{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR‐135b is frequently upregulated in diverse human malignancies and exerts potent oncogenic functions. For instance, in multiple myeloma cells maintained under chronic hypoxia, increased exosomal miR‐135b suppresses factor‐inhibiting hypoxia‐inducible factor 1 (FIH‐1) in endothelial cells, thereby promoting angiogenesis. In colorectal cancer, miR‐135b overexpression—triggered by APC loss, PTEN/PI3K pathway deregulation, and SRC overexpression—enhances tumor transformation, progression and correlates with poor clinical outcome; similarly, it targets TGF‑β receptor 2 to further compromise tumor‐suppressive signaling. In non‐small cell lung cancer, elevated miR‐135b augments cell invasiveness and migration by directly repressing components of the Hippo pathway, while in anaplastic large cell lymphoma it mediates NPM–ALK–driven oncogenicity and shifts the tumor immune‐phenotype."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "6"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn additional solid tumors and lymphomas, miR‐135b contributes to a malignant phenotype through diverse mechanisms. In diffuse large B‐cell lymphoma, for example, the long noncoding RNA SMAD5‐AS1 suppresses miR‐135b‐5p to allow adenomatous polyposis coli (APC) expression and consequent inhibition of the Wnt/β‐catenin pathway. Conversely, in non‐small cell lung cancer, lncRNA GAS5 downregulation leads to elevated miR‐135b that is linked to enhanced tumorigenesis and radioresistance. In hepatocellular carcinoma, miR‐135b is frequently amplified and directly targets metastasis suppressors RECK and EVI5 under the transcriptional control of HSF1, thereby promoting cell motility and metastasis. In pancreatic ductal adenocarcinoma, miR‐135b is induced by glutamine deprivation via ROS‐dependent mutant p53 activation; it targets phosphofructokinase‑1 (PFK1) to shift glucose utilization toward the TCA cycle, and in separate pancreatic cancer models, it promotes migration, invasion, and epithelial–mesenchymal transition by directly inhibiting NR3C2. In breast cancer, miR‐135b increases proliferation, invasion and disturbs cell cycle progression by suppressing LATS2; moreover, in gastric cancer arising in the context of Helicobacter pylori infection, NF‑κB–mediated miR‐135b‑5p induction reduces KLF4 expression and confers cisplatin resistance. In colorectal cancer, miR‐135b additionally drives chemoresistance to 5‑fluorouracil by targeting ST6GALNAC2 through the PI3K/AKT pathway, while in glioblastoma multiforme its upregulation is associated with radioresistance via direct targeting of GSK3β. In triple‑negative breast cancer, high miR‑135b expression marks a basal‐like phenotype that modulates the TGF‑β and Wnt/β‑catenin pathways via suppression of APC, and a single nucleotide polymorphism in the 3′‑UTR of CD133 creates a new binding site for miR‑135a/b that is linked to reduced lung cancer risk. Finally, in hepatocellular carcinoma, Gα12 signaling stimulates miR‑135b (via JunB/AP‑1 activation) to repress FOXO1, thereby promoting cell cycle progression and tumor growth, and in osteosarcoma, miR‑135b forms a positive feedback loop with transcriptional co‑activator TAZ, suppressing its inhibitors and reinforcing EMT and metastasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "7", "end_ref": "22"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in promoting oncogenesis, miR‑135b is critically involved in cell differentiation and microenvironmental regulation. In the context of bone biology, elevated miR‑135b in mesenchymal stem cells from multiple myeloma patients impairs osteogenic differentiation via targeting SMAD5, while a reciprocal downregulation during osteogenesis is necessary for proper mineralization in unrestricted somatic stem cells. In the cardiovascular realm, increased circulating miR‑135b‑5p in atherosclerotic patients enhances proliferation and migration of endothelial and vascular smooth muscle cells through repression of MEF2C. Likewise, during neuroectoderm development, PAX6‐induced activation of miR‑135b promotes neural lineage commitment by targeting key components of the TGF‑β and BMP signaling pathways, and in osteoblasts miR‑135b confers protection against dexamethasone‑induced toxicity by downregulating its phosphatase target Ppm1e to activate AMPK signaling."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "23", "end_ref": "27"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nmiR‑135b has also been implicated in non‑oncologic as well as microenvironmental inflammatory responses. In models of Parkinson’s disease, miR‑135b exerts a neuroprotective role by inhibiting pyroptosis through direct targeting of FoxO1, thereby mitigating inflammatory cell death. In podocyte injury models, concurrent upregulation of miR‑135b (alongside its family member miR‑135a) disrupts cytoskeletal organization via downregulation of GSK3β, contributing to glomerular pathology. Moreover, in multiple myeloma–related bone disease, increased serum levels of miR‑135b correlate with the severity of lytic lesions and predict poorer patient survival, highlighting its value as a noninvasive biomarker."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "28", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFinally, miR‑135b is emerging as a valuable diagnostic and regulatory biomarker. Its increased expression profiles in nasopharyngeal and cutaneous squamous cell carcinomas—as well as detection via stool‑based screening for colorectal cancer—underline its potential in noninvasive diagnostics. In glioblastoma stem‑like cells, restoration of miR‑135b significantly attenuates proliferation, invasion and brain infiltration, while additional evidences of its regulatory impact come from studies demonstrating that altered miRNA binding (for example, via SNPs in the 3′‑UTR of CD133) or modulation by upstream factors (as observed in studies of monocytes and in the regulation of the calcium‑sensing receptor in colorectal tumors) further cement miR‑135b’s diverse roles in tumor pathogenesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "31", "end_ref": "37"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Tomohiro Umezu, Hiroko Tadokoro, Kenko Azuma, et al. 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