong Huang *State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral & Maxillofacial Surgery, School of Stomatology, Fourth Military Medical University, Xi'an, 710032, China.ORCID 0000-0003-2997-2201
Huan Li *State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral & Maxillofacial Surgery, School of Stomatology, Fourth Military Medical University, Xi'an, 710032, China.ORCID 0000-0003-2168-3579
Zihui YangState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral & Maxillofacial Surgery, School of Stomatology, Fourth Military Medical University, Xi'an, 710032, China.
Rong LiuState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral & Maxillofacial Surgery, School of Stomatology, Fourth Military Medical University, Xi'an, 710032, China.
Yahui LiState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral & Maxillofacial Surgery, School of Stomatology, Fourth Military Medical University, Xi'an, 710032, China.
Yating HuState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral & Maxillofacial Surgery, School of Stomatology, Fourth Military Medical University, Xi'an, 710032, China.
Shengnan ZhaoState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral & Maxillofacial Surgery, School of Stomatology, Fourth Military Medical University, Xi'an, 710032, China.
Xiang GaoState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral & Maxillofacial Surgery, School of Stomatology, Fourth Military Medical University, Xi'an, 710032, China.
Xinjie YangState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral & Maxillofacial Surgery, School of Stomatology, Fourth Military Medical University, Xi'an, 710032, China. yangxinjie@fmmu.edu.cn.ORCID 0000-0003-3799-4590
Jianhua WeiState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Oral & Maxillofacial Surgery, School of Stomatology, Fourth Military Medical University, Xi'an, 710032, China. weiyoyo@fmmu.edu.cn.ORCID 0000-0002-8231-3101
Air Force Medical University · CNStomatology Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) NO.81973114
6 · The paper itself

Abstract

Radioresistance imposes a great challenge in reducing tumor recurrence and improving the clinical prognosis of individuals having oral squamous cell carcinoma (OSCC). OSCC harbors a subpopulation of CD44(+) cells that exhibit cancer stem-like cell (CSC) characteristics are involved in malignant tumor phenotype and radioresistance. Nevertheless, the underlying molecular mechanisms in CD44( + )-OSCC remain unclear. The current investigation demonstrated that methyltransferase-like 3 (METTL3) is highly expressed in CD44(+) cells and promotes CSCs phenotype. Using RNA-sequencing analysis, we further showed that Spalt-like transcription factor 4 (SALL4) is involved in the maintenance of CSCs properties. Furthermore, the overexpression of SALL4 in CD44( + )-OSCC cells caused radioresistance in vitro and in vivo. In contrast, silencing SALL4 sensitized OSCC cells to radiation therapy (RT). Mechanistically, we illustrated that SALL4 is a direct downstream transcriptional regulation target of METTL3, the transcription activation of SALL4 promotes the nuclear transport of β-catenin and the expression of downstream target genes after radiation therapy, there by activates the Wnt/β-catenin pathway, effectively enhancing the CSCs phenotype and causing radioresistance. Herein, this study indicates that the METTL3/SALL4 axis promotes the CSCs phenotype and resistance to radiation in OSCC via the Wnt/β-catenin signaling pathway, and provides a potential therapeutic target to eliminate radioresistant OSCC.

Indexed as

Carcinoma, Squamous CellHead and Neck NeoplasmsMouth NeoplasmsAdeninebeta CateninCell Line, TumorCell ProliferationHumansMethyltransferasesNeoplasm Recurrence, LocalNeoplastic Stem CellsSquamous Cell Carcinoma of Head and NeckTranscription Factors6-methyladenineAdeninebeta CateninMethyltransferasesMETTL3 protein, humanSALL4 protein, humanTranscription Factors

Identifiers

PMID38355684
PMCPMC10866932
OpenAlexW4391815907

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.