{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nThe studies collectively underscore that the cancer‐associated protein—here predominantly investigated as ENOX2 (also known as tNOX)—plays a central role in promoting cancer cell growth. Overexpression of this cell surface NADH oxidase in mouse embryonic fibroblasts and transgenic mice leads to accelerated proliferation, increased cell size, and higher carcass mass. Furthermore, these cells exhibit a pronounced sensitivity to inhibitors such as (–)-epigallocatechin-3-gallate and phenoxodiol, which selectively trigger apoptosis in the cancer cells while leaving their normal counterparts largely unaffected."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAdditional investigation into the modulation of ENOX2 expression has revealed a cancer-specific alternative splicing event. Specifically, in certain transformed cells, exon 4 is skipped from the ENOX2 transcript via a mechanism driven by hnRNP F binding to an exonic splicing silencer element. This post-transcriptional process underscores a finely tuned regulatory mechanism that might be functionally analogous to the regulation of other related genes such as FAM182A."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFinally, while the precise role of ENOX2 in the immunological interplay within the tumor microenvironment remains under active investigation, its cancer-restricted expression and contribution to unregulated growth suggest that it could influence chemosensitization and immune surveillance. Such multifaceted activity as a promoter of aberrant cell growth and potential mediator of immunosuppressive signals hints at how related factors—potentially including FAM182A—might exert similar oncogenic and regulatory functions."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Kader Yagiz, Lion-Ying Wu, Charles P Kuntz, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Mouse embryonic fibroblast cells from transgenic mice overexpressing tNOX exhibit an altered growth and drug response phenotype."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Cell Biochem (2007)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1002/jcb.21184"}], "href": "https://doi.org/10.1002/jcb.21184"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "17115410"}], "href": "https://pubmed.ncbi.nlm.nih.gov/17115410"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Kader Yagiz, Paul W Snyder, D James Morré, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Cell size increased in tissues from transgenic mice overexpressing a cell surface growth-related and cancer-specific hydroquinone oxidase, tNOX, with protein disulfide-thiol interchange activity."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Cell Biochem (2008)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1002/jcb.21962"}], "href": "https://doi.org/10.1002/jcb.21962"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "18980249"}], "href": "https://pubmed.ncbi.nlm.nih.gov/18980249"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Xiaoyu Tang, Vanessa D Kane, Dorothy M Morré, et al. "}, {"type": "b", "children": [{"type": "t", "text": "hnRNP F directs formation of an exon 4 minus variant of tumor-associated NADH oxidase (ENOX2)."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Mol Cell Biochem (2011)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1007/s11010-011-0875-5"}], "href": "https://doi.org/10.1007/s11010-011-0875-5"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "21625959"}], "href": "https://pubmed.ncbi.nlm.nih.gov/21625959"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Ngar-Woon Kam, Olivier Laczka, Xiang Li, et al. "}, {"type": "b", "children": [{"type": "t", "text": "ENOX2 inhibition enhances infiltration of effector memory T-cell and mediates response to chemotherapy in immune-quiescent nasopharyngeal carcinoma."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Adv Res (2024)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.jare.2023.04.001"}], "href": "https://doi.org/10.1016/j.jare.2023.04.001"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "37061217"}], "href": "https://pubmed.ncbi.nlm.nih.gov/37061217"}]}]}]}