Evidence map›Paper›PMID 42775292›Full record

ArticleBreast cancer (Dove Medical Press)2026

RNA-Binding Protein CSTF2 Drives Immune Evasion and Malignant Progression in Breast Cancer by Degrading THSD1 mRNA.

TangXiaoMan Wang, Lei Yan, JiaLi Jiang, Jing He

Abstract read
In one paragraph

Article in Breast cancer (Dove Medical Press), 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

What it found

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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

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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

4 authors.

TangXiaoMan WangReproductive Center, The Central Hospital of Yongzhou, Yongzhou, Hunan, 425000, People's Republic of China.
Lei YanDepartment of Neurology, The Central Hospital of Yongzhou, Yongzhou, Hunan, 425000, People's Republic of China.
JiaLi JiangDepartment of Gynecology, The Central Hospital of Yongzhou, Yongzhou, Hunan, 425000, People's Republic of China.
Jing HeDepartment of Pharmacy, The Central Hospital of Yongzhou, Yongzhou, Hunan, 425000, People's Republic of China.ORCID 0009-0002-6462-1132

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Resistance to immunotherapy in breast cancer (BC) is intimately connected to the dynamic tumor immunoediting process. RNA-binding proteins (RBPs) are recognized as pivotal modulators of BC advancement. Cleavage stimulation factor 2 (CSTF2), a core factor involved in mRNA 3'-end maturation, shows significant overexpression in numerous cancers and is correlated with adverse clinical outcomes. However, the precise molecular mechanisms through which it drives malignancy by regulating immunoediting remain incompletely understood. Methods: This study performed a systematic evaluation of CSTF2's expression profile and prognostic significance in BC using data from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO). CSTF2 expression was modulated via knockdown and overexpression approaches to study core malignant traits, such as proliferative capacity and cell migration. The role of CSTF2 in immunoediting was examined through immune landscape analysis and flow cytometry. Results: Integrated bioinformatics identified a regulatory pathway whereby CSTF2 induces transcriptional upregulation of the immune checkpoint molecule programmed death-ligand 1 (PD-L1) by promoting degradation of thrombospondin type-1 domain-containing protein 1 (THSD1) mRNA. The consequent increase in PD-L1 expression potently inhibits CD8⁺ T cell-mediated tumoricidal activity, thereby facilitating immune escape and collectively accelerating malignant progression in BC. Conclusion: This study delineates the detailed molecular mechanisms by which the RBP CSTF2 exacerbates malignant progression, offering fresh theoretical insights and potential targets for targeted immunotherapeutic strategies in BC.

Indexed as

breast cancerCSTF2immunoeditingTHSD1tumor microenvironment

Identifiers

PMID42775292
PMCPMC13596459

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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.