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Upregulation and biological function of transmembrane protein 119 in osteosarcoma

Zhen-Huan Jiang1, Jun Peng1, Hui-Lin Yang2

  • 1Department of Orthopedics, The Affiliated Yixing Hospital of Jiangsu University, Yixing, People's Republic of China.

Experimental & Molecular Medicine
|May 13, 2017
PubMed

Insights

Transmembrane protein 119 (TMEM119) is upregulated in osteosarcoma, promoting cancer cell proliferation, migration, and invasion. Downregulating TMEM119 inhibits osteosarcoma growth by affecting cell cycle and apoptosis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Osteosarcoma arises from genetic alterations disrupting osteoblast differentiation.
  • Transmembrane protein 119 (TMEM119) is implicated in osteoblast differentiation and bone development.
  • The role and expression of TMEM119 in osteosarcoma remain unclear.

Purpose of the Study:

  • To investigate TMEM119 expression levels in osteosarcoma.
  • To elucidate the functional role of TMEM119 in osteosarcoma progression.
  • To explore the underlying molecular mechanisms involving TMEM119 in osteosarcoma.

Main Methods:

  • Quantitative analysis of TMEM119 mRNA and protein expression in osteosarcoma tissues.
  • Gene Set Enrichment Analysis (GSEA) on the GEO GSE42352 dataset.
  • In vitro studies involving TMEM119 knockdown using small interfering RNA (siRNA) in osteosarcoma cell lines (U2OS, MG63).
  • Assessment of cell proliferation, cell cycle, apoptosis, migration, and invasion.
  • Investigation of the TGF-β/BMP signaling pathway.

Main Results:

  • TMEM119 expression is significantly upregulated in osteosarcoma compared to normal bone cyst tissues.
  • Elevated TMEM119 protein levels correlate with larger tumor size, advanced clinical stage, distant metastasis, and poorer overall survival.
  • TMEM119 expression is positively associated with cell cycle, apoptosis, metastasis, and TGF-β signaling pathways.
  • TMEM119 knockdown inhibits osteosarcoma cell proliferation by inducing G0/G1 cell cycle arrest and apoptosis.
  • TMEM119 knockdown suppresses cell migration and invasion, reducing TGF-β pathway factors (BMP2, BMP7, TGF-β).
  • TGF-β application reversed the inhibitory effects of TMEM119 knockdown on cell migration and invasion.
  • TMEM119 promotes osteosarcoma cell migration and invasion, partly via TGF-β/BMP signaling.

Conclusions:

  • TMEM119 acts as an oncogene in osteosarcoma.
  • TMEM119 contributes to osteosarcoma cell proliferation, migration, and invasion.
  • TMEM119 may serve as a potential therapeutic target for osteosarcoma.

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