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In some settings, genetic deletion or promoter hypermethylation results in loss of miR‐335 expression and a consequent increase in tumor aggressiveness, while restoration of miR‐335 improves drug sensitivity and reduces metastatic potential."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "25"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in cancer suppression, miR‐335 is pivotal in regulating cellular differentiation, senescence and responses in non‐malignant contexts. In human mesenchymal stem cells, high miR‐335 levels mark the undifferentiated, reparative state; its downregulation is necessary for activation of differentiation programs and proper tissue repair. Moreover, miR‐335 participates in diverse biological processes including the modulation of diabetic wound healing, adipocyte inflammation and adipogenesis, osteoarthritis and even aspects of host antiviral responses. In reproductive biology, aberrant miR‐335 expression is linked to endocrine conditions such as polycystic ovary syndrome and preeclampsia, suggesting that precise regulation of this microRNA is crucial for maintaining tissue homeostasis. Furthermore, miR‐335 activity is finely tuned through interactions with long non‐coding RNAs and epigenetic modifications, emphasizing its role as an integrative hub in cellular fate decisions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "26", "end_ref": "34"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Kim J Png, Mitsukuni Yoshida, Xiang H-F Zhang, et al. 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