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Comment
. 2019 Aug;29(8):607-608.
doi: 10.1038/s41422-019-0197-9.

AIF: an acquired metabolic liability in lung cancer

Brandon Faubert  1 , Ralph J DeBerardinis  2   3   4   5 , John D Minna  6   7
Affiliations
Comment

AIF: an acquired metabolic liability in lung cancer

Brandon Faubert et al. Cell Res. 2019 Aug.
No abstract available

PubMed Disclaimer

Conflict of interest statement

R.J.D. is an advisor for Agios Pharmaceuticals.

Figures

Fig. 1
Fig. 1
Outcomes of AIF manipulation in KRAS-driven tumor growth. Mice expressing a mutant KrasG12D allele in the presence (a) or absence (b) of AIF have different levels of tumor growth. Re-expression of mutant AIF (Δ96–110) (c), which restores the metabolic role of AIF but is unable to translocate to the nucleus to induce apoptosis, rescues the tumor growth defect of AIF knock-out tumors. WT, wild-type; KO, knock-out; CHCHD4, Coiled-Coil-Helix-Coiled-Coil-Helix Domain Containing 4; OXPHOS, oxidative phosphorylation. (This figure was created using Servier Medical Art templates, which are licensed under a Creative Commons Attribution 3.0 Unported License; https://smart.servier.com)
See this image and copyright information in PMC

Comment on

  • AIF-regulated oxidative phosphorylation supports lung cancer development.
    Rao S, Mondragón L, Pranjic B, Hanada T, Stoll G, Köcher T, Zhang P, Jais A, Lercher A, Bergthaler A, Schramek D, Haigh K, Sica V, Leduc M, Modjtahedi N, Pai TP, Onji M, Uribesalgo I, Hanada R, Kozieradzki I, Koglgruber R, Cronin SJ, She Z, Quehenberger F, Popper H, Kenner L, Haigh JJ, Kepp O, Rak M, Cai K, Kroemer G, Penninger JM. Rao S, et al. Cell Res. 2019 Jul;29(7):579-591. doi: 10.1038/s41422-019-0181-4. Epub 2019 May 27. Cell Res. 2019. PMID: 31133695 Free PMC article.

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