Moreira Ângela, Pereira Sofia S, Machado Christiane L, Morais Tiago, Costa Madalena, Monteiro Mariana P
Department of Anatomy, Multidisciplinary Unit for Biomedical Research (UMIB), Institute for Biomedical Sciences Abel Salazar (ICBAS), University of Porto Portugal.
Int J Clin Exp Pathol. 2013 Dec 15;7(1):348-52. eCollection 2014.
Lymphangiogenesis is the process that leads to new lymphatic vessels formation from preexisting blood vessels in the presence of appropriate inducing signals, which in pathologic conditions such as cancer, may contribute to tumor cells dissemination. The aim of the present study was to study the role of obesity, leptin and insulin in tumor lymphangiogenesis. For that, we have quantified the lymphatic vessels in prostate tumors through their immunohistochemistry staining by Lyve-1 in RM1 prostate tumors induced in different obese mice models (ob/ob, db/db and diet induced obese (DIO) and in normal weight C57BL/6J mice (control). Lymph vessels density was determined by Lyve-1 immunohistochemistry of prostate adenocarcinomas, while the percentage of the Lyve-1 stained area and lymphatic vessels number were obtained using a morphometric computerized tool. Obese ob/ob and DIO mice presented prostate tumors that were significantly larger (p<0.001) than controls, while tumors of db/db mice were significantly smaller (p=0.047). Lyve-1 expression was significantly higher in prostate tumors of DIO mice compared to tumors of db/db mice (p<0.05); furthermore Lyve-1 expression was negatively correlated with the percentage of the epididymal fat and body weight (p<0.01). No significantly correlations were found between Lyve-1 expression and tumor weight and leptin or insulin plasma levels. Our results suggest that obesity may have a protective effect against prostate cancer dissemination by inhibiting lymphangiogenesis through a still unidentified mechanism that appears not to involve leptin or insulin.
淋巴管生成是指在适当的诱导信号存在下,从预先存在的血管形成新的淋巴管的过程,在诸如癌症等病理状况下,这可能有助于肿瘤细胞的扩散。本研究的目的是探讨肥胖、瘦素和胰岛素在肿瘤淋巴管生成中的作用。为此,我们通过对不同肥胖小鼠模型(ob/ob、db/db和饮食诱导肥胖(DIO))以及正常体重的C57BL/6J小鼠(对照)中诱导的RM1前列腺肿瘤进行Lyve-1免疫组化染色,对前列腺肿瘤中的淋巴管进行了定量分析。通过前列腺腺癌的Lyve-1免疫组化确定淋巴管密度,同时使用形态计量计算机工具获得Lyve-1染色面积百分比和淋巴管数量。肥胖的ob/ob和DIO小鼠的前列腺肿瘤明显大于对照组(p<0.001),而db/db小鼠的肿瘤明显较小(p=0.047)。与db/db小鼠的肿瘤相比,DIO小鼠前列腺肿瘤中的Lyve-1表达明显更高(p<0.05);此外,Lyve-1表达与附睾脂肪百分比和体重呈负相关(p<0.01)。未发现Lyve-1表达与肿瘤重量以及瘦素或胰岛素血浆水平之间存在显著相关性。我们的结果表明,肥胖可能通过一种尚未明确的机制抑制淋巴管生成,从而对前列腺癌的扩散具有保护作用,这种机制似乎不涉及瘦素或胰岛素。