Evidence map›Paper›PMID 41053718›Full record

ArticleBMC cancer2025

ACOXL-AS1's pan-cancer dynamics and its proliferative impact on endometrial endometrioid carcinoma.

Hongrong Wu, Ruilin Lin, Liangli Hong

Abstract read
In one paragraph

Article in BMC cancer, 2025. 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

3 authors.

Hongrong WuDepartment of Pathology, First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, 515041, China.
Ruilin LinDepartment of Pathology, First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, 515041, China.
Liangli HongDepartment of Pathology, First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, 515041, China. hong_liangli@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLong non-coding RNAs (lncRNAs) are critically involved in carcinogenesis; however, the pan-cancer significance and functional mechanisms of ACOXL-AS1 remain largely uncharacterized. This study comprehensively investigates the expression landscape, prognostic value, and biological impact of ACOXL-AS1 across multiple malignancies, with a specific focus on its pro-proliferative role in endometrial endometrioid carcinoma (EEC).

methodsWe analyzed ACOXL-AS1 expression and its association with clinical outcomes using pan-cancer RNA-seq data from TCGA and GTEx databases. Functional validation was performed in EEC cell lines (HHUA, HEC-1 A) via lentivirus-mediated overexpression, followed by CCK-8, colony formation, and transwell migration/invasion assays. Mechanistic insights were investigated using integrated bioinformatics approaches.

resultsACOXL-AS1 was significantly downregulated in most cancers, and higher expression correlated with improved prognosis. Elevated ACOXL-AS1 levels were associated with smaller tumor size, lower disease stage, reduced metastasis, and decreased tumor mutational burden (TMB)/microsatellite instability (MSI). It also modulated the immunosuppressive tumor microenvironment. Critically, ACOXL-AS1 overexpression significantly inhibited EEC cell proliferation, migration, invasion, and tumor growth in xenograft models. Mechanistically, it may regulate RPA4 expression through the homologous recombination pathway in EEC cells.

conclusionsACOXL-AS1 may play a role as a tumor suppressor in endometrial endometrioid carcinoma (EEC), suggesting its potential as a prognostic biomarker and a candidate for further exploration as a therapeutic target.

Indexed as

Carcinoma, EndometrioidEndometrial NeoplasmsRNA, Long NoncodingAnimalsBiomarkers, TumorCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMiceMice, NudePrognosisTumor MicroenvironmentXenograft Model Antitumor AssaysBiomarkers, TumorRNA, Long NoncodingACOXL-AS1Cancer progressionEndometrial carcinomaImmune evasion

Identifiers

PMID41053718
PMCPMC12502427

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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.