ArticleCommunications biology2020
Aberrant (pro)renin receptor expression induces genomic instability in pancreatic ductal adenocarcinoma through upregulation of SMARCA5/SNF2H.
Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- How histone modifications influence cellular radiosensitivity: Pharmaceutically targeting epigenetic regulators as a promising avenue to overcome radioresistance.Acta pharmaceutica Sinica. B · 2025Review
- Advances in Understanding Renin-Angiotensin System-Mediated Anti-Tumor Activity of Natural Polyphenols.Biomolecules · 2025Review
- Identification of multiple organ metastasis-associated hub mRNA/miRNA signatures in non-small cell lung cancer.Cell death & disease · 2023Article
- Mapping the protein binding site of the (pro)renin receptor using in silico 3D structural analysis.Hypertension research : official journal of the Japanese Society of Hypertension · 2023Article
- Targeting Chromatin-Remodeling Factors in Cancer Cells: Promising Molecules in Cancer Therapy.International journal of molecular sciences · 2022Review
- Article
Corrections and comments
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Authors and funding
20 authors at 8 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
(Pro)renin receptor [(P)RR] has a role in various diseases, such as cardiovascular and renal disorders and cancer. Aberrant (P)RR expression is prevalent in pancreatic ductal adenocarcinoma (PDAC) which is the most common pancreatic cancer. Here we show whether aberrant expression of (P)RR directly leads to genomic instability in human pancreatic ductal epithelial (HPDE) cells. (P)RR-expressing HPDE cells show obvious cellular atypia. Whole genome sequencing reveals that aberrant (P)RR expression induces large numbers of point mutations and structural variations at the genome level. A (P)RR-expressing cell population exhibits tumour-forming ability, showing both atypical nuclei characterised by distinctive nuclear bodies and chromosomal abnormalities. (P)RR overexpression upregulates SWItch/Sucrose Non-Fermentable (SWI/SNF)-related, matrix-associated, actin-dependent regulator of chromatin, subfamily a, member 5 (SMARCA5) through a direct molecular interaction, which results in the failure of several genomic stability pathways. These data reveal that aberrant (P)RR expression contributes to the early carcinogenesis of PDAC.
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Registered trials
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