MUC5AC

Official Full Name

mucin 5AC, oligomeric mucus/gel-forming

Organism

Homo sapiens

GeneID

4586

Background

Predicted to enable extracellular matrix constituent, lubricant activity. Predicted to be an extracellular matrix structural constituent. Predicted to act upstream of or within maintenance of lens transparency. Located in extracellular space and mucus layer. Implicated in dry eye syndrome. Biomarker of several diseases, including Sjogren's syndrome; biliary tract disease (multiple); cystic fibrosis; eye disease (multiple); and pancreatic cancer (multiple). [provided by Alliance of Genome Resources, Feb 2025]

Synonyms

TBM; leB; MUC5; mucin;

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Detailed Information

Mucin 5AC, also known as gastric mucus, is mainly distributed in normal gastrointestinal epithelium, colon cancer, colonic precancerous epithelium and fetal colon mucosa, but not in normal adult colonic epithelium. MUC5AC is located on chromosome 11lpl5.5 and contains a tandem repeat region of 8 amino acids and a polypeptide region consisting of 130 amino acids rich in 10 repeating cysteine residues in the MUC5AC gene.

Figure 1. Secreted mucin MUC5AC regulation and secretion. (Krishn, S. R., et al. 2018)

Abnormal Expression of MUC5AC and Respiratory Diseases

By studying the SPC-A1 cell line (human lung cancer cell line), it was found that after lipopolysaccharide intervention in APC-A1 (human lung cancer cell line), aquaporin 5 (AQP5) transcriptional activity and protein expression decreased, while MUC5AC expression increased. Further studies revealed that AQP5 expression is regulated by the p38/JNK pathway and MUC5AC is regulated by the epidermal growth factor receptor (EGFR)-p38/JNK pathway. In COPD patients with chronic obstructive pulmonary disease, it may be that lipopolysaccharide stimulates p38 and JNK in the respiratory tract, overexpressing MUC5AC, decreasing AQP5 expression, increasing airway mucus secretion and thickening, triggering the clinical course of COPD.

Studies have shown that matrix metalloproteinase-9 (MMP-9) is involved in the high expression of MUC5AC induced by epithelial lipopolysaccharide in human respiratory tract. Studies have found that lipopolysaccharide can cause elevated levels of transcription and protein expression in NCI-H292 cells and normal human respiratory epithelium MMP-9 and MUC5AC, and changes in MUC5AC are associated with changes in MMP-9 transcription, protein expression and activity. Doxycycline can inhibit the transcription, protein expression and activity of MMP-9. LPS-induced MMP-9 transcriptional activity can be inhibited by EGFR inhibitors, p38 inhibitors and JNK inhibitors. EGFR inhibitors can inhibit the phosphorylation of p38 MAPK and JNK, suggesting that MMP-9 activation and EGFR-p38 MAPK/JNK pathway may be involved in the up-regulation of MUC5AC expression by lipopolysaccharide.

Studies have shown that TNF-α can stimulate the expression and secretion of MUC in the respiratory epithelium. IL-8 plays an important role in neutrophil elastase-mediated goblet cell metaplasia and increased MUC5AC content in the respiratory epithelium. Statins can impair the pro-inflammatory effects of the cytokine TNF-α and IL-8 in vitro and in vivo. MUC5AC is thought to be secreted by goblet cells, not submucosal cells. Studies have found that TNF-α, platelet activating factor (PAF) and lipopolysaccharide can induce COX-2 production and up-regulate the expression of MUC5AC, which can be inhibited by celecoxib, a COX-2 inhibitor. Inhibition of the agent suggests that there may be a common pathway involved in the upregulation of MUC5AC expression by inflammatory mediators.

MUC5AC and Lung Cancer

When the base cells and/or goblet cells proliferated and metaplasia, the expression of the mucin gene was not significantly different from normal, but the expression of MUC5AC was significantly increased. Due to epithelial cell metaplasia of squamous cell carcinoma, MUC5AC is more widely expressed and is concentrated in the normal epithelium adjacent to squamous cell carcinoma cells. MUC5AC is closely related to the differentiation of small mucous cells in squamous cell carcinoma, suggesting that squamous cell carcinoma may be derived from mucous cells. Adenocarcinoma is derived from the mucous glandular epithelium. The expression of MUC5AC in bronchial adenocarcinoma was abnormally elevated. Mucinous bronchioloalveolar carcinoma is constantly expressed. The mucin genes (MUC2, MUC5AC, MUC5B, and MUC6) on chromosome 11p 15.5 have goblet cell characteristics, clinical manifestations and prognosis are different from other adenocarcinoma subtypes. Non-mucinous bronchioloalveolar carcinoma and non-bronchiolar alveolar carcinoma express MUC1 and MUC4, and mucus secretion regions have MUC5AC and MUC5B expression.

References:

Krishn, S. R. , Ganguly, K. , Kaur, S. , & Batra, S. K. . (2018). Ramifications of secreted mucin muc5ac in malignant journey: a holistic view. Carcinogenesis.
Biemer-Huttmann, A. E. , Walsh, M. D. , Mcguckin, M. A. , Ajioka, Y. , Watanabe, H. , & Leggett, B. A. , et al. (1999). Immunohistochemical staining patterns of muc1, muc2, muc4, and muc5ac mucins in hyperplastic polyps, serrated adenomas, and traditional adenomas of the colorectum. Journal of Histochemistry & Cytochemistry, 47(8), 1039-1048.
Garvin, L. M. (2015). Steroid repression of muc5ac mucin gene expression in human lung epithelial cells. Dissertations & Theses - Gradworks.

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