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We report the identification of a novel secreted peptide, INM02. The mRNA transcript of human INM02 gene is about 3.0 kb. Its open-reading frame contains 762 bps and encodes a protein of 254 amino acids. Northern blot analysis demonstrates that INM02 mRNA is widely expressed in rat tissues, especially with abundant quantities in pancreatic islets, testis, and bladder tissue. We have expressed recombinant INM02 protein and generated rabbit anti-INM02 polyclonal antibodies. We show here that INM02 could be detectable in human serum by ELISA. We also present evidence that INM02 mRNA expression could be regulated by glucose. Experiments on both MIN6 cells and intact isolated islets demonstrate that INM02 mRNA levels are increased more than threefold by high glucose (25 mM) when compared with low glucose (5.5 mM). ELISA analysis shows that secretion of INM02 is significantly augmented by high glucose in vitro. It is speculated that as a novel secreted protein, INM02 is associated with functions of pancreatic islets, especially of β-cells.
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The solute carrier (SLC) family is a large group of membrane transport proteins. Their dysfunction plays an important role in the pathogenesis of thyroid cancer. The most well-known SLC is the sodium-iodide symporter (NIS), also known as sodium/iodide co-transporter or solute carrier family 5 member 5 (SLC5A5) in thyroid cancer. The dysregulation of NIS in thyroid cancer is well documented. The role of NIS in the uptake of iodide is critical in the treatment of thyroid cancer, radioactive iodide (RAI) therapy in particular. In addition to NIS, other SLC members may affect the autophagy, proliferation, and apoptosis of thyroid cancer cells, indicating that an alteration in SLC members may affect different cellular events in the evolution of thyroid cancer. The expression of the SLC members may impact the uptake of chemicals by the thyroid, suggesting that targeting SLC members may be a promising therapeutic strategy in thyroid cancer.
