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NOV inhibits proliferation while promoting apoptosis and migration in osteosarcoma cell lines through p38/MAPK and

Juan Yao1, Yaguang Weng1, Shujuan Yan1

  • 1Key Laboratory of Diagnostic Medicine Designated by the Chinese Ministry of Education, Chongqing Medical University, Chongqing 400016, P.R. China.

Oncology Reports
|August 5, 2015
PubMed

Insights

The nephroblastoma overexpressed (NOV) gene inhibits osteosarcoma cell proliferation and induces apoptosis by activating the MAPK pathway. However, NOV also enhances osteosarcoma cell migration in vitro.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • The nephroblastoma overexpressed (NOV) gene, part of the CCN family, is implicated in tumorigenesis and altered in various cancers, including osteosarcoma.
  • While NOV is known to promote osteosarcoma metastasis, its precise roles and molecular mechanisms in osteosarcoma proliferation remain unclear.

Purpose of the Study:

  • To investigate the biological functions of the NOV gene in osteosarcoma.
  • To elucidate the molecular mechanisms underlying NOV's role in osteosarcoma cell proliferation and migration.

Main Methods:

  • Assessed endogenous NOV expression using RT-PCR and Western blot in osteosarcoma cell lines.
  • Utilized recombinant adenovirus (AdNOV/AdsiNOV) to modulate NOV expression and evaluated effects on cell growth, apoptosis, and migration in vitro.
  • Analyzed cell proliferation via MTT assays, colony formation assays, and cell cycle analysis; apoptosis was assessed by Hoechst staining and flow cytometry.
  • Investigated the involvement of the MAPK signaling pathway, including p38 and JNK, using specific inhibitors (SB203580 and SP600125).

Main Results:

  • NOV upregulation significantly reduced osteosarcoma cell proliferation and induced apoptosis.
  • Conversely, NOV-transfected cells demonstrated increased migration capabilities in vitro.
  • NOV activation led to increased phosphorylation of p38 and JNK mitogen-activated protein kinases (MAPKs).
  • Inhibition of p38 and JNK pathways reversed the effects of NOV on proliferation and apoptosis.

Conclusions:

  • NOV plays a dual role in osteosarcoma, inhibiting proliferation and inducing apoptosis while promoting cell migration.
  • The MAPK signaling pathway, specifically p38 and JNK, is crucial for mediating NOV's effects on osteosarcoma cell growth and apoptosis.
  • NOV regulates osteosarcoma tumor growth and migration through the activation of the MAPK pathway.

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