Evidence map›Paper›PMID 29084211›Full record

ArticleOncogene2018

SPARCL1 suppresses osteosarcoma metastasis and recruits macrophages by activation of canonical WNT/β-catenin signaling through stabilization of the WNT-receptor complex.

S-J Zhao, Y-Q Jiang, N-W Xu, Q Li, Q Zhang, S-Y Wang, J Li, Y-H Wang, Y-L Zhang, S-H Jiang and 11 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.9field-weighted citation impact, top 5% of its field
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

49 citing papers in PubMed, 87 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. AAV-Sparcl1 promotes hair cell regeneration by increasing supporting cell plasticity.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. The oncogenic functions of SPARCL1 in bladder cancer.Journal of cellular and molecular medicine · 2024
    Article
  10. Article
  11. Article
  12. Review
  13. Sparcl1 and Atherosclerosis.Journal of inflammation research · 2023
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

21 authors at 5 institutions in 1 country.

S-J ZhaoDepartment of Orthopedics, the Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou, Jiangsu, China.
Y-Q JiangDepartment of Orthopedics, the Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou, Jiangsu, China.
N-W XuDepartment of Orthopedics, the Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou, Jiangsu, China.
Q LiState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Q ZhangDepartment of Orthopedics, the Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou, Jiangsu, China.
S-Y WangDepartment of Orthopedics, the Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou, Jiangsu, China.
J LiState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Y-H WangState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Y-L ZhangState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
S-H JiangState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Y-J WangDepartment of Orthopedics, the Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou, Jiangsu, China.
Y-J HuangDepartment of Orthopedics, the Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou, Jiangsu, China.
X-X ZhangState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
G-A TianState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
C-C ZhangDepartment of Obstetrics and Gynecology, Fengxian Hospital, Southern Medical University, Shanghai, China.
Y-Y LvDepartment of Obstetrics and Gynecology, Fengxian Hospital, Southern Medical University, Shanghai, China.
M DaiDepartment of Obstetrics and Gynecology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
F LiuDepartment of Obstetrics and Gynecology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
R ZhangDepartment of Obstetrics and Gynecology, Fengxian Hospital, Southern Medical University, Shanghai, China.
D ZhouDepartment of Orthopedics, the Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou, Jiangsu, China.
Z-G ZhangState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Shanghai Jiao Tong University · CNChangzhou No.2 People's Hospital · CNShanghai Cancer Institute · CNNanjing Medical University · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metastasis significantly reduces the survival rate of osteosarcoma (OS) patients. Therefore, identification of novel targets remains extremely important to prevent metastasis and treat OS. In this report, we show that SPARCL1 is downregulated in OS by epigenetic methylation of promoter DNA. In vitro and in vivo experiments revealed that SPARCL1 inhibits OS metastasis. We further demonstrated that SPARCL1-activated WNT/β-catenin signaling by physical interaction with various frizzled receptors and lipoprotein receptor-related protein 5/6, leading to WNT-receptor complex stabilization. Activation of WNT/β-catenin signaling contributes to the SPARCL1-mediated inhibitory effects on OS metastasis. Furthermore, we uncovered a paracrine effect of SPARCL1 on macrophage recruitment through activated WNT/β-catenin signaling-mediated secretion of chemokine ligand5 from OS cells. These findings suggest that the targeting of SPARCL1 as a new anti-metastatic strategy for OS patients.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisbeta CateninBiomarkers, TumorBone NeoplasmsCalcium-Binding ProteinsCell MovementCell ProliferationChemokine CCL5Extracellular Matrix ProteinsFrizzled ReceptorsHumansLow Density Lipoprotein Receptor-Related Protein-5Low Density Lipoprotein Receptor-Related Protein-6Lung Neoplasmsbeta CateninBiomarkers, TumorCalcium-Binding ProteinsCCL5 protein, humanChemokine CCL5CTNNB1 protein, humanExtracellular Matrix ProteinsFrizzled ReceptorsLow Density Lipoprotein Receptor-Related Protein-5Low Density Lipoprotein Receptor-Related Protein-6LRP5 protein, humanLRP6 protein, humanSPARCL1 protein, humanWnt Proteins

Identifiers

PMID29084211
PMCPMC5851113
OpenAlexW2766020779

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

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.