Erkasap Nilufer, Ozyurt Rumeysa, Ozkurt Mete, Erkasap Serdar, Yasar Fatih, Ihtiyar Enver, Ciftci Evrim, Canaz Funda, Colak Ertugrul
Department of Physiology, Eskisehir Osmangazi University Medical Faculty, Odunpazari, Eskisehir 26040, Turkey.
Department of General Surgery, Eskisehir Osmangazi University Medical Faculty, Odunpazari, Eskisehir 26040, Turkey.
Exp Ther Med. 2021 Jun;21(6):600. doi: 10.3892/etm.2021.10032. Epub 2021 Apr 11.
An increasing number of studies have shown that angiogenesis has an important role in the progression of cancer. The growth of a new network of blood vessels is crucial for tumor growth and metastasis, which is promoted by several proangiogenic factors. Leptin, an essential adipokine that is secreted from fat tissue, is one of these pro-angiogenic factors. It has been shown that the inhibition of leptin-induced angiogenesis resulted in decreased levels of vascular endothelial growth factor (VEGF)/VEGFR2, hypoxia inducible factor (HIF) 1α, NF-κB, IL-1 and Notch and reduced the tumor growth in breast cancer. Leptin induces angiogenesis in breast cancer either by upregulating VEGFR2 in endothelial cells or by increasing VEGF/VEGFR2 expression through the Notch, IL-1 and leptin crosstalk outcome (NILCO) pathway. NILCO is a novel mechanism that interacts with proinflammatory and proangiogenic signals, which are critical for cell proliferation and angiogenesis in cancer. Several studies have shown that components of NILCO may affect human cancer incidence and progression. However, to the best of our knowledge, the interactions between Notch, IL-1 and leptin in human colorectal cancer have not been yet studied at the molecular level. The aim of the present study was to investigate the expression levels of genes related to the NILCO pathway in human colorectal cancer specimens. The current results demonstrated that leptin, leptin receptor (ObR) b, Notch-1, Notch-4, IL-1α, IL-1β, IL-1R, IL-6, JAK-2, STAT-1, STAT-3, VEGFA, VEGFR1, VEGFR2, TNF-α and NF-κB mRNA expression levels in the cancer tissue were increased compared with the normal tissue. No significant changes in the mRNA expression levels of Jagged-1, HIF-1α and TNF receptor 1 were observed. Western blotting revealed that the protein expression levels of IκB were increased in the cancer tissue compared with normal tissue, whereas HIF-1α and phosphorylated STAT-1 levels were decreased. IL-6 and VEGFA plasma concentrations were statistically raised and the leptin plasma concentration was also raised, although significantly, patients with cancer compared with control individuals. Together, the present findings indicated that Notch, IL-1 and leptin may serve a crucial role in the development of colorectal cancer.
越来越多的研究表明,血管生成在癌症进展中起着重要作用。新血管网络的生长对于肿瘤生长和转移至关重要,这是由多种促血管生成因子促进的。瘦素是一种从脂肪组织分泌的重要脂肪因子,是这些促血管生成因子之一。研究表明,抑制瘦素诱导的血管生成会导致血管内皮生长因子(VEGF)/VEGFR2、缺氧诱导因子(HIF)1α、核因子κB(NF-κB)、白细胞介素-1(IL-1)和Notch水平降低,并减少乳腺癌的肿瘤生长。瘦素通过上调内皮细胞中的VEGFR2或通过Notch、IL-1和瘦素串扰结果(NILCO)途径增加VEGF/VEGFR2表达来诱导乳腺癌血管生成。NILCO是一种与促炎和促血管生成信号相互作用的新机制,这些信号对癌症中的细胞增殖和血管生成至关重要。多项研究表明,NILCO的组成部分可能影响人类癌症的发病率和进展。然而,据我们所知,Notch、IL-1和瘦素在人类结直肠癌中的相互作用尚未在分子水平上进行研究。本研究的目的是调查人类结直肠癌标本中与NILCO途径相关基因的表达水平。目前的结果表明,与正常组织相比,癌组织中瘦素、瘦素受体(ObR)b、Notch-1、Notch-4、IL-1α、IL-1β、IL-1R、IL-6、JAK-2、STAT-1、STAT-3、VEGFA、VEGFR1、VEGFR2、肿瘤坏死因子-α(TNF-α)和NF-κB的mRNA表达水平升高。锯齿蛋白-1(Jagged-1)、HIF-1α和TNF受体1的mRNA表达水平未观察到显著变化。蛋白质印迹法显示,与正常组织相比,癌组织中IκB的蛋白质表达水平升高,而HIF-1α和磷酸化STAT-1水平降低。与对照个体相比,癌症患者的IL-6和VEGFA血浆浓度在统计学上升高,瘦素血浆浓度也升高,尽管升高幅度显著。总之,目前的研究结果表明,Notch、IL-1和瘦素可能在结直肠癌的发生发展中起关键作用。