A better understanding of the function of the protein TAK1 may offer new insights into the development of liver disease and cancer. At least that’s what scientists from the UC San Diego School of Medicine and Osaka University in Japan claim. The team has apparently recognized a protein switch that could help prevent liver damage. It includes inflammation, fibrosis and cancer.
TAK1 is known to be a kinase that is a kind of signaling protein engaged in regulation of various cell activities like cell growth. The kinase has been associated by the experts with the activation of two specific proteins namely NF-kappaB and JNK. Both appear to be involved in immunity, inflammation, programmed cell death and cancer. While NF-kappaB seems to help safeguard liver cells from dying and also protects against cancer development, JNK in contrast promotes cell death and cancer.
“TAK1 appears to be a master regulator of liver function. Understanding its role in liver disease and cancer may eventually enable us to devise new therapeutic strategies,” remarked David A. Brenner, MD, professor of medicine and Dean of the UC San Diego School of Medicine. He and Ekihiro Seki, MD, PhD, assistant research scientist in the Department of Medicine, led the work.
Until now, however, it appears to have been foggy whether TAK1 aids or prevents the development of liver cancer. Seki, Brenner and their group built a mouse model in which liver cells lacked the gene Tak1 that was responsible for making TAK1 protein to find out. A high rate of liver cell death in young animals without TAK1 was revealed by the range of experiments conducted.
Apparently the animals’ livers were found to have gone into overdrive following this. They appeared to have produced too many liver cells supposedly to make up for the loss, eventually leading to liver damage. Inflammation and fibrosis along with liver scarring and finally cancer were observed.
This novel analysis is claimed to be the premier one to offer insights into the role of TAK1 in cancer development suggests Seki. The researcher further suggests that the protein may also play a part in cancer development in other organs. Besides, the liver cancer mouse model created by the team was also linked to sustained liver inflammation and fibrosis. The latter are considered to be key attributes of human liver cancer. Scientists hope to find them useful in examining if fibrosis could influence liver cancer development.
This analysis appears on line the week of December 14 in advance of publication in the journal Proceedings of the National Academy of Sciences.