Extracellular Superoxide Dismutase: Growth Promoter or Tumor Suppressor?

Author

Laukkanen, Mikko O.

Source

Oxidative Medicine and Cellular Longevity

Issue

Vol. 2016, Issue 2016 (31 Dec. 2016), pp.1-9, 9 p.

Publisher

Hindawi Publishing Corporation

Publication Date

2016-05-12

Country of Publication

Egypt

No. of Pages

9

Main Subjects

Biology

Abstract EN

Extracellular superoxide dismutase (SOD3) gene transfer to tissue damage results in increased healing, increased cell proliferation, decreased apoptosis, and decreased inflammatory cell infiltration.

At molecular level, in vivo SOD3 overexpression reduces superoxide anion ( O 2 - ) concentration and increases mitogen kinase activation suggesting that SOD3 could have life-supporting characteristics.

The hypothesis is further strengthened by the observations showing significantly increased mortality in conditional knockout mice.

However, in cancer SOD3 has been shown to either increase or decrease cell proliferation and survival depending on the model system used, indicating that SOD3-derived growth mechanisms are not completely understood.

In this paper, the author reviews the main discoveries in SOD3-dependent growth regulation and signal transduction.

American Psychological Association (APA)

Laukkanen, Mikko O.. 2016. Extracellular Superoxide Dismutase: Growth Promoter or Tumor Suppressor?. Oxidative Medicine and Cellular Longevity،Vol. 2016, no. 2016, pp.1-9.
https://search.emarefa.net/detail/BIM-1113843

Modern Language Association (MLA)

Laukkanen, Mikko O.. Extracellular Superoxide Dismutase: Growth Promoter or Tumor Suppressor?. Oxidative Medicine and Cellular Longevity No. 2016 (2016), pp.1-9.
https://search.emarefa.net/detail/BIM-1113843

American Medical Association (AMA)

Laukkanen, Mikko O.. Extracellular Superoxide Dismutase: Growth Promoter or Tumor Suppressor?. Oxidative Medicine and Cellular Longevity. 2016. Vol. 2016, no. 2016, pp.1-9.
https://search.emarefa.net/detail/BIM-1113843

Data Type

Journal Articles

Language

English

Notes

Includes bibliographical references

Record ID

BIM-1113843