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Muscle disorders

Combating cachexia in cancer

Nature Reviews Drug Discovery volume 14, pages 748–749 (2015)Cite this article

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Previous work has indicated that FN14 signalling has a wide range of roles; it is involved in angiogenesis, proliferation and inflammation. In this study, the authors investigated the effects of tumour overexpression of FN14. They transformed mouse embryonic fibroblasts (MEFs) using an HRAS oncogene and infected these cells with a lentivirus expressing either the full human FN14 (hFN14) or an extracellular section of hFN14 that could not induce intracellular signalling. When the transformed cells were injected subcutaneously into mice, tumours developed in both groups at similar rates; however, 8 days post-injection, mice bearing the full hFN14-expressing tumours suffered severe weight loss, implicating a role for tumour FN14 signalling in the induction of cachexia.

The authors developed FN14-specific antibodies and tested one of them, 001, in mice bearing the hFN14-expressing MEF tumours. A single dose of 001 6 days after inoculation with the MEFs prevented the symptoms of cachexia — including loss of body mass, tibialis anterior (TA) muscle mass and subscapular fat — that were observed in the control immunoglobulin G (IgG)-treated mice without affecting tumour volume, indicating that blocking tumour FN14 can protect against cachexia.

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References

  1. Johnston, A. J. et al. Targeting of Fn14 prevents cancer-induced cachexia and prolongs survival. Cell 162, 1365–1378 (2015)

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  1. Natasha Bray
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Cohen, S., Nathan, J. A. & Goldberg, A. L. Muscle wasting in disease: molecular mechanisms and promising therapies. Nat. Rev. Drug. Discov. 14, 58–74 (2015)

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Bray, N. Combating cachexia in cancer. Nat Rev Drug Discov 14, 748–749 (2015). https://doi.org/10.1038/nrd4765

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