{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMTUS1 encodes a family of proteins (collectively known as ATIPs) that act as potent tumor suppressors in a wide range of human cancers. In diverse cellular contexts—including colon, pancreatic, gastric, oral, and other tumors—MTUS1 expression is associated with inhibition of cell proliferation and induction of differentiation. Its products interact with the angiotensin II type 2 receptor (AT2R), thereby counteracting mitogenic signals such as those mediated by receptor tyrosine kinases and growth factors, reducing ERK activation and DNA synthesis, and often localizing to mitochondria to regulate energy and apoptotic pathways."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its classical role in restraining proliferation, certain MTUS1 isoforms—particularly ATIP3—regulate the dynamics of the microtubule cytoskeleton. By interacting with key microtubule‐associated proteins (such as EB1 and kinesins) and controlling spindle length and microtubule turnover, ATIP3 contributes to mitotic fidelity, limits cell polarity, and suppresses migratory behavior that is critical for metastasis. This microtubule‐stabilizing function underlies its value as a prognostic biomarker, notably in aggressive breast cancers, and supports its emerging role in predicting therapeutic responses to taxane-based chemotherapy."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "20"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMTUS1 expression itself is subject to tight regulation at multiple levels. Epigenetic modifications such as promoter DNA methylation and histone deacetylation, as well as post‐transcriptional control by a host of microRNAs and long noncoding RNAs, modulate its expression and, consequently, its tumor suppressive functions. Moreover, genetic alterations—including copy number variants and deleterious non‐synonymous SNPs—can compromise MTUS1 activity, thereby contributing to oncogenic processes in lung, colorectal, and bladder carcinomas among others."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "27"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its cell‐intrinsic tumor suppressive roles, MTUS1 contributes to vascular homeostasis and mitochondrial integrity. In endothelial cells, MTUS1 modulates p38 MAPK signaling and cytokine production, while also interfacing with mitochondrial fusion proteins to sustain an elongated mitochondrial network and reduce oxidative stress. These mechanisms not only protect vascular cells from stress-induced apoptosis but also reinforce the anti-tumor microenvironment through proper mitochondrial function."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "28", "end_ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAdditional studies have expanded the clinical and biological landscape of MTUS1. Investigations in prostate cancer, for example, corroborate its role in restraining mitochondrial fission and inhibiting cellular invasion. Furthermore, emerging regulatory networks—encompassing interactions with other growth regulatory proteins and noncoding RNAs—highlight the potential of MTUS1 as both a diagnostic marker and a therapeutic target in personalized oncologic strategies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "33", "end_ref": "36"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Stefan Seibold, Claudia Rudroff, Manfred Weber, et al. 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