Evidence map›Paper›PMID 40337977›Full record

ArticleProtein and peptide letters2025

Inhibition of Canonical Wnt Signaling in Renal Cell Carcinoma Bone Metastasis: An Immunohistochemical Analysis of DKK1 and LRP5 Expression.

Zixiong Huang, Yiqing Du, Huaqi Yin, Gongwei Wang, Tao Xu

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Article in Protein and peptide letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

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8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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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

Who cites it

8 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Zixiong HuangDepartment of Urology, Peking University People's Hospital, Beijing, China.
Yiqing DuDepartment of Urology, Peking University People's Hospital, Beijing, China.
Huaqi YinDepartment of Urology, Peking University People's Hospital, Beijing, China.
Gongwei WangDepartment of Pathology, Peking University People's Hospital, Beijing, China.
Tao XuDepartment of Urology, Peking University People's Hospital, Beijing, China.

Funding

Peking University People's Hospital Research and Development Funds RDY2021-20, RDJP2023-20
6 · The paper itself

Abstract

BACKGROUND AND

objectiveCanonical Wnt (Wnt/β-catenin) signaling maintains bone homeostasis by promoting osteoblastic activities. The inhibitory factor, Dickkopf-1 (DKK1), enhances bone resorption in malignant diseases. Low-density lipoprotein-related protein (LRP) 5 is antagonized by DKK1. This study aimed to investigate the expression of DKK1 and LRP5 in renal cell carcinoma bone metastasis (RCC-BM).

methodsRCC-BM patients with paired samples of primary and metastatic lesions were selected for the study (RCC-BM group). RCC patients without any metastasis served as the control group (RCC-only group). Immunohistochemical staining with monoclonal anti-DKK1 and polyclonal anti- LRP5 antibody was conducted on paraffin-embedded slides. The staining results were recorded using scoring according to staining intensity in the renal tissue adjacent to the tumor, primary RCC lesions, and RCC-BM lesions.

resultsDKK1 was differently expressed among normal renal tissues, primary RCC, and RCC- BM tissues (p<0.001). The DKK1 expression in primary RCC was significantly lower than that in normal renal tissues (p<0.001) without a difference between the RCC-BM and RCC-only groups. DKK1 expression in bone metastasis was significantly higher than that in primary tumors (p<0.001). For RCC-BM patients, the expression of LRP5 in the primary tumor was significantly lower than that in adjacent renal tissues (p<0.01). The tendency of lower expression was found in primary RCC from RCC-BM patients compared to RCC without metastasis (p=0.073).

conclusionA "rebound" pattern of DKK1 expression in bone metastasis lesions and the decreasing LRP5 expression in primary lesions of RCC-BM patients suggested that Wnt/β-catenin signaling was inhibited in RCC-BM. The overexpression of DKK1 and reduced expression of LRP5 suggest that these markers may be useful for the early prediction of RCC-BM.

Indexed as

Bone NeoplasmsCarcinoma, Renal CellIntercellular Signaling Peptides and ProteinsKidney NeoplasmsLow Density Lipoprotein Receptor-Related Protein-5Wnt Signaling PathwayAdultAgedFemaleHumansImmunohistochemistryMaleMiddle AgedDKK1 protein, humanIntercellular Signaling Peptides and ProteinsLow Density Lipoprotein Receptor-Related Protein-5LRP5 protein, humanbone metastasisDickkopf-1low-density lipoprotein related receptor protein 5Renal cell carcinomatyrosine kinase inhibitors.Wnt/β-catenin signaling

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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.