{Reference Type}: Journal Article
{Title}: KLF10: a point of convergence in cancer cachexia.
{Author}: Epstein SA;Doles JD;Dasgupta A;
{Journal}: Curr Opin Support Palliat Care
{Volume}: 18
{Issue}: 3
{Year}: 2024 Sep 1
{Factor}: 2.265
{DOI}: 10.1097/SPC.0000000000000711
{Abstract}: <B>OBJECTIVE: </B>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.<BR><B>RESULTS: </B>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 .<BR><B>CONCLUSIONS: </B>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.