Evidence map›Paper›PMID 30237403›Full record

ArticleCell death & disease2018

CCN6-mediated MMP-9 activation enhances metastatic potential of human chondrosarcoma.

Huey-En Tzeng, Chih-Hsin Tang, Sz-Hua Wu, Hsien-Te Chen, Yi-Chin Fong, Yung-Chang Lu, Wei-Cheng Chen, Hsien-Da Huang, Chih-Yang Lin, Shih-Wei Wang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  9. Structural insights into regulation of CCN protein activities and functions.Journal of cell communication and signaling · 2023
    Review
  10. Review
  11. Article
  12. The CCN axis in cancer development and progression.Journal of cell communication and signaling · 2021
    Review
  13. Article
  14. Article
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  16. Article
  17. Review
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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

10 authors at 7 institutions in 1 country.

Huey-En TzengTaipei Cancer Center, Taipei Medical University, Taipei, 110, Taiwan.
Chih-Hsin TangChinese Medicine Research Center, China Medical University, Taichung, 404, Taiwan.
Sz-Hua WuSchool of Pharmacy, China Medical University, Taichung, 404, Taiwan.
Hsien-Te ChenSchool of Chinese Medicine, China Medical University, Taichung, 404, Taiwan.
Yi-Chin FongDepartment of Sports Medicine, College of Health Care, China Medical University, Taichung, 404, Taiwan.
Yung-Chang LuDepartment of Medicine, Mackay Medical College, New Taipei City, 252, Taiwan.
Wei-Cheng ChenDepartment of Orthopaedics, MacKay Memorial Hospital, Taipei, 104, Taiwan.
Hsien-Da HuangDegree Program of Biomedical Science and Engineering, National Chiao Tung University, Hsinchu, 300, Taiwan.
Chih-Yang LinDepartment of Medicine, Mackay Medical College, New Taipei City, 252, Taiwan. p123400@hotmail.com.
Shih-Wei WangDepartment of Medicine, Mackay Medical College, New Taipei City, 252, Taiwan. shihwei@mmc.edu.tw.
China Medical University · TWMackay Medical College · TWMackay Memorial Hospital · TWChina Medical University Beigang Hospital · TWChina Medical University Hospital · TWNational Yang Ming Chiao Tung University · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chondrosarcomas are primary malignant bone tumors that have a poor prognosis. WNT1-inducible signaling pathway protein-3 (WISP-3, also termed CCN6) belongs to the CCN family of proteins and is implicated in the regulation of various cellular functions, such as cell proliferation, differentiation, and migration. It is unknown as to whether CCN6 affects human chondrosarcoma metastasis. We show how CCN6 promotes chondrosarcoma cell migration and invasion via matrix metallopeptidase-9 (MMP)-9 expression. These effects were abolished by pretreatment of chondrosarcoma cells with PI3K, Akt, mTOR, and NF-κB inhibitors or short interfering (si)RNAs. Our investigations indicate that CCN6 facilitates metastasis through the PI3K/Akt/mTOR/NF-κB signaling pathway. CCN6 and MMP-9 expression was markedly increased in the highly migratory JJ012(S10) cell line compared with the primordial cell line (JJ012) in both in vitro and in vivo experiments. CCN6 knockdown suppressed MMP-9 production in JJ012(S10) cells and attenuated cell migration and invasion ability. Importantly, CCN6 knockdown profoundly inhibited chondrosarcoma cell metastasis to lung. Our findings reveal an important mechanism underlying CCN6-induced metastasis and they highlight the clinical significance between CCN6 and MMP-9 in regard to human chondrosarcoma. CCN6 appears to be a promising therapeutic target in chondrosarcoma metastasis.

Indexed as

AnimalsBlotting, WesternBone NeoplasmsCCN Intercellular Signaling ProteinsCell Line, TumorCell MovementCell ProliferationChondrosarcomaGene Expression Regulation, NeoplasticHumansMaleMatrix Metalloproteinase 9MiceMice, Inbred BALB CMice, NudeNF-kappa BCCN6 protein, humanCCN6 protein, mouseCCN Intercellular Signaling ProteinsMatrix Metalloproteinase 9NF-kappa B

Identifiers

PMID30237403
PMCPMC6147788
OpenAlexW2891830250

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.