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[Effects of MnSOD silence on in vitro tumorigenicity in NCI-H446 cells]

Qing Yuan1, Min Wen1, Xiang Li1

  • 1Department of Basic Medicine, College of Medicine of Human Normal University, Changsha 410013, China.

Zhong Nan Da Xue Xue Bao. Yi Xue Ban = Journal of Central South University. Medical Sciences
|August 16, 2018
PubMed
Abstract

Insights

Manganese superoxide dismutase (MnSOD) silence reduced the tumorigenicity of small cell lung cancer cells. This suggests MnSOD promotes cancer growth by increasing urokinase plasminogen activator (uPAR) expression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Small cell lung cancer (SCLC) is an aggressive form of lung cancer.
  • Manganese superoxide dismutase (MnSOD) is an enzyme involved in cellular defense against oxidative stress.
  • The role of MnSOD in SCLC tumorigenicity requires further elucidation.

Purpose of the Study:

  • To investigate the impact of silencing manganese superoxide dismutase (MnSOD) on the in vitro tumorigenicity of human small cell lung cancer NCI-H446 cells.
  • To explore the underlying molecular mechanisms, specifically the role of urokinase type plasminogen activator (uPAR).

Main Methods:

  • NCI-H446 cells were cultured in suspension to obtain sphere formation cells.
  • Manganese superoxide dismutase (MnSOD) was silenced using adenovirus infection.
  • Tumorigenicity was assessed via sphere formation and soft-agar colony formation assays.
  • Expression levels of MnSOD and urokinase type plasminogen activator (uPAR) were analyzed by Western blot.

Main Results:

  • Sphere formation and colony formation rates were significantly increased in NCI-H446 cells compared to controls.
  • Silencing MnSOD significantly inhibited sphere and colony formation rates.
  • MnSOD silencing also led to a significant decrease in uPAR expression.

Conclusions:

  • Manganese superoxide dismutase (MnSOD) appears to promote in vitro tumorigenicity in NCI-H446 cells.
  • This promotion may be mediated through the up-regulation of urokinase type plasminogen activator (uPAR) expression.
  • Targeting MnSOD could be a potential therapeutic strategy for SCLC.

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