Evidence map›Paper›PMID 40161756›Full record

ArticlebioRxiv : the preprint server for biology2025

NCOR2 represses MHC class I molecule expression to drive metastatic progression of breast cancer.

Pavla Ticha, Jason J Northey, Kelly Kersten, Hugo González Velozo, Alastair J Ironside, Martin Zidek, Allison Drain, Jonathan N Lakins, Yunn-Yi Chen, Kelvin K Tsai and 1 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Pavla TichaDepartment of Surgery and Center for Bioengineering and Tissue Regeneration, University of California, San Francisco, San Francisco, CA 94143, USA.ORCID 0000-0002-1959-8618
Jason J NortheyDepartment of Surgery and Center for Bioengineering and Tissue Regeneration, University of California, San Francisco, San Francisco, CA 94143, USA.
Kelly KerstenDepartment of Pathology, University of California, San Francisco, San Francisco, CA 94143, USA.
Hugo González VelozoDepartment of Anatomy, University of California, San Francisco, San Francisco, CA 94143, USA.
Alastair J IronsideDepartment of Pathology, Western General Hospital, NHS Lothian, Edinburgh, UK.
Martin ZidekDepartment of Surgery and Center for Bioengineering and Tissue Regeneration, University of California, San Francisco, San Francisco, CA 94143, USA.
Allison DrainDepartment of Surgery and Center for Bioengineering and Tissue Regeneration, University of California, San Francisco, San Francisco, CA 94143, USA.
Jonathan N LakinsDepartment of Surgery and Center for Bioengineering and Tissue Regeneration, University of California, San Francisco, San Francisco, CA 94143, USA.
Yunn-Yi ChenDepartment of Pathology, University of California, San Francisco, San Francisco, CA 94143, USA.
Kelvin K TsaiLaboratory of Advanced Molecular Therapeutics, Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, 110301, Taiwan.
Valerie M WeaverDepartment of Surgery and Center for Bioengineering and Tissue Regeneration, University of California, San Francisco, San Francisco, CA 94143, USA.ORCID 0000-0003-4786-6752

Funding

Tissue mechanics reprograms the tissue to malignancy and metastasisR35CA242447 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI VALERIE MARIE WEAVER · 2020 to 2026
$6.6M
NCI NIH HHS R35 CA242447
6 · The paper itself

Abstract

Metastatic progression depends upon the ability of disseminated tumor cells to evade immune surveillance. MHC molecule expression facilitates T cell recognition and activation to permit the eradication of metastatic tumor cells. We identified nuclear corepressor 2 (NCOR2) as a key epigenetic regulator of MHC class I molecule expression on breast tumor cells. Patients with triple negative breast cancers (TNBC) that expressed high levels of NCOR2 also exhibited reduced metastasis free survival and decreased MHC class I expression, and the metastatic lesions in patients with TNBC had high nuclear NCOR2 and reduced CD8 T cell levels and activity. Genetically and experimentally reducing NCOR2 expression in tumor cells permitted interferon gamma upregulation of MHC class I, and potentiated CD8 T cell activity and induction of apoptosis to repress metastatic progression of disseminated breast cancer cells. These studies provide evidence to support NCOR2 as a targetable epigenetic regulator of metastasis towards which therapies could be developed to reduce patient mortality.

Identifiers

PMID40161756
PMCPMC11952456

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.