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LINE-1 Methylation Analysis in Mesenchymal Stem Cells Treated with Osteosarcoma-Derived Extracellular Vesicles
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Hypermethylated PODN represses the progression of osteosarcoma by inactivating the TGF-β/Smad2/3 pathway

Xiuxin Han1, Yan Zhang1, Feng Lu1

  • 1Department of Bone and Soft Tissue Tumors, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin 300060, China.

Pathology, Research and Practice
|August 29, 2022
PubMed
Abstract

Insights

Podoplanin (PODN) suppresses osteosarcoma (OS) development by inhibiting cell proliferation, migration, and invasion. PODN overexpression inactivates the TGF-β/Smad2/3 pathway, offering a potential therapeutic target for OS.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Podoplanin (PODN) is a promising prognostic biomarker for osteosarcoma (OS).
  • The specific function and mechanism of PODN in OS remain underexplored.
  • This study investigates the role and underlying mechanisms of PODN in OS.

Purpose of the Study:

  • To elucidate the functional role of PODN in osteosarcoma.
  • To investigate the molecular mechanisms by which PODN affects OS progression.
  • To explore PODN as a potential therapeutic target in osteosarcoma.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) and Western blot for gene and protein expression analysis.
  • Methylation-specific PCR to assess PODN methylation status.
  • Cell proliferation (CCK-8, colony formation) and invasion/migration (Transwell) assays.
  • Xenograft mouse models and immunohistochemical staining for in vivo validation.

Main Results:

  • PODN expression was significantly downregulated and hypermethylated in OS tissues and cells.
  • PODN overexpression suppressed OS cell proliferation, migration, and invasion in vitro.
  • PODN overexpression inhibited tumor growth in vivo and reduced TGF-β1 and p-Smad2/3 levels.
  • TGF-β1 partially reversed the inhibitory effects of PODN overexpression.

Conclusions:

  • PODN functions as a tumor suppressor in osteosarcoma.
  • PODN overexpression inhibits osteosarcoma progression by inactivating the TGF-β/Smad2/3 signaling pathway.
  • PODN represents a potential therapeutic target for osteosarcoma treatment.
Keywords:
MethylationOsteosarcomaPODNTGF-β/Smad2/3

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