The cyclic AMP responsive element-binding protein 3-like 4 (CREB3L4) is a transcription factor highly expressed in multiple human cancers. This study aimed to investigate the regulatory effects of CREB3L4 on GC progression and angiogenesis. CREB3L4 was overexpressed in GC tissues and cell lines, and was positively correlated with advanced tumor stage and poor survival in GC patients. The upregulation of CREB3L4 in GC cells increased cell viability, promoted cell proliferation, reduced apoptosis, enhanced cell migration and invasion, and induced the formation of tubule-like endothelial structures, whereas CREB3L4 knockdown impeded tumor cell growth, attenuated cell motility, and prevented human umbilical vein endothelial cells from forming tubule-like structures. In addition, mice inoculated with CREB3L4-deficient GC cells showed significantly suppressed tumor growth compared to the group harboring wild-type tumors.
Cellular repressor of E1A genes (CREG) is an evolutionarily conserved lysosomal protein, and an important new factor in regulating tissue homeostasis that has been shown to antagonize injury of tissues or cells. CREG contains three mannose 6-phosphate (M6P) markers, and depends on interactions with M6P receptors for efficient delivery to lysosomes, which is implicated in the regulation of lysosomal functions. This protein shares limited sequence similarity with E1A and binds both the general transcription factor TBP and the tumor suppressor pRb in vitro. CREG plays an important role in the control of cell growth and differentiation. It has been shown that CREG antagonizes transcriptional and cellular transformation by the adenoviral E1A oncoprotein, induces differentiation while attenuating cellular proliferation, regulates the levels of the signaling kinases ERK1/2, and mediates glucocorticoid-induced proliferation of ileal epithelial cells. CREG is widely expressed in adult tissues, such as the brain, heart, lungs, liver, intestines and kidneys in mice, but is not markedly expressed in pluripotent embryonic stem cells.
CRELD1 is a transmembrane glycoprotein. Epidermal growth factor(EGF)like domain exists in CRELD1. EGF-like repeats are a class of cysteine-rich domains that mediate interactions between proteins of diverse function. EGF domains are found in proteins that are either completely secreted or have transmembrane regions that tether the protein to the cell surface. CRELD1 contains a 333 amino acid acid (aa) extracellular domain (ECD), two tandem transmembrane segments, and a second ECD of 15 aa. Defects in CRELD1 may cause susceptibility to atrioventricular septal defect type 2 which results in a persistent common atrioventricular canal.
Cysteine-Rich with EGF-Like Domain Protein 2 (CRELD2) is a secreted protein that is a member of the CRELD family. Human CRELD2 is synthesized as a 353 amino acid precursor protein with a signal peptide, a highly conserved domain rich in glutamic acid and tryptophan (WE) and EGF-like repeats. CRELD2 is ubiquitously expressed in many tissues. CRELD2 may interact with CHRNA4 and regulate transport of α4-β2 neuronal acetylcholine receptor. In addition, CRELD2 could be a novel mediator in regulating the onset and progression of various ER stress-associated diseases.
Corticotropin-Releasing Factor-Binding Protein (CRHBP) is a 37 kDa secreted glycoprotein that binds both CRH and urocortin in a 42 kDa extracellular complex. The molecule is approximately 300 amino acids in length and demonstrates five intrachain disulfide bonds. Difference between CRHBP from different species exist, human CRHBP is found in plasma while rodent and sheep CRHBP is limited to neuroendocrine tissues. CRHBP may inactivate CRH and may prevent inappropriate pituitary-adrenal stimulation in pregnancy. CRHBP is presumed to either sequester CRH, rendering it unavailable to cells or transport it to target tissues. Although CRF-BP concentration in the human peripheral circulation is normally low, it increases throughout pregnancy and fall back rapidly after parturition.
Hormone regulating the release of corticotropin from pituitary gland. Induces NLRP6 in intestinal epithelial cells, hence may influence gut microbiota profile.
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