Abstract
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-1α 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 TNFα-stimulated NF-κB activation. These findings demonstrate that LCN2 is a critical regulator of cell proliferation, autophagy, and mitochondrial biogenesis.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 165-172 |
| Number of pages | 8 |
| Journal | Molecular and cellular biochemistry |
| Volume | 351 |
| Issue number | 1-2 |
| DOIs | |
| State | Published - May 2011 |
Bibliographical note
Funding Information:Acknowledgments The project described was supported by Grant Number R01DK080743 (to X.C.) from the National Institute of Diabetes and Digestive and Kidney Diseases. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institute of Diabetes and Digestive and Kidney Diseases or the National Institutes of Health. We thank Wendy Wright from the Department of Biochemistry, Molecular Biology and Biophysics at the University of Minnesota for the technical assistance in establishment of mouse embryonic fibroblasts.
Keywords
- Autophagy
- Cell proliferation
- Lipocalin 2
- Mitochondrial biogenesis
- Tumorigenesis
