Slc34a2, encoding the sodium-dependent phosphate transport protein 2B (NaPi-2b), is crucial for phosphate transport. It is involved in pathways related to phosphate homeostasis and has overall biological importance in maintaining normal physiological functions. Genetic models, like KO/CKO mouse models, are valuable for studying its functions [1,4].

The generation of a conditional NaPi-IIb (product of Slc34a2) knockout mouse demonstrated its critical role in maintaining skeletal integrity during phosphate restriction. Under normal physiological conditions, the passive sodium-independent pathway may be more dominant for intestinal phosphate absorption [1].

Mutations in Slc34a2 are responsible for pulmonary alveolar microlithiasis (PAM), a rare autosomal recessive disorder characterized by calcium phosphate microlith deposition in the lungs [2,4].

In cancer research, knockdown of Slc34a2 in glioma inhibits cell proliferation, metastasis, and elevates chemosensitivity. In esophageal squamous cell carcinoma, it promotes cell proliferation by activating STX17-mediated autophagy. In colorectal cancer, it promotes cancer proliferation and cell cycle progression by targeting TMPRSS3 [3,5,6].

In conclusion, Slc34a2 is essential for phosphate homeostasis and skeletal integrity. Its mutations are linked to PAM. In cancer, it plays roles in promoting cell proliferation, metastasis, and chemoresistance. The study of Slc34a2 using KO/CKO mouse models has provided insights into these disease-related mechanisms, facilitating a better understanding of related biological processes and potential therapeutic strategies [1,2,3,4,5,6].