{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n Research on CRYBG3 has revealed that this gene product functions in a multifaceted manner in cancer cells, particularly in non‐small cell lung cancer. In several studies, a long noncoding RNA (lncRNA) form of CRYBG3 has been shown to regulate key aspects of tumor cell behavior. For instance, CRYBG3 can interact with the translation factor eEF1A1 to upregulate MDM2 expression, thereby promoting p53 degradation and contributing to enhanced metastatic ability and radioresistance."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In contrast, another study demonstrated that ionizing radiation induces lncRNA CRYBG3, which interferes with mechanotransduction by dysregulating F‐actin organization and activating the LATS1/2 kinases; this in turn leads to the nuclear exclusion of YAP/TAZ and suppression of cell proliferation and invasion."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Moreover, CRYBG3 has been implicated in the regulation of mitosis. It can directly bind to Bub3, disrupting its interaction with CDC20 and thereby impairing the mitotic checkpoint. This disruption facilitates aneuploidy and tumorigenesis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": " Similarly, by binding G‐actin, CRYBG3 inhibits actin polymerization and the assembly of contractile rings, leading to M‐phase arrest; alterations in its expression were associated with changes in malignant phenotypes."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n In addition, CRYBG3 appears to modulate tumor energetics, as it has been found to interact with lactate dehydrogenase A—a key enzyme in glycolysis—and is highly upregulated in lung cancer tissues, suggesting a role in reprogramming metabolic pathways to favor tumor progression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": " \n "}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Complementary to its regulatory functions in cancer cells, structural studies of a βγ‐crystallin domain of non–lens CRYBG3 from mouse brain have revealed unique unfolding pathways and specialized biophysical properties, suggesting that evolutionary changes—such as the loss of canonical Ca²⁺‐binding sites—may underlie distinct functional adaptations in non–lens tissues."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": " \n "}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n In summary, CRYBG3 emerges as a pleiotropic factor that can both promote tumor progression—by fostering metastasis, radioresistance, and aneuploidy through interactions with proteins governing the cell cycle, cytoskeletal dynamics, and metabolic regulation—and, under certain conditions, trigger cell-cycle arrest and cell death. These multifaceted roles make CRYBG3 a promising candidate for targeted therapeutic intervention in cancer.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Anqing Wu, Jiaxin Tang, Ziyang Guo, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Long Non-Coding RNA CRYBG3 Promotes Lung Cancer Metastasis via Activating the eEF1A1/MDM2/MTBP Axis."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Int J Mol Sci (2021)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.3390/ijms22063211"}], "href": "https://doi.org/10.3390/ijms22063211"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "33809929"}], "href": "https://pubmed.ncbi.nlm.nih.gov/33809929"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Anqing Wu, Jiaxin Tang, Yingchu Dai, et al. 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