Leptin-Induced JAK/STAT Signaling and Cancer Growth.
Leptin-Induced JAK/STAT Signaling and Cancer Growth.
复制标题
DOI：
10.3390/vaccines4030026
复制
发表时间：
2016-07-26
期刊：
影响因子：
7.8
通讯作者：
Gonzalez-Perez RR
中科院分区：
文献类型：
--
作者：
Mullen M;Gonzalez-Perez RR
生长因子和细胞因子信号传导可以影响多种癌症类型的发展。在癌症发展中的关键参与者之一是Janus激酶（JAK）信号转导转录激活因子（STAT）信号通路。大多数生长因子和细胞因子与其膜结合受体的相互作用触发JAK-STAT激活。肥胖和癌症之间的影响关系是一个事实。然而，有一个复杂的事件序列有助于调节这种机制，以促进肿瘤生长，尚未完全阐明。JAK-STAT通路受到肥胖相关变化的影响，这些变化已被证明会影响癌症的生长和进展。这一复杂的过程受到大量脂肪因子和细胞因子的高度调节，这些脂肪因子和细胞因子对癌细胞发挥多效性作用，以增强向远处靶位点的转移。瘦素是一种细胞因子，或者更准确地说，是一种主要由脂肪组织分泌的脂肪因子，需要JAK-STAT激活才能发挥其生物学功能。瘦素是能量平衡和食欲的中央调节器。瘦素与其受体OB-R结合进而激活JAK-STAT，JAK-STAT在表达受体的正常细胞和恶性细胞中诱导增殖、血管生成和抗凋亡事件。瘦素还诱导与Notch和IL-1（NILCO）的串扰，这涉及促进肿瘤生长的其他血管生成因子。因此，靶向JAK/STAT通路的多种新型治疗剂的存在具有重要的临床意义。然后，识别调节肥胖-癌症联系的信号网络和因子，可以对其实施潜在的药理学干预以抑制肿瘤生长和转移。本文就leptin-JAK-STAT信号通路与肿瘤的关系作一综述。
Growth factor and cytokine signaling can influence the development of several cancer types. One of the key players in the development of cancer is the Janus kinas (JAK) signal transducer of activators of transcription (STAT) signaling pathway. The majority of growth factors and cytokine interactions with their membrane-bound receptors trigger JAK-STAT activation. The influential relationship between obesity and cancer is a fact. However, there is a complex sequence of events contributing to the regulation of this mechanism to promote tumor growth, yet to be fully elucidated. The JAK-STAT pathway is influenced by obesity-associated changes that have been shown to impact cancer growth and progression. This intricate process is highly regulated by a vast array of adipokines and cytokines that exert their pleiotropic effects on cancer cells to enhance metastasis to distant target sites. Leptin is a cytokine, or more precise, an adipokine secreted mainly by adipose tissue that requires JAK-STAT activation to exert its biological functions. Leptin is the central regulator of energy balance and appetite. Leptin binding to its receptor OB-R in turn activates JAK-STAT, which induces proliferation, angiogenesis, and anti-apoptotic events in normal cells and malignant cells expressing the receptor. Leptin also induces crosstalk with Notch and IL-1 (NILCO), which involves other angiogenic factors promoting tumor growth. Therefore, the existence of multiple novel classes of therapeutics that target the JAK/STAT pathway has significant clinical implications. Then, the identification of the signaling networks and factors that regulate the obesity-cancer link to which potential pharmacologic interventions can be implemented to inhibit tumor growth and metastasis. In this review, we will discuss the specific relationship between leptin-JAK-STAT signaling and cancer.
登录
查看更多内容
影响因子：
5.6
作者：
Cascio, Sandra;Ferla, Rita;Russo, Antonio
通讯作者：
Russo, Antonio
影响因子：
--
作者：
Dorritie, Kathleen A.;Redner, Robert L.;Johnson, Daniel E.
通讯作者：
Johnson, Daniel E.
DOI：
10.1073/pnas.95.11.6061
发表时间：
1998-05-26
影响因子：
11.1
作者：
Carpenter, LR;Farruggella, TJ;Stahl, N
通讯作者：
Stahl, N
影响因子：
5.5
作者：
Frank, Philippe G.;Pavlides, Stephanos;Lisanti, Michael P.
通讯作者：
Lisanti, Michael P.
影响因子：
--
作者：
Andorfer P;Heuwieser A;Heinzel A;Lukas A;Mayer B;Perco P
通讯作者：
Perco P