Cancer-associated cachexia is a wasting syndrome entailing loss in body mass and a shortened life expectancy. There is currently no effective treatment to abrogate this syndrome, which leads to 20-30% of deaths in patients with cancer.

While there have been advancements in defining signaling factors/pathways in cancer-induced muscle wasting, targeting the same in the clinic has not been as successful. Krüppel-like factor 10 (KLF10), a transcription factor implicated in muscle regulation, is regulated by the transforming growth factor-beta signaling pathway.

This review proposes KLF10 as a potential convergence point of diverse signaling pathways involved in muscle wasting. KLF10 was discovered as a target of transforming growth factor-beta decades ago but more recently it has been shown that deletion of KLF10 rescues cancer-induced muscle wasting.

Moreover, KLF10 has also been shown to bind key atrophy genes associated with muscle atrophy in vitro . There is an elevated need to explore targets in cachexia, which will successfully translate into the clinic.

Investigating a convergence point downstream of multiple signaling pathways might hold promise in developing effective therapies for cachexia.