Journal
MOLECULAR AND CELLULAR BIOCHEMISTRY
Volume 351, Issue 1-2, Pages 165-172Publisher
SPRINGER
DOI: 10.1007/s11010-011-0724-6
Keywords
Lipocalin 2; Cell proliferation; Autophagy; Mitochondrial biogenesis; Tumorigenesis
Categories
Funding
- National Institute of Diabetes and Digestive and Kidney Diseases [R01DK080743]
Ask authors/readers for more resources
Lipocalin 2 (LCN2) has been recently implicated as a critical player in multiple cancer tumorigeneses. However, the molecular mechanisms for its tumorigenic role are poorly understood. Herein, we investigated the effects of LCN2 on cell proliferation, autophagy, and mitochondrial biogenesis in MEF cells. We observed that LCN2 deficiency significantly inhibited cell proliferation and autophagy in MEF cells. Furthermore, mitochondrial DNA content, mRNA expression levels of mitochondrial-encoded gene cytochrome oxidase 2 and PGC-1 alpha were all markedly reduced in LCN2-/- MEF cells. Additionally, when compared with wild-type MEF cells, LCN2-/- MEF cells expressed significantly higher levels of IRS-1, and displayed more potent TNF alpha-stimulated NF-kappa B activation. These findings demonstrate that LCN2 is a critical regulator of cell proliferation, autophagy, and mitochondrial biogenesis.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available