{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nNeuroepithelial transforming gene 1 (NET1) is a RhoA‐specific guanine nucleotide exchange factor that plays a central role in orchestrating cytoskeletal dynamics, cell adhesion, and motility. By activating RhoA, NET1 stimulates the formation of actin stress fibers and focal adhesions, thereby modulating extracellular matrix degradation and promoting invasive behavior in diverse cellular contexts. Extracellular cues (including lysophosphatidic acid and transforming growth factor‐β) and metabolic kinases (such as AMPK) regulate its catalytic actions, underscoring its importance during early steps of cell invasion in cancers like gastric adenocarcinoma and in epithelial–mesenchymal transition events."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "7"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its well‐characterized catalytic function, NET1 activity is tightly regulated by its subcellular localization and protein–protein interactions. Predominantly confined to the nucleus under basal conditions, NET1 can be relocalized to the cytosol via phosphorylation events mediated by kinases such as PAK1 and JNK—events that alleviate its inhibitory restraints. Moreover, interactions with PDZ domain–containing proteins influence NET1’s stability and transformation potential, with alterations in its nuclear–cytoplasmic shuttling contributing to oncogenic signaling. These regulatory adaptations illustrate how post‐translational modifications and binding partnerships modulate NET1’s ability to activate RhoA and drive pathological cytoskeletal reorganization."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "18"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in cytoskeletal regulation and cell motility, aberrant NET1 expression has emerged as a pivotal contributor to cancer progression, chemoresistance, and adverse clinical outcomes across multiple tumor types including hepatocellular carcinoma, non‐small cell lung cancer, and colorectal cancer. Elevated NET1 levels promote tumor cell proliferation, invasion, and angiogenesis via modulation of mitotic spindle organization, apoptotic signaling, and DNA damage responses. Its expression is frequently controlled by regulatory non‐coding RNAs and transcription factors, further integrating NET1 into complex oncogenic networks. Collectively, these findings position NET1 not only as a master regulator of RhoA‐dependent signaling but also as a promising prognostic biomarker and therapeutic target in malignancy."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "19", "end_ref": "39"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Arthur S Alberts, Huajun Qin, Heather S Carr, et al. 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