{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nIn hematologic malignancies, PBX3 plays a central role as part of a homeobox gene signature that is associated with adverse outcomes. In cytogenetically abnormal acute myeloid leukemia, down‐regulation of miR‐181 family members leads to up‐regulation of PBX3 (with HOXA7/HOXA9/HOXA11), correlating with poor survival."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In MLL‐rearranged AML, PBX3 is consistently coexpressed with HOXA9 and functions as a critical cofactor for HOXA9–mediated leukemic transformation; its depletion dramatically impairs MLL‐fusion–driven cell transformation."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": " Moreover, co‐expression of PBX3 with MEIS1 is sufficient to induce AML in experimental models"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": ", while epigenetic aberrations in leukemic stem cells yield high PBX3 levels that are essential for leukemia maintenance."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": " A four‐gene HOXA/TALE signature that includes PBX3 predicts adverse outcome in cytogenetically normal AML and appears to contribute to chemoresistance"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": ", and in NPM1‐mutated AML, PBX3 up‐regulation—partially via DOT1L–mediated H3K79 hypermethylation—is critical for leukemic cell survival."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn a diverse range of solid tumors, PBX3 overexpression promotes malignant phenotypes by enhancing proliferation, migration, invasion, and the epithelial–mesenchymal transition. In hepatocellular carcinoma (HCC), PBX3 is necessary and sufficient for the acquisition and maintenance of tumor‐initiating properties, with several microRNAs (eg, miR‐33a‐3p and miR‐302a) shown to directly target PBX3 and thereby suppress tumor progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "7", "end_ref": "9"}]}, {"type": "t", "text": " In colorectal cancer, PBX3 contributes to a full EMT phenotype and its expression—as regulated by WNT activation and EMT transcription factors—is linked to metastasis and poor survival."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "13"}]}, {"type": "t", "text": " In prostate cancer, androgen regulation of PBX3 and its unusual shift from nuclear to cytosolic localization together have prognostic implications."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": " In gastric cancer, PBX3 is commonly overexpressed where it drives EMT, with repression by miR‐144‑3p limiting cell proliferation and invasion."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "16", "end_ref": "18"}]}, {"type": "t", "text": " Similar oncogenic roles have been elucidated in pilocytic astrocytoma"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "19"}]}, {"type": "t", "text": ", multiple myeloma"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "20"}]}, {"type": "t", "text": ", and glioma where PBX3 sustains cell cycle progression and tumor growth."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "23"}]}, {"type": "t", "text": " In addition, in pancreatic and papillary thyroid carcinomas, PBX3 fosters proliferation, migration, and angiogenesis"}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "24", "end_ref": "26"}]}, {"type": "t", "text": ", while in melanoma, competitive regulation by miR‑4458 and HuR modulates PBX3 levels to impact cell growth and migration."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "27"}]}, {"type": "t", "text": " Furthermore, in breast cancer, stabilization of PBX3 via USP14‐mediated deubiquitination downstream of ATRAP contributes to enhanced tumor aggressiveness"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "28"}]}, {"type": "t", "text": ", and in cervical and bladder cancers, PBX3 is similarly targeted by tumor‐suppressive miRNAs or modulated through competing endogenous RNAs to regulate EMT and cell survival."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its direct oncogenic functions, PBX3 is subject to diverse regulatory and epigenetic modifications that bear prognostic and therapeutic significance. Aberrant promoter methylation of PBX3 in peripheral blood leukocytes has been explored as a prognostic marker in colorectal and gastric cancers."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "31"}]}, {"type": "t", "text": " In sepsis, the 3′‐UTR of PBX3 acts as a competing endogenous RNA to modulate HMGB1 expression and thereby elicit inflammatory responses."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "33"}]}, {"type": "t", "text": " Similarly, in the context of preeclampsia, noncoding RNAs—including miR‑655‑3p and circRNAs—regulate PBX3 in trophoblasts, affecting cell invasion and migration."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "34"}]}, {"type": "t", "text": " Finally, genetic studies evaluating PBX3 polymorphisms in congenital heart defects and celiac disease have underscored its potential role as a modifier gene, although not all associations reach significance."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "36"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Zejuan Li, Hao Huang, Yuanyuan Li, et al. 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