Regulatory BC200 RNA promotes breast carcinogenesis by repressing BRCA1 gene expression.

Valerio Berardi, Ilham A Muslimov, Dan Sun, Giuseppe Militello, Prem Premsrirut, Henri Tiedge

Abstract read

In one paragraph

Article in iScience, 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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0citing 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

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3 · Its place in the literature

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Valerio BerardiDepartment of Physiology and Pharmacology, State University of New York Downstate Health Sciences University, Brooklyn, NY 11203, USA.

Ilham A MuslimovDepartment of Physiology and Pharmacology, State University of New York Downstate Health Sciences University, Brooklyn, NY 11203, USA.

Dan SunMirimus Inc., Brooklyn, NY 11226, USA.

Giuseppe MilitelloMirimus Inc., Brooklyn, NY 11226, USA.

Prem PremsrirutMirimus Inc., Brooklyn, NY 11226, USA.

Henri TiedgeDepartment of Physiology and Pharmacology, State University of New York Downstate Health Sciences University, Brooklyn, NY 11203, USA.

Funding

Translational Control in NeuronsR01NS046769 · NINDS · SUNY DOWNSTATE MEDICAL CENTER · PI TIEDGE, HENRI · 2003 to 2019

$4.8M

NINDS NIH HHS R01 NS046769

6 · The paper itself

Abstract

Downregulation of the BRCA1 gene expression has been implicated in hereditary and sporadic breast cancer. Expression of regulatory BC200 RNA, which is normally restricted to neurons, is dysregulated in invasive breast carcinoma cells, giving rise to high cellular RNA levels. However, the molecular mechanisms by which BC200 RNA contributes to breast cancer malignancy remain poorly understood. Here, we show that atypical BC200 RNA expression in breast epithelial cells results in malignant transformation. By repressing the translation of BRCA1 mRNA, BC200 RNA reduces BRCA1 protein expression in breast epithelial cells, leading to increased DNA damage and carcinogenesis. RNAi-mediated downregulation of BC200 RNA restores the normal, non-malignant phenotype. Tumor innervation stimulates BC200 RNA expression, indicating a role of the nervous system in tumor formation. Thus, in a hitherto unreported molecular mechanism, neuronal BC200 RNA promotes breast carcinogenesis by repressing the expression of the tumor suppressor BRCA1. These findings indicate the utility of BC200 RNA in breast cancer therapy.

Indexed as

Biological sciencesCancerCancer systems biologyMolecular mechanism of gene regulation

Identifiers

PMID41907432

DOI10.1016/j.isci.2026.115267

PMCPMC13018867

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LicenceCC BY-NC-ND

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