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.
A 54-year-old woman with hairy cell leukemia developed severe polymorphic erythema and blisters on the trunk and limbs after injection of interferon (IFN) α-2b. Skin biopsy revealed lymphocytic exocytosis and perivascular lymphocytic infiltrate in the dermis, and the lesions improved after methylprednisolone pulse therapy. Although injection-site reactions have been observed after injection of IFNα-2b, this is the first report of a widespread cutaneous reaction to IFNα-2b.
Cisplatin (CDDP) has been widely used in cancer therapy, but it has been linked to side effects such as nephrotoxicity. Crocin is a carotenoid found in crocus and gardenia flowers that has been shown to have anti-oxidant properties, inhibit tumor growth, and provide neuroprotection. The purpose of this study was to investigate the protective effect of crocin against CDDP-induced nephrotoxicity in a mouse model. Kunming mice were administered orally with crocin for 7 days at the dose of 6.25 mg/kg and 12.5 mg/kg per body weight daily and were injected with CDDP via intraperitoneal route at the dose of 10 mg/kg per body weight. Using commercial kits, the oxidative stress markers glutathione, malondialdehyde, catalase, glutathione peroxidase, and superoxide dismutase were measured in the kidneys of mice. Immunohistochemistry was used to assess the levels of p53, cleaved caspase-3, and phospho-p38 mitogen-activated protein kinase in the kidneys. Crocin significantly reduced CDDP-induced changes in serum creatinine and blood urea nitrogen levels, according to the findings. Crocin reduced malondialdehyde levels and increased glutathione, glutathione peroxidase, catalase, and superoxide dismutase levels in CDDP-induced lipid peroxidation. Crocin also significantly inhibited p38 mitogen-activated protein kinase activation, p53 expression, and caspase-3 cleavage. In conclusion, crocin protects against CDDP-induced oxidative stress and nephrotoxicity by attenuating the activation of p38 mitogen-activated protein kinase and caspase-3 cleavage.
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