Abcc2, also known as MRP2, is a member of the ABC transporter family. It is expressed at major physiological barriers like the canalicular membrane of liver cells, kidney proximal tubule epithelial cells, enterocytes of the small and large intestine, and syncytiotrophoblast of the placenta, always localizing in the apical membranes. It functions as a multispecific transporter with dominant excretory functions, preferentially transporting phase II conjugates such as endogenous compounds (e.g., bilirubin-glucuronides), drugs, toxic chemicals, nutraceuticals, and their conjugates [1].

Mutations in ABCC2 lead to Dubin-Johnson syndrome, characterized by conjugate hyperbilirubinemia [1]. In gastric cancer, ABCC2 high expression is correlated with better prognosis, and it can induce metabolic vulnerability and cellular ferroptosis via enhanced glutathione efflux. The ABCC2 24C > T polymorphism is a key factor influencing its expression [2]. In non-small cell lung cancer, PFKP can upregulate ABCC2 through the activation of NF-κB, promoting chemoresistance [3]. In Plutella xylostella, up-regulated ABCC2 expression is related to insecticide resistance [4]. In Spodoptera litura, ABCC2 is a functional receptor of Bacillus thuringiensis Cry1Ca [6]. In papillary renal cell carcinoma, ABCC2 brush-border expression correlates with higher gene expression and independently predicts survival outcomes [5].

In conclusion, Abcc2 plays a crucial role in the excretion of various substances at physiological barriers. Its function is closely related to multiple diseases and biological processes, such as hyperbilirubinemia in Dubin-Johnson syndrome, prognosis and ferroptosis in gastric cancer, chemoresistance in non-small cell lung cancer, insecticide resistance in insects, and survival outcomes in papillary renal cell carcinoma. Studies on Abcc2 using various models help to understand its biological functions and the underlying mechanisms of related diseases.