{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMAPKAPK5‐AS1 is a long noncoding RNA implicated in the regulation of tumorigenesis across multiple cancer types. In colorectal cancer, early investigations noted its unclear clinical significance"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ", while subsequent functional studies revealed that MAPKAPK5‐AS1 is significantly upregulated, acting as an oncogene. Elevated expression in colorectal tissues is associated with larger tumor size and advanced pathological stage. Knockdown experiments demonstrated that reducing MAPKAPK5‐AS1 levels inhibits cell proliferation and induces apoptosis, in part by modulating p21, thereby underscoring its role in promoting malignant progression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}, {"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn hepatitis B virus–related hepatocellular carcinoma, MAPKAPK5‐AS1 (also referred to as MAAS) is markedly overexpressed. Mechanistic studies indicate that MAAS enhances cell proliferation by stabilizing the c‐Myc protein, which in turn facilitates the transcriptional activation of cell cycle regulators such as CDK4, CDK6, and SKP2, thereby expediting the G1/S cell cycle transition. Notably, the upregulation of MAAS in M2 macrophages—cells that secrete exosomes transferring the RNA to neighboring hepatocellular carcinoma cells—further amplifies this oncogenic signaling, contributing to tumor progression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn thyroid cancer, MAPKAPK5‐AS1 is also overexpressed compared to normal thyroid cells. Functional assays have demonstrated that interference with MAPKAPK5‐AS1 significantly reduces cell proliferation and invasion while promoting apoptosis. These effects appear to be mediated via a competing endogenous RNA mechanism, whereby MAPKAPK5‐AS1 sponges miR-519e-5p, leading to an upregulation of the downstream target YWHAH, and thus contributing to the progression of thyroid malignancy."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond solid tumors, dysregulation of MAPKAPK5‐AS1 has been observed in non-malignant conditions. In rheumatoid arthritis, altered expression of MAPKAPK5‐AS1 in peripheral blood mononuclear cells correlates with clinical indexes and self-perception parameters, suggesting its potential as a biomarker for disease monitoring."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": " Similarly, in non‐functioning pituitary adenomas, overexpression of MAPKAPK5‐AS1 further supports its role as a candidate diagnostic biomarker in diverse pathological contexts."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Ting Yang, Wei-Cong Chen, Pei-Cong Shi, et al. 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