Pkn2, also known as Protein kinase N2, PRK2 or PKNγ, is a PKC-related serine/threonine-protein kinase. It is involved in multiple biological processes such as cytoskeleton organization, cell mobility, adhesion, and the cell cycle [3]. It is also part of key signaling pathways, like the DUSP6-Erk1/2 pathway, and has significance in development and disease contexts. Genetic models, especially knockout mouse models, have been crucial in studying its functions.

In gene knockout studies, constitutive disruption of the mouse Pkn2 gene led to growth retardation and lethality before embryonic day 10.5, with issues in axial turning and neural tube closure [4]. Mouse embryonic fibroblasts from Pkn2-/-embryos failed to grow, and Cre-mediated ablation in Pkn2flox/flox MEFs showed impaired cell proliferation [4]. In cardiomyocytes, Pkn2 knockout embryos had abnormalities in the compact myocardium, and adult heterozygous Pkn2 knockout mice had reduced cardiac hypertrophy in response to angiotensin II-induced hypertension [2]. In pancreatic stellate cells, loss of Pkn2 reduced proliferation, contractility, and α-SMA stress fibers, and promoted invasive cancer cell outgrowth [1].

In conclusion, Pkn2 is essential for mouse embryonic development, cell proliferation, and plays important roles in heart development and response to stress. Its loss-of-function in various mouse models has revealed its significance in cancer development, especially in colon, pancreatic, and colorectal cancers. These findings from model-based research contribute to understanding disease mechanisms and may potentially lead to new therapeutic strategies targeting Pkn2-related pathways.