Evidence map›Paper›PMID 38566554›Full record

ArticleCancer science2024

YTHDC1-dependent m6A modification modulated FOXM1 promotes glycolysis and tumor progression through CENPA in triple-negative breast cancer.

Xi Shen, Jianxin Zhong, Pan Yu, Feng Liu, Haoran Peng, Nianyong Chen

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

14 citing papers in PubMed, 15 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

6 authors at 6 institutions in 2 countries.

Xi ShenDepartment of Oncology, The Eighth Affiliated Hospital, Sun Yat-sen University, Shenzhen, China.ORCID https://orcid.org/0000-0001-7832-9154
Jianxin ZhongKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Breast Oncology, Peking University Cancer Hospital & Institute, Beijing, China.ORCID https://orcid.org/0000-0002-9525-6222
Pan YuDepartment of Health Management, The Second Hospital Affiliated to Chongqing Medical University, Chongqing, China.
Feng LiuDepartment of Thyroid and Breast Surgery, Wuhan Fourth Hospital, Wuhan, China.ORCID https://orcid.org/0009-0006-4314-1649
Haoran PengDepartment of Stomatology, Shenzhen Hospital, University of Chinese Academy of Sciences, Shenzhen, China.ORCID https://orcid.org/0009-0003-9818-9103
Nianyong ChenDepartment of Radiation Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, China.ORCID https://orcid.org/0000-0003-0825-3048
Chinese University of Hong Kong, Shenzhen · CNDalian Medical University · CNPeking University · CNSichuan University · CNSun Yat-sen University · CNWuhan Puai Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) exhibits heightened aggressiveness compared with other breast cancer (BC) subtypes, with earlier relapse, a higher risk of distant metastasis, and a worse prognosis. Transcription factors play a pivotal role in various cancers. Here, we found that factor forkhead box M1 (FOXM1) expression was significantly higher in TNBC than in other BC subtypes and normal tissues. Combining the findings of Gene Ontology (GO) enrichment analysis and a series of experiments, we found that knockdown of the FOXM1 gene attenuated the ability of TNBC cells to proliferate and metastasize both in vivo and in vitro. In addition, Spearman's test showed that FOXM1 significantly correlated with glycolysis-related genes, especially centromere protein A (CENPA) in datasets (GSE76250, GSE76124, GSE206912, and GSE103091). The effect of silencing FOXM1 on the inhibition of CENPA expression, TNBC proliferation, migration, and glycolysis could be recovered by overexpression of CENPA. According to MeRIP, the level of m6A modification on FOMX1 decreased in cells treated with cycloleucine (a m6A inhibitor) compared with that in the control group. The increase in FOXM1 expression caused by YTHDC1 overexpression could be reversed by the m6A inhibitor, which indicated that YTHDC1 enhanced FOXM1 expression depending on m6A modification. Therefore, we concluded that the YTHDC1-m6A modification/FOXM1/CENPA axis plays an important role in TNBC progression and glycolysis.

Indexed as

Cell ProliferationDisease ProgressionForkhead Box Protein M1Gene Expression Regulation, NeoplasticGlycolysisTriple Negative Breast NeoplasmsAdenosineAnimalsCell Line, TumorCell MovementCentromere Protein AChromosomal Proteins, Non-HistoneFemaleHumansMiceMice, NudeAdenosineCENPA protein, humanCentromere Protein AChromosomal Proteins, Non-HistoneForkhead Box Protein M1FOXM1 protein, humanNerve Tissue ProteinsN-methyladenosineRNA Splicing FactorsYTHDC1 protein, humanCENPAFOXM1 transcription factorglycolysisTNBCYTHDC1‐dependent m6A modification

Identifiers

PMID38566554
PMCPMC11145146
OpenAlexW4393864081

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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.