EVA1A is encoded by the EVA1A gene and is also known as TMEM166 (transmembrane protein 166) or FAM176A (family with sequence similarity 176). EVA1A acts as a regulator of programmed cell death, mediating both autophagy and apoptosis. EVA1A is highly conserved in humans, chimpanzees, rats, mice, and dogs, indicating its importance in vertebrate animals. The expression profile analysis indicates that the expression of the EVA1A protein in most cancer tissues is negative or lower compared with that of normal tissues.
|Basic Information of EVA1A|
|Protein Name||Protein eva-1 homolog A|
|Aliases||Protein FAM176A, Transmembrane protein 166,TMEM166|
|Organism||Homo sapiens (Human)|
EVA1A is expressed in a cell- and tissue-specific manner and the expression level is decreased in many types of human tumors, such as gastric cancer, esophagus cancer, adrenal cortical carcinoma, pituitary adenoma, and parathyroid adenoma. In vivo and in vitro experiments have demonstrated that EVA1A overexpression inhibits the proliferation of tumor cells and induces both autophagy and apoptosis even under nutrient-rich conditions, and the appearance of autophagy usually precedes cell death. EVA1A stimulates autophagy by interacting with WD repeats of ATG16L1. Furthermore, it acts on downstream of the BECN1 complex and upstream of ATG16L1 and may be responsible for ATG12–5/16L1 recruitment to the isolation membrane. EVA1A, potentially as a component of the autophagosomal membrane, is closely related to the development and maturation of the autophagosome. The restoration of EVA1A in some cancer cell lines can induce cell death through both autophagy and apoptosis, suggesting that EVA1A is an effective tumor-suppressing molecule. So, EVA1A could be combined with chemotherapy in the treatment of tumors, which needs further exploration.
Fig.1 EVA1A (TMEM166) in cell death mechanisms (Mrschtik, 2015).
The findings of this article show that EVA1A is a novel regulator involved in both autophagy and apoptosis for the first time because the suppression of EVA1A inhibits starvation-induced autophagy.
The results of this article provide a comprehensive view of our understanding of the pathways involved in the role of EVA1A in autophagy and programmed cell death.
Authors of this article generate a specific rabbit polyclonal antibody against human EVA1A and assess the expression of this protein in various human normal and tumor tissue samples by tissue microarray-based immunohistochemical analysis, suggesting that EVA1A expression was widely downregulated in the cancer tissues.
This article reports a recombinant adenovirus 5- EVA1A vector (Ad5-TMEM166) and evaluates its expression and anti-tumor activities in vitro and in vivo, indicating that Ad5- EVA1A may be a novel gene therapy candidate for cancer.
This article demonstrates that EVA1A regulates embryonic neurogenesis by modulating autophagy and provides potential implications for understanding the pathogenesis of neurodevelopmental disorders caused by autophagy dysregulation.
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