Evidence map›Paper›PMID 31578655›Full record

ReviewClinical & experimental metastasis2020

Harnessing the versatile role of OPG in bone oncology: counterbalancing RANKL and TRAIL signaling and beyond.

Maria V Deligiorgi, Mihalis I Panayiotidis, John Griniatsos, Dimitrios T Trafalis

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical & experimental metastasis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  3. Review
  4. Article
  5. MiR-217 regulates autophagy through OPG/RANKL/RANK in giant cell tumors.Journal of orthopaedic surgery and research · 2023
    Article
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  7. Article
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  10. 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

4 authors at 2 institutions in 2 countries.

Maria V DeligiorgiClinical Pharmacology Unit, Laboratory of Pharmacology, Faculty of Medicine, National and Kapodistrian University of Athens, 75 Mikras Asias Str, Goudi, 11527, Athens, Greece. mdeligiorgi@yahoo.com.ORCID http://orcid.org/0000-0002-0480-954X
Mihalis I PanayiotidisDepartment of Applied Sciences, Northumbria University, Ellison Building, Room A516, Newcastle upon Tyne, NE1 8ST, UK.
John Griniatsos1st Department of Surgery, Faculty of Medicine, National and Kapodistrian University of Athens, Laikon General Hospital, 17 Agiou Thoma Str, Goudi, 115-27, Athens, Greece.
Dimitrios T TrafalisClinical Pharmacology Unit, Laboratory of Pharmacology, Faculty of Medicine, National and Kapodistrian University of Athens, 75 Mikras Asias Str, Goudi, 11527, Athens, Greece.
National and Kapodistrian University of Athens · GRNorthumbria University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

More than 2 decades ago, the discovery of osteoprotegerin (OPG) as inhibitor of the receptor of activator of nuclear factor Kb (RANK) ligand (RANKL) revolutionized our understanding of bone biology and oncology. Besides acting as decoy receptor for RANKL, OPG acts as decoy receptor for tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). OPG, RANKL, and TRAIL are ubiquitously expressed, stimulating per se pivotal signaling cascades implicated in cancer. In the context of cancer cell-bone cell interactions, cancer cells skew the OPG/RANKL/RANK (RANKL cognate receptor) balance towards bone destruction and tumor growth through favoring the RANKL/RANK interface, circumventing OPG. Numerous preclinical and clinical studies demonstrate the dual role of OPG in cancer: antitumor and tumor-promoting. OPG potentially conveys an antitumor signal through inhibiting the tumor-promoting RANKL signaling-both the osteoclast-dependent and the osteoclast-independent-and the tumor-promoting TRAIL signaling. On the other hand, the presumed tumor-promoting functions of OPG are: (i) abrogation of TRAIL-induced apoptosis of cancer cells; (ii) abrogation of RANKL-induced antitumor immunity; and (iii) stimulation of oncogenic and prometastatic signaling cascades downstream of the interaction of OPG with diverse proteins. The present review dissects the role of OPG in bone oncology. It presents the available preclinical and clinical data sustaining the dual role of OPG in cancer and focuses on the imbalanced RANKL/RANK/OPG interplay in the landmark "vicious cycle" of skeletal metastatic disease, osteosarcoma, and multiple myeloma. Finally, current challenges and future perspectives in exploiting OPG signaling in bone oncology therapeutics are discussed.

Indexed as

AnimalsAntineoplastic AgentsApoptosisBone and BonesBone NeoplasmsClinical Trials as TopicDisease Models, AnimalDrug Screening Assays, AntitumorHumansImmunoconjugatesNeoplasm MetastasisOsteoblastsOsteoclastsOsteolysisOsteoprotegerinRANK LigandAntineoplastic AgentsImmunoconjugatesOsteoprotegerinRANK LigandTNF-Related Apoptosis-Inducing LigandBoneMetastasisMultiple myelomaOPGOsteosarcomaRANKLTRAIL

Identifiers

PMID31578655
OpenAlexW2977902215

What OpenQuestion holds

Textmetadata
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.