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pmid:28496199

Upregulation and biological function of transmembrane protein 119 in osteosarcoma.

Zhen-Huan Jiang · Jun Peng · Hui-Lin Yang · Xing-Li Fu · Jin-Zhi Wang · Lei Liu · Jian-Nong Jiang · Yong-Fei Tan · Zhi-Jun Ge

Experimental & molecular medicine · 2017 doi:10.1038/emm.2017.41

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Experiment

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Data

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pmid:28496199
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title
Upregulation and biological function of transmembrane protein 119 in osteosarcoma.
doi
10.1038/emm.2017.41
pmid
28496199
authors array · 9 items
[0]
Zhen-Huan Jiang
[1]
Jun Peng
[2]
Hui-Lin Yang
[3]
Xing-Li Fu
[4]
Jin-Zhi Wang
[5]
Lei Liu
[6]
Jian-Nong Jiang
[7]
Yong-Fei Tan
[8]
Zhi-Jun Ge
journal
Experimental & molecular medicine
year
2017
abstract
Osteosarcoma is suggested to be caused by genetic and molecular alterations that disrupt osteoblast differentiation. Recent studies have reported that transmembrane protein 119 (TMEM119) contributes to osteoblast differentiation and bone development. However, the level of TMEM119 expression and its roles in osteosarcoma have not yet been elucidated. In the present study, TMEM119 mRNA and protein expression was found to be up-regulated in osteosarcoma compared with normal bone cyst tissues. The level of TMEM119 protein expression was strongly associated with tumor size, clinical stage, distant metastasis and overall survival time. Moreover, gene set enrichment analysis (GSEA) of the Gene Expression Omnibus (GEO) GSE42352 dataset revealed TMEM119 expression in osteosarcoma tissues to be positively correlated with cell cycle, apoptosis, metastasis and TGF-β signaling. We then knocked down TMEM119 expression in U2OS and MG63 cells using small interfering RNA, which revealed that downregulation of TMEM119 could inhibit the proliferation of osteosarcoma cells by inducing cell cycle arrest in G0/G1 phase and apoptosis. We also found that TMEM119 knockdown significantly inhibited cell migration and invasion, and decreased the expression of TGF-β pathway-related factors (BMP2, BMP7 and TGF-β). TGF-β application rescued the inhibitory effects of TMEM119 knockdown on osteosarcoma cell migration and invasion. Further in vitro experiments with a TGF-β inhibitor (SB431542) or BMP inhibitor (dorsomorphin) suggested that TMEM119 significantly promotes cell migration and invasion, partly through TGF-β/BMP signaling. In conclusion, our data support the notion that TMEM119 contributes to the proliferation, migration and invasion of osteosarcoma cells, and functions as an oncogene in osteosarcoma.
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To determine differentially expressed genes associated with TMEM119 expression, gene set enrichment analysis (GSEA) was performed based on the GSE42352 dataset using GSEA version 2.0 from the Broad Institute at MIT, as previously described.
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To determine differentially expressed genes associated with TMEM119 expression, gene set enrichment analysis (GSEA) was performed based on the GSE42352 dataset using GSEA version 2.0 from the Broad Institute at MIT, as previously described.
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Osteosarcoma gene expression data were obtained from Gene Expression Omnibus (GEO) using accession numbers GSE42352 and GSE39055. To determine differentially expressed genes associated with TMEM119 expression, gene set enrichment analysis (GSEA) was performed based on the GSE42352 dataset using GSEA version 2.0 from the Broad Institute at MIT, as previously described.
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Moreover, gene set enrichment analysis (GSEA) of the Gene Expression Omnibus (GEO) GSE42352 dataset revealed TMEM119 expression in osteosarcoma tissues to be positively correlated with cell cycle, apoptosis, metastasis and TGF-β signaling.
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Correlation of TMEM119 expression with clinicopathological features of osteosarcoma
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Increased TMEM119 expression is associated with the prognosis of osteosarcoma patients
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Correlation of TMEM119 expression with clinicopathological features of osteosarcoma
