{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n FGD5 plays multifaceted roles in both normal vascular biology and cancer progression through its protein‐coding product and its antisense long noncoding RNA (FGD5‑AS1). The protein‐coding FGD5 is highly expressed in endothelial cells, where it functions as a Rho guanine nucleotide exchange factor (GEF) that activates small GTPases such as Cdc42 and Rac1. Through these actions, FGD5 regulates cytoskeletal reorganization, cell adhesion, survival, and angiogenic responses by sustaining key signaling cascades including those mediated by vascular endothelial growth factor receptor 2 (VEGFR2) as well as by modulating receptor recycling and downstream PI3K–Akt/mTORC2 pathways. In addition, FGD5 contributes to vascular integrity during inflammation—for example, its activation downstream of Tie‑2 prevents leakage during neutrophil extravasation—and has been implicated in the identification of hematopoietic stem cells as well as in rare congenital cardiovascular defects."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "6"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n In parallel, the antisense transcript FGD5‑AS1 is emerging as a potent oncogenic regulator in a wide range of malignancies. Multiple studies have reported that elevated FGD5‑AS1 expression promotes tumor cell proliferation, migration, invasion, and chemoresistance in cancers including non‐small cell lung cancer, colorectal cancer, glioblastoma, oral cancer, pancreatic cancer, cervical cancer, gastric cancer, melanoma, osteosarcoma, hepatocellular carcinoma, and breast cancer. Mechanistically, FGD5‑AS1 typically functions as a competing endogenous RNA (ceRNA) that sponges tumor‐suppressive microRNAs, resulting in the derepression of oncogenic targets such as CDCA7, FGFRL1, DDX5, TWF1, GTPBP4, and even factors that stabilize critical transcription regulators like Sox2; these events, in turn, drive cancer stem cell–like traits and resistance to therapy."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "7", "end_ref": "20"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Moreover, gene amplification and epigenetic alterations involving FGD5 have been associated with increased tumor cell proliferation and poorer prognosis in breast cancer, while disruption of FGD5 expression in gastric cancer has been linked to the maintenance of cancer stem cell–like traits and chemoresistance."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "23"}]}, {"type": "t", "text": " Finally, emerging data also suggest that FGD5 modulates pro‐angiogenic signals from chemokine receptors such as CXCR4 by regulating Rac1/PI3K‑β activity, further underscoring its central role in angiogenesis"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "24"}]}, {"type": "t", "text": ", and that miRNA targeting of FGD5 itself can influence cancer cell invasiveness."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "25"}]}, {"type": "t", "text": " Epigenetic inactivation of FGD5 has also been observed in certain cervical carcinomas."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "26"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n In summary, FGD5 exhibits dual functionality. Its protein product is a critical mediator of endothelial function, angiogenesis, and vascular homeostasis by orchestrating actin cytoskeletal dynamics and receptor signaling, while its antisense transcript FGD5‑AS1 acts as an oncogenic driver in diverse malignancies through microRNA sponging and upregulation of downstream effectors. Together, these insights highlight FGD5 and its regulatory network as promising targets for therapeutic intervention in both vascular disorders and cancer.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Roi Gazit, Pankaj K Mandal, Wataru Ebina, et al. 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