Creative Biolabs is a world-leading services provider of application-specific antibody development. We have launched high-quality in vitro diagnostic (IVD) antibody development and immunoassay development services targeting a wide range of disease biomarkers and pathogens. Here, briefly introduce NFE2L2 as a potential cancer biomarker and our customized services targeting this biomarker.
Nuclear factor erythroid-derived 2-like 2, also known as NFE2L2 or Nrf2, is a member of the cap ‘n' collar family (CNC-family) that encoded by the human NFE2L2 gene and abundantly expressed in numerous cancer cells. It is extensively involved in the regulation of the expression of various proteins, including detoxifying enzymes, antioxidant proteins, metal-binding proteins, drug-metabolizing enzymes, molecular chaperones, and drug efflux transporters. Under normal or unstressed conditions, Nrf2 is kept in the cytoplasm by a cluster of proteins that degrade it quickly. Under oxidative stress, Nrf2 is not degraded but instead travels to the nucleus where it binds to a DNA promoter and initiates transcription of antioxidative genes and their proteins. Furthermore, NFE2L2 plays a pivotal role in endogenous protection against oxidative stress by preventing oxidation of macromolecules.
Studies have reported that NFE2L2 is abundantly expressed in many cancer cells and relates to proliferation, invasion, and chemoresistance. The high expression level of NFE2L2 usually indicates a poor prognosis in kinds of cancers such as human hepatocellular carcinoma and lung cancer. NFE2L2 also has a function of activating six proteins, including CCT7, ESD, HPRT1, PSMD12, PSMD5, and RPLP0. Based on the expression of these six proteins, it has been predicted that NFE2L2 was activated in the follicular adenoma tissue. Besides, the level of NFE2L2 genes is higher in pleomorphic adenoma tissue in comparison to the healthy parotid gland. Whereas, decreasing the expression of NFE2L2 can lead to inhibiting proliferation and tumorigenicity of cancer cells which makes NFE2L2 a drug target candidate of follicular adenoma.
Fig.1 Links between NFE2L2 signalling and epithelial-to-mesenchymal transition (EMT).1
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