{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‐655 functions in a context‐dependent manner across diverse biological systems. In lung adenocarcinoma cells, miR‐655 is part of a cluster (with miR‐134 and miR‐487b) that becomes upregulated following TGF‑β1–induced epithelial–mesenchymal transition (EMT) and contributes to gefitinib resistance by targeting MAGI2 (reducing PTEN stability) (a."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In contrast, function‐based screening in pancreatic cancer models revealed that enforced expression of miR‑655 restores epithelial markers (e.g. E‑cadherin) while suppressing EMT inducers and thereby limits cell migration and invasion (b."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": " In pituitary tumor cells, miR‑655, along with several 14q32–mapped microRNAs, targets the oncogene PTTG1 to inhibit proliferation, migration and invasion (c"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": ", and aberrant expression of miR‑655 has also been linked to hepatocellular carcinoma development (d."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn other cancer types, the role of miR‑655 appears even more dichotomous. In human breast cancer cells, COX‑2/EP4 signaling stimulates miR‑655 overexpression, which in turn promotes proliferation, migration, invasion, EMT and stem‐like properties via activation of NOTCH/WNT pathways and resistance to TGF‑β signaling (a."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": " Similarly, increased miR‑655 (co‐operating with miR‑526b) enhances oxidative stress by upregulating TXNRD1 and suppressing its negative regulators, which further drives aggressive breast cancer phenotypes (b."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": " In esophageal squamous cell carcinoma, low plasma levels of miR‑655 correlate with lymphatic invasion and metastasis, and restoration of miR‑655 levels inhibits proliferation, migration, invasion and EMT (c."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": " Moreover, in osteoarthritis, suppression of miR‑655 via CCN2‐mediated signaling leads to increased IL‑17 production and osteoclastogenesis (d."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": " Notably, preliminary studies also indicate roles for miR‑655 in ovarian cancer (e"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": "and in the multifactorial etiology of cleft lip with or without cleft palate (f."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nA recurrent regulatory theme emerging from several studies is the modulation of miR‑655 activity by long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs). For instance, in laryngeal squamous cell carcinoma, LINC01194 acts as a sponge for miR‑655, thereby promoting the expression of the oncogene SOX18 (a."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": " Similarly, in endometrial carcinoma, lncRNA SNHG14 promotes malignancy through sequestration of miR‑655‑3p (b"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": ", while in hepatocellular carcinoma, both LINC01194 and circ_0001955 have been shown to sponge miR‑655‑3p, leading to derepression of SMAD5 and ACER3 respectively, and promoting tumor growth (c"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "13"}]}, {"type": "t", "text": "; d."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": " In oral squamous cell carcinoma and T-cell acute lymphoblastic leukemia, similar ceRNA mechanisms have been reported where lncRNAs (or related transcripts) negatively regulate miR‑655‑3p, facilitating oncogenic signaling (e"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "15"}]}, {"type": "t", "text": "; f."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "16"}]}, {"type": "t", "text": " Additionally, in liver-derived cells, treatment with Echinacea purpurea extract downregulates miR‑655‑3p, which in turn relieves repression of ABCG2, influencing drug transporter expression (g."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "17"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond cancer, miR‑655‑3p plays important roles in other physiological and pathological processes. In preeclampsia, miR‑655‑3p regulates trophoblast growth and invasiveness, potentially impacting placental development (a."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "18"}]}, {"type": "t", "text": " In bone biology, overexpression of miR‑655‑3p under conditions simulating microgravity promotes osteogenic differentiation and reduces apoptosis via targeting LSD1 and activating the BMP‑2/Smad pathway, suggesting therapeutic potential in osteoporosis (b."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "19"}]}, {"type": "t", "text": " Finally, in papillary thyroid carcinoma, circ‑LDLRAD3 sponges miR‑655‑3p, leading to increased MAPK1 expression and tumor progression; restoration of miR‑655‑3p levels attenuates cell proliferation and invasion (c."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "20"}]}, {"type": "t", "text": " Additional investigations in osteosarcoma (d"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "21"}]}, {"type": "t", "text": "and studies exploring the impact of oxidative stress on miR‑655 expression (e"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "22"}]}, {"type": "t", "text": "further underscore the versatile, context-specific functions of this microRNA.\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Kazuhiro Kitamura, Masahiro Seike, Tetsuya Okano, et al. 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