{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMUC6 is a prototypical secreted, gel‐forming mucin that is predominantly produced by the mucous cells of gastric glands—and is also expressed in the pancreas and duodenum—to generate a viscoelastic mucus barrier that protects the underlying epithelium from acid, proteases, mechanical trauma, and pathogens. Detailed biochemical and genomic investigations have revealed that MUC6 is synthesized as a large oligomeric glycoprotein with multiple glycoforms, and its gene is located within a cluster on chromosome 11p15.5. Its expression is tightly regulated at the transcriptional level by key promoter elements including NF‐κB and Sp family transcription factors, while epigenetic modifications and polymorphic repeats within its coding sequence further contribute to cell‐type–specific expression and the generation of functionally distinct glycoforms."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn various neoplastic settings, the expression pattern of MUC6 serves as an important indicator of tumor differentiation and progression. For instance, its aberrant or ectopic expression has been documented in precursor lesions—such as pancreatic intraepithelial neoplasia, intraductal papillary mucinous neoplasms, and serrated colonic polyps—often correlating with a more differentiated, less aggressive tumor phenotype. Conversely, absence or down‐regulation of MUC6 expression in invasive carcinomas has been associated with poorer prognoses. Furthermore, distinct mucin expression profiles that include MUC6 are being exploited to aid in the pathological subclassification of gastrointestinal and gastric epithelial dysplasias, thereby offering potential prognostic as well as diagnostic value in conditions ranging from Barrett esophagus to colorectal carcinoma."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "25"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its classical barrier‐forming role, post‐translational modifications of MUC6—such as aberrant glycosylation and Tn antigen presentation—can markedly alter its immunogenicity and functional interactions with other molecules. Modified MUC6 has been implicated in mediating cell–cell adhesion signals and even in interactions with innate immune receptors, as exemplified by its identification as a DC‐SIGN–binding component in seminal plasma that may influence viral transmission. Moreover, altered MUC6 glycoforms have been linked to Helicobacter pylori infection and the mechanistic down‐regulation of MUC6 appears to contribute to the progression of gastric cancer. These multifaceted roles underscore MUC6 as a critical player in normal epithelial homeostasis whose dysregulation may promote tumorigenesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "26", "end_ref": "37"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Henrik Nordman, Julia R Davies, Gert Lindell, et al. 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