Anti-FAM3D monoclonal antibody, clone 469304

Dysregulated glucagon secretion is a hallmark of type 2 diabetes (T2D). To date, few effective therapeutic agents target on deranged glucagon secretion. Family with sequence similarity 3 member D (FAM3D) is a novel gut-derived cytokine-like protein, and its secretion timing is contrary to that of glucagon. However, the roles of FAM3D in metabolic disorder and its biological functions are largely unknown. In the present study, we investigated whether FAM3D modulates glucagon production in mouse pancreatic alpha TC1 clone 6 (alpha TC1-6) cells. Glucagon secretion, prohormone convertase 2 (PC2) activity, and mitogen-activated protein kinase (MAPK) pathway were assessed. Exogenous FAM3D inhibited glucagon secretion, PC2 activity, as well as extracellular-regulated protein kinase 1/2 (ERK1/2) signaling and induced MAPK phosphatase 1 (MKP1) expression. Moreover, knockdown of MKP1 and inhibition of ERK1/2 abolished and potentiated the inhibitory effect of FAM3D on glucagon secretion, respectively. Taken together, FAM3D inhibits glucagon secretion via MKP1-dependent suppression of ERK1/2 signaling. These results provide rationale for developing the therapeutic potential of FAM3D for dysregulated glucagon secretion and T2D.

Although numerous differential long noncoding RNAs (IncRNAs) have been identified, the relationship between lncRNA and colorectal cancer (CRC) still remains largely unclear. In the present study, we investigated the function and provided a possible mechanism of lncRNA FAM3D-AS1 in CRC. CCK8, transwell, and trypan blue staining were used to evaluate the proliferation, invasion, and cell death rates. Real-time PCR was used to elucidate the expression level of FAM3D-AS1. We found that lncRNA FAM3D-AS1 located in cytoplasm. Overexpression of FAM3D-AS1 significantly inhibited the cell proliferation, cell survival rates, and invaded cells. We also provided evidence that FAM3D-AS1 reversed the EMT process. Moreover, we proved that FAM3D-AS1 inhibits CRC development through NF-kappa B signaling pathway. Taken together, we performed functional analysis of FAM3D-AS1 and provided a possible mechanism in the development of CRC. Our study provided new targets for clinical treatment.