The availability of reliable circulating markers is vital for prognostic stratification, improving diagnostics, follow-up and definition of the treatment strategy. Owing to its main expression throughout the neuroendocrine system, chromogranin A (CgA) is widely recognized as a biomarker in patients with the assessment of neuro-endrocrine tumors. With advanced and high-end technologies, rich experienced scientists, Creative Biolabs is an excellent service provider in the field of tumor marker assay. After long years ahead to fully comprehend tumor markers, we launch our CgA assay portfolio service which can be used in targeted cancer therapy and diagnosis.
CgA is a 49 kDa acidic glycoprotein primary produced by neuroendocrine and endocrine cells and constitutes one of the most profuse components of secretory granules. With the discovery of CgA in the chromaffin granules of the adrenal medulla and its high level in patients with neuroendocrine tumors, it has been proved that associated with a lot of diseases. CgA is overexpressed in those patients with certain neuroendocrine tumors, prostate cancer, small cell lung cancer.
CgA is synthesized at the rough endoplasmic reticulum where it is inserted via the N-terminal signal peptide and then transported to the Golgi complex. CgA is next packaged together with other secretory proteins into immature granules, where it may be cleaved into the various derived peptides by specific processing enzymes. After acidification, secretory granules mature, thus becoming ready for stimulation-induced release.
Fig.1 Physiology of production and secretion of CgA. (Marotta, 2018)
Peptides derived from CgA include vasostatins (VST I and VST II), catestatin (CST), pancreastatin (PST), a 14-amino-acid peptide with N-terminal tryptophan and C-terminal glutamic acid and serpinin. CgA and the derived peptides display several biological functions.
VST I and VST II have vasodilator and antimicrobial properties.
VST I inhibits PTH secretion, promotes cell adhesion and inhibits VEGF-induced endothelial cell proliferation/migration.
VST I exists immune-endocrine crosstalk due to promote calcium entry into neutrophils.
PST induces hyperglycemia by inhibiting glucose-stimulated insulin release from β-cells and glucose uptake in adipocytes and hepatocytes and by stimulating glucagon secretion and glycogenolysis.
PST inhibits PTH release and stimulates histamine release.
CST inhibits nicotine-induced catecholamine secretion.
CST inhibits lipolysis and fatty acid oxidation by regulating adrenergic and leptin signaling.
CST acts as a potent vasodilator due to its capacity to stimulate histamine release.
CST induces endothelial cell proliferation/migration and reduces cardiac contractility.
Intact CgA prevents uncontrolled osmotic swelling of secretory vesicles, functioning as a matrix condenser for soluble intra-vesicular components.
CgA participates in the regulation of cytosolic calcium stores, granule exocytosis in secretory cells and prohormone convertase activity.
CgA is involved in blood pressure regulation through the stimulation of the sympathetic tone.
In addition, CgA processing into CST induces opposite effects on blood pressure due to the inhibited effect on catecholamine secretion.
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