{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRBM3 is a highly conserved, cold‐inducible RNA‐binding protein that is rapidly upregulated under cellular stress conditions such as mild hypothermia, hypoxia, and other adverse microenvironments. Its induction occurs via increased transcription that is independent of the classical hypoxia‐inducible factor pathway and mitochondrial signaling, and it functions to enhance mRNA stability and translation of key survival and growth regulators (for example, COX‑2, VEGF and IL‑8) while counteracting apoptosis. Such responses have been documented in leukemia and other cell models exposed to low oxygen tension and cold stress."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the oncologic setting, RBM3 displays multifaceted roles that appear context dependent. Elevated nuclear RBM3 expression has been associated with favorable clinical outcomes in breast, ovarian, prostate, colorectal, bladder, esophageal, lung, and pancreatic cancers—often correlating with lower-grade tumors, reduced proliferation markers, and improved survival. In contrast, experimental overexpression of RBM3 in vitro can potentiate anchorage‑independent growth and promote cell cycle progression by modulating alternative splicing (for example, of CD44 isoforms) and activating β‑catenin signaling cascades that enhance stem‑like properties. Moreover, non‑coding RNAs and splicing regulators have been shown to modulate RBM3 levels and related tumor phenotypes, underscoring its integral role in tumor biology."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in tumorigenesis, RBM3 confers significant neuroprotective and cytoprotective benefits. In neural cells, upregulation of RBM3 under mild hypothermia or stress conditions alleviates apoptotic cell death induced by ultraviolet irradiation and neurotoxins through inhibition of key MAPK pathways (p38, JNK and ERK). Its abundant expression in the developing brain further supports a role in neuronal survival. In models of hepatic and myocardial ischemia‑reperfusion injury, RBM3 induction mitigates tissue damage by activating autophagy and suppressing apoptotic signaling, while in systemic inflammatory settings such as sepsis‑associated acute lung injury, RBM3 appears to temper the inflammatory cascade via NF‑κB/NLRP3 regulation. Structural studies have elucidated that RBM3 harbors a canonical RNA recognition motif along with flexible, disordered regions that facilitate temperature‑dependent oligomerization—a feature likely pivotal for its RNA‑regulatory functions. Reviews and targeted studies further underscore RBM3’s importance as a mediator of cellular adaptation to stress and as a promising candidate for therapeutic modulation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "25", "end_ref": "37"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Sven Wellmann, Christoph Bührer, Eva Moderegger, et al. 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