Laboratorio de Biología Celular del Cáncer, Facultad de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Av. Lázaro Cárdenas s/n, Chilpancingo, GRO 39090, Mexico.
Laboratorio de Biomedicina Molecular, Facultad de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Chilpancingo, GRO, 39090, Mexico.
Cytokine Growth Factor Rev. 2021 Dec;62:23-41. doi: 10.1016/j.cytogfr.2021.10.006. Epub 2021 Oct 23.
The acquired ability to induce the formation of a functional vasculature is a hallmark of cancer. Blood vessels in tumors are formed through various mechanisms, among the most important in cancer biology, angiogenesis, and vasculogenic mimicry have been described. Leptin is one of the main adipokines secreted by adipocytes in normal breast tissue and the tumor microenvironment. Here, we provide information on the relationship between leptin and the development of angiogenesis and vasculogenic mimicry in different types of cancer. Here, we report that leptin activates different pathways such as JAK-STAT3, MAPK/ERK, PKC, JNK, p38, and PI3K-Akt to induce the expression of various angiogenic factors and vasculogenic mimicry. In vivo models, leptin induces blood vessel formation through the PI3K-Akt-mTOR pathway. Interestingly, the relationship between leptin and vasculogenic mimicry was more significant in breast cancer. The information obtained suggests that leptin could be playing an essential role in tumor survival and metastasis through the induction of vascular mechanisms such as angiogenesis and vasculogenic mimicry; thus, leptin-induced pathways could be suggested as a promising therapeutic target.
获得诱导功能性血管形成的能力是癌症的一个标志。肿瘤中的血管通过各种机制形成，其中在癌症生物学中最重要的是血管生成和血管生成拟态。瘦素是正常乳腺组织和肿瘤微环境中脂肪细胞分泌的主要脂肪因子之一。在这里，我们提供了有关瘦素与不同类型癌症中血管生成和血管生成拟态发展之间关系的信息。在这里，我们报告说，瘦素通过 JAK-STAT3、MAPK/ERK、PKC、JNK、p38 和 PI3K-Akt 等不同途径激活，诱导各种血管生成因子和血管生成拟态的表达。在体内模型中，瘦素通过 PI3K-Akt-mTOR 途径诱导血管形成。有趣的是，在乳腺癌中，瘦素与血管生成拟态之间的关系更为显著。获得的信息表明，瘦素可能通过诱导血管生成和血管生成拟态等血管机制在肿瘤存活和转移中发挥重要作用；因此，瘦素诱导的途径可能被认为是一种有前途的治疗靶点。