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Osteosarcoma gene expression data were obtained from Gene Expression Omnibus (GEO) using accession numbers GSE42352 and GSE39055. To determine differentially expressed genes associated with TMEM119 expression, gene set enrichment analysis (GSEA) was performed based on the GSE42352 dataset using GSEA version 2.0 from the Broad Institute at MIT, as previously described.
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to be positively correlated with cell cycle, apoptosis, metastasis and TGF-β signaling. We then kno
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nducing cell cycle arrest in G0/G1 phase and apoptosis. We also found that TMEM119 knockdown signif
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. We then knocked down TMEM119 expression in U2OS and MG63 cells using small interfering RNA,
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ells, including Saos2, MG63, HOS, SW1353 and U2OS, and human embryonic kidney HEK293T cells we
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CO2 atmosphere. MG63, HOS, Saos2, SW1353 and HEK293 cells were grown in DMEM (Life Technologies;
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M (Life Technologies; Carlsbad, CA, USA) and U2OS cells in RPMI 1640 medium (Life Technologies
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se and apoptosis. We also found that TMEM119 knockdown significantly inhibited cell migration and i
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on rescued the inhibitory effects of TMEM119 knockdown on osteosarcoma cell migration and invasion.
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the International Union against Cancer. For real-time PCR assays, 45 osteosarcoma and 20 bone cyst sam
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uid nitrogen and stored at −80 °C until use. Immunohistochemical (IHC) analysis was performed on archived par
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of TMEM119 expression and patient prognosis. IHC staining was performed on 100 human osteosar
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ts were divided into two groups according to IHC results: high TMEM119 expression group (n=59
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Complete file
{"sci_version": "1.2", "schema": "https://corpus.bntrg.co.uk/sci/1.0/sci.schema.json", "id": "pmid:28496199", "kind": "science-record", "revision": 8, "content_hash": "sha256:cd10668f835f157c772a4bfc133a388856ce6fa07a2cf21a3eb6c8042a66e8fa", "created_at": "2026-11-01T15:40:25Z", "updated_at": "2026-11-01T21:59:22Z", "generator": {"name": "corpus-assay-engine", "run_id": "reading-sci-2026-11-01"}, "paper": {"state": "complete", "title": "Upregulation and biological function of transmembrane protein 119 in osteosarcoma.", "doi": "10.1038/emm.2017.41", "pmid": "28496199", "authors": ["Zhen-Huan Jiang", "Jun Peng", "Hui-Lin Yang", "Xing-Li Fu", "Jin-Zhi Wang", "Lei Liu", "Jian-Nong Jiang", "Yong-Fei Tan", "Zhi-Jun Ge"], "journal": "Experimental & molecular medicine", "year": 2017, "abstract": "Osteosarcoma is suggested to be caused by genetic and molecular alterations that disrupt osteoblast differentiation. Recent studies have reported that transmembrane protein 119 (TMEM119) contributes to osteoblast differentiation and bone development. However, the level of TMEM119 expression and its roles in osteosarcoma have not yet been elucidated. In the present study, TMEM119 mRNA and protein expression was found to be up-regulated in osteosarcoma compared with normal bone cyst tissues. The level of TMEM119 protein expression was strongly associated with tumor size, clinical stage, distant metastasis and overall survival time. Moreover, gene set enrichment analysis (GSEA) of the Gene Expression Omnibus (GEO) GSE42352 dataset revealed TMEM119 expression in osteosarcoma tissues to be positively correlated with cell cycle, apoptosis, metastasis and TGF-β signaling. We then knocked down TMEM119 expression in U2OS and MG63 cells using small interfering RNA, which revealed that downregulation of TMEM119 could inhibit the proliferation of osteosarcoma cells by inducing cell cycle arrest in G0/G1 phase and apoptosis. We also found that TMEM119 knockdown significantly inhibited cell migration and invasion, and decreased the expression of TGF-β pathway-related factors (BMP2, BMP7 and TGF-β). TGF-β application rescued the inhibitory effects of TMEM119 knockdown on osteosarcoma cell migration and invasion. Further in vitro experiments with a TGF-β inhibitor (SB431542) or BMP inhibitor (dorsomorphin) suggested that TMEM119 significantly promotes cell migration and invasion, partly through TGF-β/BMP signaling. 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