Slc16a1, also known as monocarboxylate transporter 1 (MCT1), is a proton-dependent transporter that serves as a lactate transporter [1,2]. It is involved in multiple biological processes, and its function is crucial for maintaining normal physiological conditions. It participates in regulating the internal and external environment, glycolysis, and redox homeostasis in cells [4]. Mutations in SLC16A1 have been associated with congenital hyperinsulinism, as it is one of the key genes involved in the regulation of insulin secretion from pancreatic β-cells [3].

In hepatocellular carcinoma (HCC), HCC exosomal SLC16A1-AS1 (antisense RNA of SLC16A1) enhances mRNA stabilization of SLC16A1 in macrophages by promoting the interaction between 3' untranslated regions (3'UTR) of SLC16A1 mRNA and heterogeneous nuclear ribonucleoprotein A1 (HNRNPA1). SLC16A1 then accelerates lactate influx and activates c-Raf/ERK signaling to induce M2 polarization of macrophages. Reciprocally, M2 macrophages secrete IL-6 to promote HCC cell proliferation, invasion, and glycolysis [1]. In cervical cancer, SLC16A1 is highly expressed and is a critical hub for regulating the internal and external environment, glycolysis, and redox homeostasis. Inhibiting SLC16A1 provides a new approach to eliminate cervical cancer [4].

In conclusion, SLC16A1 plays essential roles in multiple biological processes and is closely associated with diseases such as congenital hyperinsulinism, hepatocellular carcinoma, and cervical cancer. Functional studies, especially those using gene knockout or conditional knockout mouse models, could further reveal its detailed functions and underlying mechanisms in these diseases, providing potential therapeutic targets for related disorders [1,3,4].