{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n LGALS7B, which encodes the β‐galactoside–binding lectin galectin‑7, functions as a multifunctional mediator in epithelial homeostasis and cancer. Although not directly involved in double‐strand break resection in DNA repair pathways"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ", and while p53 orchestrates diverse metabolic and stress responses"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": ", galectin‑7 is a well‐documented p53‐induced gene whose expression integrates into these broader cellular responses. In epithelial tissues, galectin‑7 promotes wound re–epithelialization and modulates cell–cell and cell–extracellular matrix interactions, as demonstrated in corneal models where exogenous galectin‑7 accelerates healing."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": " In the epidermis, galectin‑7 influences keratinocyte apoptosis, migration, proliferation, and differentiation—functions that are mediated, at least in part, through regulation of intracellular signaling pathways such as the JNK1/miR‑203/p63 axis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n In cancer, galectin‑7 displays context–dependent roles. In several malignancies, including T cell lymphomas"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": ", breast cancer"}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "10"}]}, {"type": "t", "text": ", and cervical or oral carcinomas"}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "13"}]}, {"type": "t", "text": ", elevated levels of galectin‑7 are associated with increased tumor invasiveness, metastasis, and poor clinical outcomes. Mechanistically, galectin‑7 has been shown to promote metastatic behavior by upregulating proteolytic enzymes such as MMP‑9"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}, {"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": ", and its expression can be induced by mutant p53 through NF‑κB–dependent mechanisms."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": " In contrast, in some settings such as gastric cancer, galectin‑7 may act as a tumor suppressor by inhibiting cell proliferation, migration, and invasion."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "15"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Additional studies have provided structural insights into galectin‑7, showing that lactose binding stabilizes its dimer formation and alters its dynamics, features that likely contribute to both extracellular and intracellular functions."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "16"}]}, {"type": "t", "text": " Moreover, galectin‑7 can interact with key apoptotic regulators such as Bcl‑2 to sensitize mitochondria to apoptotic signals"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "17"}]}, {"type": "t", "text": ", and secreted galectin‑7 may also modulate the immune microenvironment by inducing death of T cells."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": " Collectively, these studies highlight that galectin‑7 acts as a critical regulator of epithelial repair and tumor progression by modulating cell survival, differentiation, and motility. Its pleiotropic functions, which range from promoting wound healing to influencing metastatic behavior, underscore its potential as both a prognostic marker and a therapeutic target in diverse pathologies, including cancers and inflammatory skin disorders."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "18"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Zachary Mirman, Francisca Lottersberger, Hiroyuki Takai, et al. 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