Figure 4 The circulating EPC numbers. Leptin treated melanoma tumor bearing mice have more EPCs in peripheral blood than all other study groups. There was no significant difference between three other study groups. * (p < 0.05). The plasma concentration of NOx significantly increased in leptin group and significantly decreased in 9f8 treated

mice compare to respective control groups (Figure 5). Figure 5 The plasma concentration of NOx. The plasma concentration of NOx significantly increased in leptin group and significantly decreased in 9f8 treated mice compare to Selleckchem JIB04 respective control groups. Furthermore leptin treated mice had significantly more NOx levels than 9F8 group. * (p < 0.05). Discussion Adipose tissue secretes several adipokines that are supposed to stimulate inflammation, cell proliferation and angiogenesis. One of the most important member of such adipokines family is leptin, which increases cell proliferation in several Selleckchem BTK inhibitor tumor cell lines, enhances endothelial cell migration in vitro, and has been suggested to be an angiogenic/vasculogenic factor [12–17, 20].

It has been suggested that leptin may contribute to tumor growth. However, a direct cause and effect role of leptin in accelerating tumor DMXAA in vivo growth is uncertain. Besides, most of the data supporting leptin’s role in stimulating cell proliferation and angiogenesis have been derived

from invitro studies. In our study, the tumors weight of leptin treated mice were significantly more than tumors from all other groups of mice. Leptin has been identified in several types of human cancers and may also be linked to poor prognosis. In two studies, leptin and leptin receptor expression were significantly increased in primary and metastatic breast cancer relative to noncancerous tissues in women [24]. In a clinical study of colorectal cancer, leptin expression was associated with tumor G2 grade [25]. In renal cell carcinomas leptin and leptin receptor expression was well correlated with progression-free survival, venous invasion and lymph node metastasis [26]. Leptin has also been suggested to have a role in uterine and endometrial PJ34 HCl cancers [27]. There is very little previous information on the relationship between leptin and melanoma. Just one epidemiological study demonstrated that high serum leptin was positively correlated with melanoma risk [19]. The limited published animal studies trying to find whether leptin promote tumor growth have reported different results. Some studies support the hypothesis that the absence of leptin signaling diminishes mammary tumor growth in mice [10, 20, 28, 29]. Brandon et al, in their well-designed study have shown that leptin deficiency attenuates but does not abolish melanoma tumor growth [20].