Plac8, also known as placenta-specific 8 or Onzin, is a multifaceted protein involved in various biological processes. It has been implicated in regulating autophagy, cell proliferation, apoptosis, and the immune response. Plac8 is associated with pathways such as Wnt/β-Catenin, ERK, AKT/mTOR, and is involved in diseases like cancer and sepsis [1-8]. Genetic models, such as gene knockout mouse models, can be valuable in studying its functions.

In cancer, Plac8 shows diverse roles. In lung cancer, its overexpression promotes cell growth via the Wnt/β-Catenin signaling pathway [1]. In breast cancer, higher Plac8 expression is linked to adriamycin resistance by blocking autophagy, and in triple-negative breast cancer, it affects tumor proliferation and immune response by modulating PD-L1 levels [2,4]. In cervical cancer, Plac8 contributes to malignant behaviors by activating the SOX4-mediated AKT pathway [5]. In nasopharyngeal carcinoma, knocking out Plac8 induces autophagy, apoptosis, and inhibits cell proliferation and EMT via the AKT/mTOR pathway [6]. In sepsis, Plac8 upregulation promotes monocyte survival, proliferation, and activation by activating the ERK pathway [3].

In conclusion, Plac8 is a key protein involved in multiple biological functions and disease conditions. Studies using gene knockout models have revealed its roles in cancer and sepsis, providing insights into potential therapeutic targets. Its functions in regulating cell growth, autophagy, and immune responses suggest its importance in understanding disease mechanisms and developing novel treatment strategies.