ZG16B

Official Full Name

zymogen granule protein 16B

Organism

Homo sapiens

GeneID

124220

Background

Predicted to enable carbohydrate binding activity. Involved in cell migration. Located in apicolateral plasma membrane; cytoplasm; and extracellular region. [provided by Alliance of Genome Resources, Feb 2025]

Synonyms

EECP; PAUF; JCLN2; HRPE773; PRO1567;

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Detailed Information

The ZG16B gene encodes zymogen granule protein 16B and is located on human chromosome 16p11.2. As suggested by its name, this protein was initially associated with zymogen granules in pancreatic acinar cells, but subsequent studies have shown that its expression is not restricted to the pancreas. ZG16B is a small secreted protein characterized by a carbohydrate-recognition domain, a hallmark of the lectin family, indicating its ability to bind specific carbohydrate structures. Both bioinformatic predictions and experimental studies support ZG16B's carbohydrate-binding capacity, although the precise physiological ligand spectrum remains under investigation. The protein localizes to the apical plasma membrane, cytoplasm, and extracellular space, suggesting potential roles in intracellular trafficking, cell–cell adhesion, or extracellular functions. ZG16B is notably expressed in normal gastrointestinal mucosa and pancreas, and its dysregulation in pathological states, especially tumor development, is increasingly being explored.

Figure 1. Human ZG16p and ZG16b have a b-prism fold. (Kanagawa M, et al., 2010)

Biological Significance

ZG16B's biological function is not fully elucidated, but evidence indicates that it plays an important role in maintaining mucosal homeostasis and regulating cell behavior. As a putative lectin, ZG16B may interact with specific glycosylated structures on cell surfaces or extracellular matrix components, mediating cell–cell and cell–matrix interactions crucial for epithelial tissue integrity and barrier function. In pancreatic cancer, ZG16B exhibits a complex, context-dependent role. Studies have shown that ZG16B can promote pancreatic cancer cell migration and invasion by activating Toll-like receptor 4 (TLR4) and its downstream MyD88–NF-κB signaling axis, notably independent of the TLR4/TRIF pathway. This finding links a classical lectin molecule to innate immune signaling pathways, suggesting that ZG16B may drive malignant behavior by mimicking pathogen-associated molecular patterns. Conversely, there is evidence that ZG16B may act as a tumor suppressor in certain contexts, with reduced expression associated with tumor progression. Its functions are therefore likely tissue-specific and context-dependent. Under physiological conditions, ZG16B may participate in sensing the gut microbiota or their products, organizing the mucus layer, or regulating epithelial cell turnover, while dysregulation in pathological conditions may be exploited by tumor cells to promote progression and metastasis.

Clinical Relevance

ZG16B's clinical significance mainly lies in its potential as a disease biomarker, particularly in pancreatic ductal adenocarcinoma (PDAC). PDAC is highly aggressive with a poor prognosis, highlighting the urgent need for early diagnostic and prognostic biomarkers. Multiple studies indicate that ZG16B expression is significantly altered in pancreatic cancer tissues and correlates with clinicopathological features and patient outcomes, making it a promising candidate biomarker. Assessing ZG16B levels in tissue samples or liquid biopsies may aid early diagnosis or risk stratification. Moreover, since ZG16B promotes pancreatic cancer cell migration and invasion via the TLR4/MyD88/NF-κB axis, this signaling pathway and its upstream regulators represent potential therapeutic targets. In theory, blocking ZG16B–B-receptor interactions or inhibiting downstream signaling could reduce metastatic potential and improve patient prognosis. Translating these findings into clinical applications remains challenging, requiring a deeper understanding of ZG16B interactions within the tumor microenvironment, its precise role at different cancer stages, and the development of specific, effective therapeutic agents. Beyond pancreatic cancer, ZG16B's role in inflammatory bowel diseases and other gastrointestinal conditions is under investigation, with its function as a mucosal immune and barrier regulator suggesting broader clinical relevance.

References

Kanagawa M, Satoh T, Ikeda A, et al. Crystal structures of human secretory proteins ZG16p and ZG16b reveal a Jacalin-related β-prism fold. Biochem Biophys Res Commun. 2011 Jan 7;404(1):201-5.
Youn SE, Jiang F, Won HY, et al. PAUF Induces Migration of Human Pancreatic Cancer Cells Exclusively via the TLR4/MyD88/NF-κB Signaling Pathway. Int J Mol Sci. 2022 Sep 27;23(19):11414.

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