Evidence map›Paper›PMID 42305506›Full record

ArticleTranslational cancer research2026

WT1-AS acts as a tumor suppressor in cervical cancer via OSR2-mediated transcriptional activation.

Gulimire Buranjiang, Li Xie, Yang Wang, Shiying Jin, Yina Wang

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Article in Translational cancer research, 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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5 · Who and what money

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5 authors.

Gulimire BuranjiangDepartment of Gynecologic Oncology Radiation Therapy (Ward II), Xinjiang Medical University, Xinjiang Medical University Third Clinical Medical College (Affiliated Tumor Hospital), Urumqi, China.
Li XieFirst Department of Gynecological Tumor Radiotherapy, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China.
Yang WangSecond Department of Thoracic Surgery, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China.
Shiying JinSecond Department of Thoracic Surgery, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China.
Yina WangFirst Department of Gynecological Tumor Radiotherapy, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Cervical cancer (CESC) remains a major global health burden, and its molecular mechanisms are not fully understood. Long non-coding RNAs (lncRNAs) have emerged as critical regulators in tumor biology. Among them, Wilms tumor 1 antisense RNA (WT1-AS) has been implicated in several cancers, but its role in CESC is largely unknown. Therefore, this study aimed to investigate the expression pattern, prognostic significance, biological function, and upstream transcriptional regulation of WT1-AS in CESC. Methods: We performed a comprehensive analysis integrating The Cancer Genome Atlas (TCGA) pan-cancer and CESC datasets to examine the expression profile and prognostic relevance of WT1-AS. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment, and single-cell RNA sequencing analyses were conducted to explore its biological functions. Functional assays, including Western blotting, flow cytometry, and xenograft mouse models, were performed to validate the effects of WT1-AS on apoptosis and tumor growth. Upstream transcriptional regulation was investigated using transcription factor prediction, co-expression analysis, and luciferase reporter assays. Results: WT1-AS was significantly dysregulated across multiple cancers and correlated with poor prognosis in several tumor types. In CESC, WT1-AS was primarily expressed in malignant epithelial cells and fibroblasts and was functionally enriched in apoptosis- and extracellular matrix-related pathways. Overexpression of WT1-AS promoted apoptosis, as evidenced by increased cleaved-caspase3 and cleaved-PARP expression, and suppressed tumor growth Conclusions: Our findings reveal that WT1-AS functions as a tumor suppressor in CESC by promoting apoptosis and identify OSR2 as a novel upstream regulator. The WT1-AS/OSR2 axis may have biological and potential prognostic relevance in CESC, although its clinical applicability requires further validation.

Indexed as

apoptosisCervical cancer (CESC)long non-coding RNAs (lncRNAs)pan-cancertranscriptional regulationWilms tumor 1 antisense RNA (WT1-AS)

Identifiers

PMID42305506
PMCPMC13265220

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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.