Golgi Protein 73 (GP73)

 Golgi Protein 73 (GP73) is a type II transmembrane glycoprotein present on the Golgi containing 402 amino acids and a relative molecular weight of 73 kDa.GP73 has no homology to known glycosyltransferases or to any of the known nucleotide, sugar, or ATP transport proteins of the Golgi. It is mainly expressed by epithelial lineage cells but is expressed at low levels in hepatocytes of the normal liver, but increases in response to liver injury, viral infection, or endoplasmic reticulum stress.GP73 is a novel serum indicator of liver disease and is considered one of the most promising molecular markers for hepatocellular carcinoma (HCC). In addition, the physiological function of GP73 as a Golgi-resident protein and its biological role in chronically elevated levels inside hepatocytes can have important effects on the body.

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The inventory of reagents associated with Golgi Protein 73 (GP73) that KMD Bioscience can offer:

Relationship between GP73, AFP and hepatocellular carcinoma

Golgi protein 73 (GP73) has a single N-terminal transmembrane structural domain located on the luminal surface of the Golgi lumen and an extensive C-terminal coiled-coil structural domain. All proteins residing in the Golgi are either peripheral membrane proteins or integral membrane proteins, most of which are involved in the intracellular modification of secreted proteins.

AFP serves as an oncoprotein that contributes to HCC progression, and intracellularly AFP acts as a signaling molecule that mediates a variety of cellular processes.Interaction between AFP and PTEN inhibits the latter's function, leading to malignant proliferation of HCC cells through activation of the PI3K/AKT signaling pathway.Interaction between AFP and caspase-3 leads to malignant proliferation of HCC cells by blocking caspase signaling cascades The interaction between AFP and caspase-3 inhibits apoptosis in HCC cells by blocking the caspase signaling cascade [9, 10]. In addition, AFP prevents the formation of complexes between retinoic acid and its receptor, which reduces the expression of GADD153, GADD45A, and Fn14, and promotes the abnormal growth of HCC cells [11,12,13].AFP promotes the migration and invasion of HCC cells through the up-regulation of metastasis-associated genes such as K19, EpCAM, MMP2, MMP9, and CXCR4 [14,15,16]. AFP promotes HCC cell migration and invasion by upregulating the expression of metastasis-related genes such as K19, EpCAM, MMP2, MMP9 and CXCR4 [14, 15]. Binding of extracellular AFP to its receptor (AFPR) activates Ca2+ and cyclic adenosine monophosphate (cAMP) signaling pathways, which promotes the proliferation and metastasis of HCC cells.

GP73 is a potential serum marker for HCC and is highly expressed in several types of tumor cells.GP73 regulates its cell surface recycling through interaction with the epidermal growth factor (EGFR) receptor, thereby promoting epithelial-mesenchymal transition of HCC cells to drive metastasis. In addition, GP73 interacts with MMP2 or MMP7 in HCC cells to promote their transport and secretion, thereby facilitating HCC cell transformation.GP73 is involved in the development of HCC through multiple mechanisms.

The assay of GP73 has higher sensitivity and specificity than that of AFP, and the serum level of GP73 increases with the malignant potential of liver diseases such as hepatitis, cirrhosis and HCC.

Figure 1 Schematic diagram of the molecular structure of GP73

Coordination between GP73 and AFP

Golgi protein 73 (GP73) and alpha-fetoprotein (AFP) are biomarkers for the diagnosis of hepatocellular carcinoma (HCC), and GP73 increases the secretion of AFP by binding directly to it, thereby promoting the proliferation and metastasis of HCC cells expressing AFP and its receptor (AFPR). Extracellular GP73 contributes to the proliferation and metastasis of HCC cells independently of AFP and AFPR. furthermore, extracellular AFP and GP73 synergistically enhance the malignant phenotype of HCC cells and synergistically increase drug resistance of HCC cells.

GP73 mediates AFP secretion and the increased level of secreted AFP depends on the interaction of GP73 with AFP, specifically requiring amino acid residues 56-92 of GP73. Promotes the malignant phenotype of HCC cells by upregulating the expression of proteins involved in proliferation and metastasis in HCC, but has no effect on the growth of normal hepatocytes.

GP73-mediated AFP and extracellular secretion of GP73 synergistically promote proliferation, migration and invasion of HCC cells.GP73 is a secreted protein and secretion requires an intact signal peptide (RVRR) and transmembrane structural domain (TMD) structure while promoting AFP secretion. Extracellular AFP or GP73 synergistically increase the malignant phenotype of HCC cells by enhancing the malignant phenotype of HCC cells through their respective specific receptors.

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