Evidence map›Paper›PMID 25997540›Full record

ArticleOncology reports2015

AMD3100 reduces CXCR4-mediated survival and metastasis of osteosarcoma by inhibiting JNK and Akt, but not p38 or Erk1/2, pathways in in vitro and mouse experiments.

Yu-Xin Liao, Ze-Ze Fu, Cheng-Hao Zhou, Lian-Cheng Shan, Zhuo-Ying Wang, Fei Yin, Long-Po Zheng, Ying-Qi Hua, Zheng-Dong Cai

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

36 citing papers in PubMed, 54 citations in OpenAlex.

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  14. Osteosarcoma and Metastasis.Frontiers in oncology · 2021
    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

9 authors at 3 institutions in 1 country.

Yu-Xin LiaoDepartment of Orthopaedics, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, P.R. China.
Ze-Ze FuDepartment of Orthopaedics, Shanghai First People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200080, P.R. China.
Cheng-Hao ZhouDepartment of Orthopaedics, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, P.R. China.
Lian-Cheng ShanDepartment of Orthopaedics, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, P.R. China.
Zhuo-Ying WangDepartment of Orthopaedics, Shanghai First People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200080, P.R. China.
Fei YinDepartment of Orthopaedics, Shanghai First People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200080, P.R. China.
Long-Po ZhengDepartment of Orthopaedics, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, P.R. China.
Ying-Qi HuaDepartment of Orthopaedics, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, P.R. China.
Zheng-Dong CaiDepartment of Orthopaedics, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, P.R. China.
Shanghai First People's Hospital · CNShanghai Tenth People's Hospital · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteosarcoma (OS) has an unfavorable prognosis and tends to metastasize to lung tissue. Although the CXCL12-CXCR4 axis appears to affect progression and metastasis in numerous tumors, its mechanism and downstream pathways in OS remain unclear. We used western blotting and flow cytometry to detect CXCR4 and CXCR7 expression in two OS cell lines (LM8 and Dunn). An MTT assay was used to evaluate the effects of CXCL12 and AMD3100, a specific CXCR4 antagonist, on cell viability. Flow cytometry was utilized to analyze changes in apoptosis induced by serum deprivation following treatment with CXCL12 and AMD3100. A Transwell assay was used to assess cell migration in response to CXCL12 and AMD3100. Western blotting was performed to identify the phosphorylation of signaling molecules (JNK, c-Jun, Akt, p38 and Erk1/2) and expression of caspase-3 and -8, and PARP. Mouse models were employed to evaluate AMD3100 inhibition of primary OS growth and lung metastasis in vivo. CXCR4 expression was detected in LM8 but not Dunn cells, and neither cell line expressed CXCR7. The addition of CXCL12 induced the survival and migration of serum-starved CXCR4+ LM8 cells activating JNK and Akt pathways, which were abrogated by adding AMD3100. However, similar results were not observed in CXCR4- Dunn cells. CXCL12 protected LM8, but not Dunn cells, from apoptosis induced by serum deprivation by suppressing PARP cleavage, which was partly reversed by AMD3100. In a mouse model, AMD3100 reduced primary tumor growth and lung metastasis compared with the controls. Thus, the CXCL12-CXCR4 axis regulated OS survival and metastasis through the JNK and Akt pathways, and blocking them with AMD3100 was found to be a potential OS treatment.

Indexed as

AnimalsApoptosisBenzylaminesCaspase 3Cell Line, TumorCell MovementCell ProliferationCell SurvivalChemokine CXCL12CyclamsGene Expression Regulation, NeoplasticHeterocyclic CompoundsHumansMAP Kinase Kinase 4MAP Kinase Signaling SystemMiceACKR3 protein, humanBenzylaminesCaspase 3Chemokine CXCL12CXCL12 protein, humanCXCR4 protein, humanCyclamsHeterocyclic CompoundsMAP Kinase Kinase 4Oncogene Protein v-aktp38 Mitogen-Activated Protein KinasesplerixaforReceptors, CXCRReceptors, CXCR4

Identifiers

PMID25997540
PMCPMC4484610
OpenAlexW1945249145

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.