Evidence map›Paper›PMID 32494918›Full record

ArticleJournal of cancer research and clinical oncology2020

Bone marrow adipocytes enhance osteolytic bone destruction by activating 1q21.3(S100A7/8/9-IL6R)-TLR4 pathway in lung cancer.

Guojing Luo, Mengjia Tang, Qian Zhao, Lingyun Lu, Ying Xie, Yujue Li, Chang Liu, Li Tian, Xiang Chen, Xijie Yu

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 24% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. The 1q21.3 region driver geneTranslational cancer research · 2022
    Article
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  11. Article
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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 1 institution in 1 country.

Guojing LuoLaboratory of Endocrinology and Metabolism, Department of Endocrinology and Metabolism, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu, China.
Mengjia TangLaboratory of Endocrinology and Metabolism, Department of Endocrinology and Metabolism, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu, China.
Qian ZhaoDepartment of General Practice, West China Hospital, Sichuan University, Chengdu, China.
Lingyun LuLaboratory of Endocrinology and Metabolism, Department of Endocrinology and Metabolism, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu, China.
Ying XieLaboratory of Endocrinology and Metabolism, Department of Endocrinology and Metabolism, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu, China.
Yujue LiLaboratory of Endocrinology and Metabolism, Department of Endocrinology and Metabolism, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu, China.
Chang LiuLaboratory of Endocrinology and Metabolism, Department of Endocrinology and Metabolism, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu, China.
Li TianLaboratory of Endocrinology and Metabolism, Department of Endocrinology and Metabolism, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu, China.
Xiang ChenLaboratory of Endocrinology and Metabolism, Department of Endocrinology and Metabolism, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu, China.
Xijie YuLaboratory of Endocrinology and Metabolism, Department of Endocrinology and Metabolism, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu, China. xijieyu@scu.edu.cn.ORCID http://orcid.org/0000-0002-3504-7664
Sichuan University · CN

Funding

1.3.5 project for disciplines of excellence, West China Hospital, Sichuan University 2020HXFH0081.3.5 project for disciplines of excellence, West China Hospital, Sichuan University ZYGD18022Department of Science and Technology of Sichuan Province (CN) 2018SZ0142National Natural Science Foundation of China 81572639National Natural Science Foundation of China 81770875Sichuan University 2018SCUH0093the National Clinical Research Center for Geriatrics of West China Hospital Z2018B05
6 · The paper itself

Abstract

purposeBone metastasis is the result of complex crosstalk between tumor cells and bone marrow cells. Bone marrow adipocytes (BMAs) are the most abundant cell type in adult bone marrow. Therefore, we explore the effects of BMAs on bone metastasis in lung cancer.

methodsRNA-seq was used to compare the mRNA expression level of bone metastatic SBC5 cells and non-bone metastatic SBC3 cells. Rosiglitazone-induced marrow adiposity and intra-femoral injection of SBC5 cells were used to demonstrate the relationship between BMAs and SBC5 cells in vivo. Co-culture system, gene co-expression, gene ontology (GO) enrichment analysis and protein-protein interaction (PPI) network were used to explore the potential mechanism.

resultsBMAs specially enhance the invasion of bone metastatic SBC5 instead of non-bone metastatic SBC3 in vitro. SBC5 instead of SBC3 promoted osteoblast and osteoclast differentiation as well as de-differentiation of mature BMAs. Rosiglitazone-induced marrow adiposity significantly enhanced osteolytic lesion induced by SBC5 in vivo. RNA-seq revealed that compared with SBC3, S100A9 and S100A8 genes were the most prominent genes up-regulated in SBC5 cells. High expression of S100A8/9 in SBC5 could be responsible for the crosstalk between lung cancer cells and BMAs. More importantly, interleukin 6 receptor (IL6R), which is adjacent to S100A8/A9 in 1q21.3, was significantly up-regulated by BMAs in vitro. S100A8/A9 (1 μg/ml) could obviously enhance the osteoblastic differentiation and inhibit adipogenic differentiation, whereas TLR4 inhibitor TAK242 (10 μmol/l) significantly attenuated this effect.

conclusionsOur study suggested that bone marrow adipocyte may communicate with lung cancer cells via 1q21.3 (S100A8/A9-IL6R)-TLR4 pathway to promote osteolytic bone destruction. 1q21.3 (S100A8/A9-IL6R) is a potential target for the treatment of lung cancer bone metastasis.

Indexed as

AdipocytesAnimalsBone and BonesBone MarrowBone Marrow CellsCell Line, TumorCoculture TechniquesFemaleHumansLung NeoplasmsMiceMice, Inbred BALB CMice, Inbred C57BLOsteoblastsOsteolysisReceptors, Interleukin-6IL6R protein, humanReceptors, Interleukin-6S100 ProteinsTLR4 protein, humanToll-Like Receptor 41q21.3Bone marrow adipocyteBone metastasisIL6Lung cancer

Identifiers

PMID32494918
PMCPMC11804520
OpenAlexW3030624535

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.