{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‐216b is emerging as an important microRNA with diverse tumor‐suppressive roles in a wide variety of human cancers. In multiple studies across malignancies – including hepatocellular carcinoma, esophageal squamous cell carcinoma, ovarian cancer, breast cancer, melanoma, and glioma among others – miR‐216b is frequently downregulated, and its decreased expression correlates with aggressive clinical features such as increased cell proliferation, invasion, metastasis, and poor prognosis. In some hematological malignancies like acute myeloid leukemia, however, aberrant levels of miR‐216b have also been reported to serve as potential biomarkers. These studies, conducted in both tissue specimens and in vitro models, underscore the general tumor‐suppressive and diagnostic potential of miR‐216b."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "13"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistically, miR‐216b exerts its tumor‐suppressive functions through direct targeting and repression of several oncogenic transcripts. For example, in colorectal cancer, miR‐216b is sponged by long noncoding RNAs such as SNHG7 and KCNQ1OT1, thereby releasing targets like GALNT1 and ZNF146 that promote tumor progression. Similarly, miR‐216b has been shown to target key signaling molecules, including c‐Jun (thereby attenuating AP‐1 transcription in endoplasmic reticulum stress–induced apoptosis), PARP1 (to overcome cisplatin resistance in ovarian cancer), FOXM1 in both cervical cancer and melanoma, cyclin T2 in gastric cancer, and HK2 in breast cancer, leading to modulation of proliferation, apoptosis, autophagy, and drug sensitivity. In addition, miR‐216b influences metabolic enzymes and drug‐metabolizing proteins (such as members of the UGT2B family) and modulates pathways like USP28/c‐Myc and PI3K/Akt signaling. These molecular insights highlight miR‐216b as a central node integrating various cellular processes that are critical for cancer cell survival and chemoresistance."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "14", "end_ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its mechanistic roles, miR‐216b holds significant promise as a therapeutic target and biomarker. Restoration of miR‐216b expression via mimic delivery has been shown to inhibit tumor growth, enhance chemosensitivity (for example, improving the efficacy of Taxol in gastric cancer and vemurafenib in melanoma), and reverse drug resistance in several cancer models. In some contexts, its expression is regulated by competing endogenous RNAs – including lncRNAs such as SNHG1, LINC01518, MYCNOS, and GAS5 – that sequester miR‐216b to modulate downstream oncogenic pathways. Moreover, circulating levels of miR‐216b correlate with disease status in cancers such as acute myeloid leukemia, non‐small cell lung cancer, and even in non‐malignant pathologies like atherosclerotic plaque stability. Collectively, these findings underscore the potential of targeting the SNHG/lncRNA–miR‐216b–mRNA axes for personalized cancer therapy and early diagnosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "25", "end_ref": "35"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Xinyu Xu, Yuxuan Fu, Jun Tong, et al. 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