{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nIn colorectal cancer, several studies have highlighted a distinct dysregulation of miR‑625 expression. Notably, high levels of the miR‑625‑3p isoform have been linked to poor clinical response to oxaliplatin‐based treatments and overall chemoresistance. Functional analyses revealed that miR‑625‑3p enhances resistance by directly targeting signaling mediators such as MAP2K6, leading to subsequent alterations in p38 MAPK activity. In addition, aberrant miR‑625 expression has been associated with metastatic potential in this tumor type."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nConversely, in other gastrointestinal and related malignancies—including esophageal carcinoma, hepatocellular carcinoma, thyroid cancer, and malignant melanoma—miR‑625 is frequently downregulated, which in turn seems to release suppression of several oncogenic targets. For example, restoration of miR‑625 levels suppresses cell proliferation, migration, invasion, and metastatic dissemination by targeting key molecules such as Sox2 in esophageal cancer, IGF2BP1 in hepatocellular carcinoma, and SCAI in melanoma; in thyroid cancer, miR‑625‑3p appears to modulate proliferative and invasive behaviors."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "9"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn non‐small cell lung cancer and cervical carcinoma, altered levels of miR‑625‑5p have been implicated in the development of chemoresistance and tumor progression. In lung cancer, for instance, diminished expression of miR‑625‑3p correlates with resistance to agents such as gefitinib and cisplatin through modulation of regulators including AXL and WEE1. Meanwhile, in cervical cancer, miR‑625‑5p exerts tumor‐suppressive effects by targeting components of the NF‑κB pathway, thereby inhibiting cell proliferation and invasion."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFurthermore, a growing body of evidence supports the notion that miR‑625 activity is finely tuned by a network of competing endogenous RNAs. Oncogenic circular RNAs and long noncoding RNAs—such as circ_0007534 in pancreatic ductal adenocarcinoma, circ‑SNAP47 in non‐small cell lung cancer, LINC00511 in gastric cancer, LINC00909 in pediatric acute myeloid leukemia, and circSEC62 in hepatocellular carcinoma—act as molecular sponges that sequester miR‑625‑5p. This sequestration effectively relieves miR‑625’s inhibition of downstream targets (including STAT3, IGF‑1R, and SNRPA), thereby promoting tumor progression and therapeutic resistance."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Mads H Rasmussen, Niels F Jensen, Line S Tarpgaard, et al. 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