Prkd3, encoding protein kinase D3, is a serine/threonine protein kinase belonging to the protein kinase D family. It can be activated by stimuli like phorbol esters and G-protein-coupled receptor agonists, and is involved in promoting cell proliferation, growth, migration, and invasion in multiple cancer types [3].

In cancer research, PRKD3 knockdown in OSCC cells attenuated their migration and invasiveness, and high PRKD3 expression was associated with distant metastasis and poor prognosis [1]. In HCC, PRKD3 knockdown reduced cell proliferation and induced cell cycle arrest at G2/M phase [2]. In GC, PRKD3 knockdown impaired cell malignancy with a decline in proliferation, migration, and invasion, along with G2/M phase arrest [4]. In invasive breast cancer, depletion of PRKD3 led to alternation of cell cycle and decrease of cell migration ability [5]. In addition, deletion of Prkd3 in mice promoted liver fibrosis through profibrotic macrophage activation [6].

In conclusion, Prkd3 plays a significant role in promoting the malignant progression of various cancers and in liver fibrosis development. The use of Prkd3 knockout or knockdown models in these studies has been crucial in revealing its oncogenic functions in specific disease conditions, providing potential therapeutic targets for cancer treatment and insights into the mechanism of liver fibrosis.