Evidence map›Paper›PMID 40637745›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2026

FBXO45 enhances cell viability and glycolysis in cervical cancer via DUSP2 ubiquitination-mediated ERK1/2 activation.

Huaguo Xiang, Junfang Sun, Lingyue Kong, Yingzhen Wang, Xiaorou Qiu, Guo Li, Jiehong He, Jinting Zeng

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Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Huaguo Xiang *Department of Clinical Laboratory, Fuyong Peoples Hospital of Baoan District, Shenzhen, 518103, China.
Junfang Sun *Department of Clinical Laboratory, Fuyong Peoples Hospital of Baoan District, Shenzhen, 518103, China.
Lingyue KongDepartment of Clinical Laboratory, Fuyong Peoples Hospital of Baoan District, Shenzhen, 518103, China.
Yingzhen WangDepartment of Clinical Laboratory, Fuyong Peoples Hospital of Baoan District, Shenzhen, 518103, China.
Xiaorou QiuDepartment of Clinical Laboratory, Fuyong Peoples Hospital of Baoan District, Shenzhen, 518103, China.
Guo LiDepartment of Clinical Laboratory, Fuyong Peoples Hospital of Baoan District, Shenzhen, 518103, China.
Jiehong HeDepartment of Clinical Laboratory, Fuyong Peoples Hospital of Baoan District, Shenzhen, 518103, China.
Jinting ZengDepartment of Clinical Laboratory, Fuyong Peoples Hospital of Baoan District, Shenzhen, 518103, China. 13902472463@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

F-box protein 45 (FBXO45) is implicated in tumorigenesis and progression. However, the functions and underlying mechanisms of FBXO45 in cervical cancer (CC) have not been elucidated. This study investigated the role of FBXO45 in the malignant progression of CC cells. Gene expression profiling interactive analysis, tissue microarrays, quantitative real-time PCR, and gene enrichment analysis confirmed the correlation between FBXO45 and CC. FBXO45-knockdown and FBXO45-overexpressing HeLa cells and Caski cells were utilized to evaluate cell viability, metabolic characteristics and protein expression via CCK-8, Seahorse assays, measurement of lactate production, and Western blotting (WB). A mouse xenograft model validated the effects of FBXO45 knockdown. Concurrently, FBXO45-dual specificity phosphatase 2 (DUSP2) interaction was investigated using co-immunoprecipitation and WB. Overexpression of FBXO45 in CC tissues and cell lines was observed. Functional studies revealed that FBXO45 promoted cell viability, glycolysis, and ERK1/2 activation. FBXO45 interacted with and ubiquitinated DUSP2, leading to ERK1/2 activation and enhanced glycolysis. Tissue microarrays and Spearman correlation analysis confirmed the negative correlation between FBXO45 and DUSP2 in CC tissues. In summary, our results suggest that FBXO45 enhances cell viability and glycolysis in CC via DUSP2 ubiquitination-mediated ERK1/2 activation. Our findings identify FBXO45 as a therapeutic target for CC, guiding the development of new drugs.

Indexed as

Dual Specificity Phosphatase 2F-Box ProteinsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Uterine Cervical NeoplasmsAnimalsCell Line, TumorCell SurvivalFemaleGlycolysisHeLa CellsHumansMAP Kinase Signaling SystemMiceMice, Inbred BALB CMice, NudeDual Specificity Phosphatase 2F-Box ProteinsMAPK1 protein, humanMAPK3 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Cervical cancerDUSP2ERK1/2FBXO45GlycolysisUbiquitination

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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 Socratic graph.