Evidence map›Paper›PMID 34447693›Full record

ArticleFrontiers in oncology2021

FOXM1 Promotes Head and Neck Squamous Cell Carcinoma

Xiao Ma, Hong Zhang, Qian Li, Erik Schiferle, Yao Qin, Suifang Xiao, Tiancheng Li

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
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  9. FOXM1 promotes TGF-β2-induced injury of human lens epithelial cells by up regulating VEGFA expression.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2023
    Article
  10. Review
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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

7 authors at 5 institutions in 2 countries.

Xiao MaDepartment of Head and Neck Surgery, Perking University Cancer Hospital and Institute, Beijing, China.
Hong ZhangDepartment of Pathology, Peking University First Hospital, Beijing, China.
Qian LiDepartment of Radiology, Massachusetts General Hospital, Boston, MA, United States.
Erik SchiferleCenter for Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA, United States.
Yao QinDepartment of Otorhinolaryngology-Head and Neck Surgery, Peking University First Hospital, Beijing, China.
Suifang XiaoDepartment of Otorhinolaryngology-Head and Neck Surgery, Peking University First Hospital, Beijing, China.
Tiancheng LiDepartment of Otorhinolaryngology-Head and Neck Surgery, Peking University First Hospital, Beijing, China.
Peking University First Hospital · CNHarvard University · USMassachusetts General Hospital · USPeking University · CNPeking University Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimPrevious literature has implicated the sustained expression of FOXM1 in numerous human cancers, including head and neck squamous cell carcinoma (HNSCC). The current study aimed to elucidate the function and regulatory mechanism of FOXM1 in HNSCC.

methodsWestern blot and RT-qPCR methods were performed to evaluate the expression of Linc-ROR, FOXM1, and LMO4 in HNSCC tissue samples and cells. The binding between FOXM1 and Linc-ROR was analyzed using a ChIP assay. Various cellular processes including proliferation and invasion abilities were assessed following alteration of FOXM1, Linc-ROR and LMO4 expression in HNSCC cells. Xenograft mouse models were established to validate the

resultsLinc-ROR and FOXM1 were highly expressed in HNSCC tissues and cells. FOXM1 operated as a potential transcription factor to bind to the promoter region of Linc-ROR. Linc-ROR and FOXM1 exhibited high expression levels in both the clinical tissue samples as well as the HNSCC cells, which could facilitate the proliferation and invasion of HNSCC cells. Linc-ROR upregulated the expression of LMO4 and promoted activation of the AKT/PI3K signaling pathway, thus stimulating the proliferation and invasion of HNSCC cells. Silencing of Linc-ROR brought about a contrasting effect relative to that seen when FOXM1 was overexpressed in HNSCC

conclusionsOverall, FOXM1 promoted the expression of Linc-ROR and induced the activation of the LMO4-dependent AKT/PI3K signaling pathway, thus facilitating the occurrence and development of HNSCC.

Indexed as

Akt/PI3KFoxM1head and neck squamous cell carcinomainvasionlinc-RORLMO4proliferation

Identifiers

PMID34447693
PMCPMC8383294
OpenAlexW3192117953

What OpenQuestion holds

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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.