Plxnc1, also known as plexin C1, is a neuronal guidance receptor. It is involved in various biological processes. In the immune response, it dampens the intracellular response to lipopolysaccharide (LPS) by interacting with adenylate cyclase 4 (ADCY4) and protein kinase A activity, diminishing caspase-11 expression [4]. In the olfactory system, it participates in Sema7A/PlxnC1 signaling within glomeruli, which is crucial for the olfactory critical period, promoting post-synaptic events and dendrite selection in mitral/tufted cells [6].

In disease-related research, Plxnc1 has been implicated in multiple conditions. In gastric cancer, it is frequently up-regulated and associated with poor prognosis. Knockdown of Plxnc1 significantly reduces gastric cancer cell proliferation and migration, while overexpression accelerates carcinogenesis. It promotes these malignant behaviors through transcriptional activation of IL6ST [1]. In stomach adenocarcinoma, it is an immune-related gene regulated by IRF5, significantly associated with M2 macrophages and poor outcome [2]. In osteoarthritis, its expression is elevated in cartilage tissues of patients and IL-1β-treated chondrocytes. Silencing Plxnc1 mitigates the apoptosis, inflammation, and extracellular matrix degradation of IL-1β-insulted chondrocytes by interacting with and down-regulating GRP78 [3]. In papillary thyroid cancer, miR-4500 inhibits the malignant transformation of cancer cells by directly targeting and repressing Plxnc1 [5].

In conclusion, Plxnc1 plays important roles in immune response, olfactory development, and is closely associated with multiple diseases such as gastric cancer, stomach adenocarcinoma, osteoarthritis, and papillary thyroid cancer. Studies using gene knockdown or knockout models in these diseases have revealed its functional mechanisms, providing potential therapeutic targets and new insights into disease pathogenesis.