Ptosis can market aggressiveness and poor progThe resistance of tumor cells to 2-Methoxyestradiol site apoptosis can market aggressiveness and poor prog nosis in many physiological situations, which include hypoxia, nutrient deprivation, and nosis in various physiological circumstances, including hypoxia, nutrient deprivation, and an anticancer drug remedy. Hence, the identification of strategies to overcome the reticancer drug therapy. Consequently, the identification of approaches to overcome the re sistance of tumor cells to apoptosis will significantly enable boost the effectiveness of sistance of tumor cells to apoptosis will significantly aid enhance the effectiveness of tumor remedy. In addition, NDRG2 expression is positively correlated with apoptumor therapy. In addition, NDRG2 expression is positively correlated with apoptosis tosis induced by metabolic stressors, for instance oxygen deprivation, glucose deprivation, induced by metabolic stressors, including oxygen deprivation, glucose deprivation, or both, or both, and anticancer drug treatments. Though mechanisms that regulate NDRG2 and anticancer drug remedies. Though mechanisms that regulate NDRG2 gene expres gene expression and NDRG2-mediated improvements of tumor cell apoptosis happen to be sion and NDRG2mediated improvements of tumor cell apoptosis have already been presented, presented, the molecular mechanisms of those aspects are unclear. Though its Exendin-4 web functional the molecular mechanisms of these elements are unclear. Despite the fact that its functional domain is domain just isn’t well-known, NDRG2 has not too long ago been reported to interact with kinases or not well-known, NDRG2 has not too long ago been reported to interact with kinases or phospha phosphatases (or both). Its prospective as an adapter protein that mediates protein rotein tases (or each). Its possible as an adapter protein that mediates protein rotein interac interactions appears to induce antitumor phenotypes in various tumor cells. In the future, tions appears to induce antitumor phenotypes in various tumor cells. In the future, the the continued discovery of and functional research on proteins that interact with NDRG2 continued discovery of and functional studies on proteins that interact with NDRG2 needs to be carried out. It can be anticipated that tumor therapy tactics that account for the need to be conducted. It can be expected that tumor treatment methods that account for theCells 2021, 10, x ten, 2649 Cells 2021,9 eight of 12 ofexpression pattern of NDRG2 or that regulate NDRG2 expression ought to improve the expression pattern of NDRG2 or that regulate NDRG2 expression must enhance the ef efficiency of tumor treatment options. ficiency of tumor treatments.Figure 5. Overview of NDRG2 function in several stimuli-mediated apoptosis. Figure 5. Overview of NDRG2 function in different stimulimediated apoptosis.Author Contributions: K.D.K. drafted the manuscript outline; K.D.K., G.K., and S.L. conceived the suggestions and prepared the figures. All authors have study and agreed for the published version of your concepts and prepared the figures. All authors have study and agreed towards the published version with the manuscript. manuscript.Funding: This function was supported by the BioGreen21 Agri-Tech Innovation Plan (SA00016073), Author Contributions: K.D.K. drafted the manuscript outline; K.D.K., G.K., and S.L. conceived theFunding: This perform was supported Korea, andBioGreen21 Investigation Foundation of Korea the Rural Improvement Administration, b.