ESM-1: A Novel Tumor Biomaker and its Research Advances

Abstract

Background: Cancer kills nearly 9,000,000 people worldwide, and its mortality was reported up to 28% in the past decade. Few available tumor markers have been known to help early stage diagnosis. In this study, Endocan was taken as a novel tumor marker, which has been found in many cancers related to cancer cell proliferation, neoangiogenesis, etc. Methods: Studies on Endocan and its correlation with cancer were reviewed, and key points of meaningful studies on the structure, pathways and targeted agents of Endocan were drawn. Results: Endocan leads to tumorigenesis and promotes tumor cells proliferation via HGF/SF signal transmission pathway, suppresses tumor cells apoptosis via NF-κB signaling pathway and promotes angiogenesis within tumors via VEGF and HIF pathway. Medicine suppressing the expression of Endocan could prevent tumorigenesis and even improve survival rate of mice with tumor significantly. Conclusion: Endocan is capable of promoting prognosis of cancer patients. Moreover, Endocan is supposed to a potential target of tumor-targeted therapy.

ESM1/VEGFα/ERK signaling axis augments cell proliferation and tumor angiogenesis in human cervical squamous cell carcinoma

“…In normal tissues, ESM1 is mainly expressed in vascular endothelial cells, distal renal tubular epithelial cells, and pulmonary endothelial cells, and is mainly involved in the in ammatory response [32] and angiogenesis [33]. Accumulative studies have shown that ESM1 was hyper-expressed in a variety of malignancies and was associated with tumor prognosis [34]. In hepatocellular carcinoma, ESM1 was an early-stage biomarker via augmenting the formation of tumor angiogenesis [21].…”

Endocan serum levels in patients with low- and high-grade meningiomas: does this biomarker have an indicative role?

“…Due to the potential role of both inflammatory cytokines and intercellular adhesion molecules in an inflammatory response and ischemia/reperfusion injuries, it is now hypothesized that the over-expression of endocan can activate both inflammatory and tumoral processing through activation of inflammatory mediators and adhesion molecules. Recent studies have focused on the central role of endocan over-expression in angiogenesis and tumorigenesis and thus this biomarker seems to be a selective target for cancer therapy [16]. This hypothesis has been examined and even demonstrated in subgroups of patients suffering malignancies of liver, kidney, lungs, breast, pancreas, prostate, ovary, and brain glioblastoma [17][18][19][20][21][22].…”

A pair of long intergenic non-coding RNA LINC00887 variants act antagonistically to control Carbonic Anhydrase IX transcription upon hypoxia in tongue squamous carcinoma progression

“…1C). All of these genes have been shown to play important roles in tumor progression [32][33][34][35][36][37][38][39][40][41][42][43][44][45][46][47]. Interestingly, 8 of these 17 genes have been identified as hypoxia-associated genes, including CA9, gamma-glutamyltransferase 6 (GGT6), KISS1 receptor (KISS1R), enolase 2 (ENO2), hypoxia-inducible lipid droplet-associated protein (HILPDA), EGL-9 family hypoxia inducible factor 3 (EGLN3), endothelial cell specific molecule 1 (ESM1), and NDUFA4 mitochondrial complex-associated like 2 (NDUFA4L2) (Fig.…”