Evidence map›Paper›PMID 39821576›Full record

ArticleCancer medicine2025

YTHDF1 Regulates RELA m6A Modification and Activates the NF-Kappa B Signaling Pathway to Promote the Mechanism of Gastric Cancer.

Yangyuan Huang, Shihao Liang, Liping Li, Qingyu Zeng, Bin Li

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Article in Cancer medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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2citing papers in PubMed
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2 citing papers in PubMed.

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5 · Who and what money

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5 authors.

Yangyuan HuangDepartment of Gastroenterology, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, People's Republic of China.
Shihao LiangDepartment of Gastroenterology, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, People's Republic of China.
Liping LiDepartment of Gastroenterology, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, People's Republic of China.
Qingyu ZengDepartment of Gastroenterology, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, People's Republic of China.
Bin LiDepartment of Gastroenterology, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, People's Republic of China.ORCID https://orcid.org/0009-0005-7862-9284

Funding

General Program of National Natural Science Foundation of China 82173075Innovation Project of Guangxi Graduate Education YCBZ2024182the Department of Science and Technology of Guangxi Zhuang Autonomous Region, Guangxi Science and Technology Program Project under grant, Guangxi Clinical Medical Research Center for Early Diagnosis and Treatment of Gastric Cancer AD23026091
6 · The paper itself

Abstract

backgroundGastric cancer (GC) is an important cause of death. Molecular targeted therapy and immunotherapy are progressing rapidly. It is very important to explore the pathogenesis pathways of GC and provide strong support for its treatment. However, the mechanism of occurrence and development of GC is still unclear.

methodsOnline databases and immunohistochemistry (IHC) of clinical samples were used to analyze the differential expression of YTHDF1 in the GC and nearby tissues, and its effect on survival prognosis. In vitro experimental study of GC, other mechanisms and functional analyses were specifically designed and performed too.

resultsOnline data and clinical samples analysis showed that the expression of YTHDF1 in GC was markedly elevated compared to surrounding tissues. Higher YTHDF1 levels were correlated with worse survival outcomes. Analysis of correlation with clinical parameters showed that the expression level of YTHDF1 exhibited a favorable correlation with lymphatic metastases, as well as with PD-1 and PD-L1 levels. In vitro studies of YTHDF1 overexpression have demonstrated its ability to enhance GC cell growth and migration while inhibiting apoptosis. Based on our results, RELA is a downstream target of YTHDF1, and YTHDF1 triggers the NF-κB signaling pathway by regulating RELA translation.

conclusionIn comparison to adjacent tissues, GC exhibits significantly elevated YTHDF1 expression. Increased YTHDF1 expression in the GC is correlated with decreased patient survival. Lymph node metastasis and the expression of PD-1 and PD-L1 are positively correlated with YTHDF1 levels. YTHDF1 inhibits apoptosis while promoting the migration and proliferation of GC. Additionally, it stimulates the NF-κB pathway and controls the translation of RELA.

Indexed as

NF-kappa BRNA-Binding ProteinsStomach NeoplasmsTranscription Factor RelAApoptosisB7-H1 AntigenCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMaleMiddle AgedPrognosisSignal TransductionB7-H1 AntigenCD274 protein, humanNF-kappa BRELA protein, humanRNA-Binding ProteinsTranscription Factor RelAYTHDF1 protein, humangastric cancerNF‐kappa B signaling pathwayRELAYTHDF1

Identifiers

PMID39821576
PMCPMC11740084

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