Evidence map›Paper›PMID 29190493›Full record

ArticleNeoplasia (New York, N.Y.)2018

BIGH3 Promotes Osteolytic Lesions in Renal Cell Carcinoma Bone Metastasis by Inhibiting Osteoblast Differentiation.

Tianhong Pan, Song-Chang Lin, Kai-Jie Yu, Guoyu Yu, Jian H Song, Valerae O Lewis, Justin E Bird, Bryan Moon, Patrick P Lin, Nizar M Tannir and 6 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neoplasia (New York, N.Y.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.2field-weighted citation impact, top 40% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

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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

16 authors at 2 institutions in 2 countries.

Tianhong PanDepartment of Orthopedic Oncology, University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
Song-Chang LinDepartment of Translational Molecular Pathology, University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
Kai-Jie YuDepartment of Urology, University of Texas, MD Anderson Cancer Center, Houston, TX, USA; Division of Urology, Department of Surgery, Chang Gung Memorial Hospital at Linkou, Chang Gung University College of Medicine, Taoyuan, Taiwan; Department of Chemical Engineering and Biotechnology and Graduate Institute of Biochemical and Biomedical Engineering, National Taipei University of Technology, Taipei, Taiwan.
Guoyu YuDepartment of Translational Molecular Pathology, University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
Jian H SongDepartment of Genitourinary Medical Oncology, University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
Valerae O LewisDepartment of Orthopedic Oncology, University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
Justin E BirdDepartment of Orthopedic Oncology, University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
Bryan MoonDepartment of Orthopedic Oncology, University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
Patrick P LinDepartment of Orthopedic Oncology, University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
Nizar M TannirDepartment of Genitourinary Medical Oncology, University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
Eric JonaschDepartment of Genitourinary Medical Oncology, University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
Christopher G WoodDepartment of Urology, University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
Gary E GallickDepartment of Genitourinary Medical Oncology, University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
Li-Yuan Yu-LeeDepartment of Medicine, Baylor College of Medicine, Houston, TX, USA.
Sue-Hwa LinDepartment of Translational Molecular Pathology, University of Texas, MD Anderson Cancer Center, Houston, TX, USA; Department of Genitourinary Medical Oncology, University of Texas, MD Anderson Cancer Center, Houston, TX, USA. Electronic address: slin@mdanderson.org.
Robert L SatcherDepartment of Orthopedic Oncology, University of Texas, MD Anderson Cancer Center, Houston, TX, USA. Electronic address: rlsatcher@mdanderson.org.
The University of Texas MD Anderson Cancer Center · USNational Taipei University of Technology · TW

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Targeting Tumor Microenvironment-Induced Therapy Resistance in Prostate Cancer Bone MetastasisP50CA140388 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LOGOTHETIS, CHRISTOPHER J., THOMPSON, TIMOTHY CHARLES · 2009 to 2022
$23.4M
Endothelial-to-osteoblast transition in prostate cancer bone metastasisR01CA174798 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LIN, SUE-HWA · 2013 to 2023
$3.0M
NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA140388NCI NIH HHS R01 CA174798
6 · The paper itself

Abstract

backgroundBone metastasis is common in renal cell carcinoma (RCC), and the lesions are mainly osteolytic. The mechanism of bone destruction in RCC bone metastasis is unknown.

methodsWe used a direct intrafemur injection of mice with bone-derived 786-O RCC cells (Bo-786) as an in vivo model to study if inhibition of osteoblast differentiation is involved in osteolytic bone lesions in RCC bone metastasis.

resultsWe showed that bone-derived Bo-786 cells induced osteolytic bone lesions in the femur of mice. We examined the effect of conditioned medium of Bo-786 cells (Bo-786 CM) on both primary mouse osteoblasts and MC3T3-E1 preosteoblasts and found that Bo-786 CM inhibited osteoblast differentiation. Secretome analysis of Bo-786 CM revealed that BIGH3 (Beta ig h3 protein), also known as TGFBI (transforming growth factor beta-induced protein), is highly expressed. We generated recombinant BIGH3 and found that BIGH3 inhibited osteoblast differentiation in vitro. In addition, CM from Bo-786 BIGH3 knockdown cells (786-BIGH3 KD) reduced the inhibition of osteoblast differentiation compared to CM from vector control. Intrafemural injection of mice with 786-BIGH3 KD cells showed a reduction in osteolytic bone lesions compared to vector control. Immunohistochemical staining of 18 bone metastasis specimens from human RCC showed strong BIGH3 expression in 11/18 (61%) and moderate BIGH3 expression in 7/18 (39%) of the specimens.

conclusionsThese results suggest that suppression of osteoblast differentiation by BIGH3 is one of the mechanisms that enhance osteolytic lesions in RCC bone metastasis, and raise the possibilty that treatments that increase bone formation may improve therapy outcomes.

Indexed as

AnimalsbetaIG-H3 ProteinBone and BonesBone NeoplasmsCarcinoma, Renal CellCell DifferentiationCell Line, TumorCell ProliferationDisease Models, AnimalExtracellular Matrix ProteinsGene ExpressionGene Knockout TechniquesHeterograftsHumansKidney NeoplasmsMass SpectrometrybetaIG-H3 ProteinExtracellular Matrix ProteinsTransforming Growth Factor beta

Identifiers

PMID29190493
PMCPMC5711998
OpenAlexW2769387999

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LicenceCC BY-NC-ND
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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.