Rhcg, also known as Rhesus C glycoprotein, is a key ammonia transporter. It plays a vital role in urinary acid excretion, mainly expressed in the intercalated cells of the renal collecting duct. Aldosterone regulates Rhcg membrane expression via the mineralocorticoid receptor and PKC pathways, modulated by extracellular potassium level [1].

In cancer research, high Rhcg expression in gastric cancer is correlated with poor differentiation, TNM stage, high HER-2 level, and worse prognosis, promoting migration and proliferation by maintaining intracellular alkalinity [2]. In endometrial cancer, Rhcg is highly expressed, promoting malignant proliferation, migration, and anti-apoptotic activity [3]. Conversely, in cervical, esophageal squamous cell carcinomas, Rhcg is down-regulated. In cervical cancer, over-expression reduces cell proliferation and migration, induces apoptosis regulated by TGF-β1 [4]. In esophageal squamous cell carcinoma, it suppresses tumorigenicity and metastasis via inhibiting NF-κB signaling and MMP1 expression [5].

In summary, Rhcg is crucial for urinary acid excretion regulated by aldosterone. In cancer, its expression pattern varies among different cancer types, either promoting or suppressing cancer progression. The study of Rhcg through various research models helps understand its functions in normal physiological and disease conditions, especially in cancer-related areas.