Evidence map›Paper›PMID 41296387›Full record

ArticleCurrent issues in molecular biology2025

CNPY3 Promotes Human Breast Cancer Progression and Metastasis via Modulation of the Tumor Microenvironment.

Xiaofeng Duan, Ran Zhao, Shaoli Sun, Beichu Guo, Zihai Li, Bei Liu

Abstract read
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Article in Current issues in molecular biology, 2025. 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

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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

6 authors.

Xiaofeng DuanDepartment of Microbiology & Immunology, Hollings Cancer Center, Medical University of South Carolina, 86 Jonathan Lucas Street, Charleston, SC 29425, USA.
Ran ZhaoDepartment of Microbiology & Immunology, Hollings Cancer Center, Medical University of South Carolina, 86 Jonathan Lucas Street, Charleston, SC 29425, USA.
Shaoli SunDepartment of Pathology, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA.
Beichu GuoDepartment of Microbiology & Immunology, Hollings Cancer Center, Medical University of South Carolina, 86 Jonathan Lucas Street, Charleston, SC 29425, USA.
Zihai LiDivision of Medical Oncology, Department of Internal Medicine, The Ohio State University Comprehensive Cancer Center, Columbus, OH 43210, USA.
Bei LiuDepartment of Microbiology & Immunology, Hollings Cancer Center, Medical University of South Carolina, 86 Jonathan Lucas Street, Charleston, SC 29425, USA.

Funding

Extrinsic and intrinsic factors regulating commensal-specific T helper-17 cellsU01AI125859 · NIAID · OHIO STATE UNIVERSITY · PI LIU, BEI · 2016 to 2020
$2.5M
Mechanism of gp96/grp94 in regulating plasma cells and myelomaR01CA193939 · NCI · OHIO STATE UNIVERSITY · PI LIU, BEI · 2016 to 2020
$1.7M
NCI NIH HHS R01 CA193939NIAID NIH HHS U01 AI125859NIH HHS CA193939, AI125859
6 · The paper itself

Abstract

Canopy FGF signaling regulator 3 (CNPY3) is a cochaperone of the molecular chaperone GRP94. CNPY3 is critical for the post-translational maturation of toll-like receptors and for regulating inflammasome signaling. However, the role of CNPY3 in cancer development and progression is still not fully understood. In this study, we aimed to investigate the role of CNPY3 in human breast cancer progression and metastasis. We used genomic and clinical information from multiple databases to profile CNPY3 and GRP94 in human cancers. We found that CNPY3 and GRP94 were elevated in human breast cancers compared to normal tissue. Higher expression of CNPY3 correlated with cancer progression and poor clinical outcomes in breast cancers. We confirmed these findings using a human breast cancer tissue array. We silenced CNPY3 in human breast cancer cells using a CRISPR/Cas9 system. For the first time, we found that deletion of CNPY3 significantly reduced tumor growth and metastasis in vitro and in vivo. Additionally, network and enrichment analyses revealed that changes in the unfolded protein response pathway and immune-related genes were significantly dependent on alterations in CNPY3 and GRP94. This study suggests that CNPY3 is a potential biomarker and novel therapeutic target for cancers.

Indexed as

CNPY3molecular chaperonetherapeutic targettumor microenvironmentunfolded protein response

Identifiers

PMID41296387
PMCPMC12651230

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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.