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首页> 外文期刊>Indian Journal of Pathology and Microbiology >Expression of erythropoietin and its receptor increases in colonic neoplastic progression: The role of hypoxia in tumorigenesis
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Expression of erythropoietin and its receptor increases in colonic neoplastic progression: The role of hypoxia in tumorigenesis

机译：促红细胞生成素及其受体的表达在结肠肿瘤进展中增加：缺氧在肿瘤发生中的作用

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Background: Tissue hypoxia is a characteristic patho-physiologic property of colorectal cancer. This process may also add to a therapeutic problem of solid tumor resistance to chemo- and radiation therapy. Erythropoietin (Epo) expression is induced by tissue hypoxia. Acting via its receptor (EpoR), Epo inhibits apoptosis of erythroid cells and has been shown to rescue neurons from hypoxic damage. Increased Epo and EpoR expression has been recently described in human breast, renal and cervical carcinoma. Given the characteristic tumor diathesis present in majority of colorectal cancers, we examined whether Epo signaling may play a role in colonic neoplastic progression. Materials and Methods: Expression of Epo and EpoR was examined using immunohistochemistry in 24 cases of primary colorectal and metastatic adenocarcinomas versus adenomas and normal colonic mucosa. Immunohistochemical stains were evaluated semiquantitatively based on a four-tiered scale. Based on the combination of extent and intensity of immunoreactivity, an immunostaining score (0-300) was determined for each sample. Expression of Epo and EpoR protein and mRNA was examined using Western blot and reverse transcriptase-polymerase chain reaction (RT-PCR), respectively, in both normal colonic tissue and carcinoma specimens in five cases. Results: Epo expression was sequentially increased in normal colonic mucosa (8.3 ± 5.6, mean ± SEM), adenoma (26.4 ± 9.1), primary carcinoma (96.1 ± 12.8) and metastatic carcinoma (122 ± 51.3). EpoR expression was also sequentially increased in normal colonic mucosa (22.3 ± 11.8), adenoma (108.7 ± 24.2), primary carcinoma (178.7 ± 16.6) and metastatic carcinoma (220 ± 58.3) (P 0.05 for all results). Epo and EpoR showed enhanced expression in the areas adjacent to ischemiaecrosis. Western blot and RT-PCR analysis revealed increased EpoR protein and mRNA levels in carcinoma compared to normal mucosal colon specimens. Focal stromal Epo and EpoR immunoreactivity was present in 10 and 12 cases, respectively. Conclusions: The uniform increase in the expression of Epo and EpoR along the colonic neoplastic sequence and further increase in ischemicecrotic areas indicates that the Epo signaling pathway is an important component in colon carcinogenesis including possible epithelial-stromal interactions.
机译：背景：组织缺氧是大肠癌的典型病理生理特性。该过程还可能增加实体瘤对化学疗法和放射疗法的抵抗力的治疗问题。促红细胞生成素（Epo）的表达是由组织缺氧诱导的。 Epo通过其受体（EpoR）起作用，抑制红系细胞的凋亡，并已显示出可以挽救神经元免受缺氧损伤的影响。最近在人乳腺癌，肾癌和宫颈癌中描述了Epo和EpoR表达增加。考虑到大多数大肠癌中存在的特征性肿瘤，我们检查了Epo信号传导是否可能在结肠肿瘤进展中起作用。材料和方法：采用免疫组织化学方法检测24例原发性结直肠和转移性腺癌与腺瘤和正常结肠粘膜的Epo和EpoR的表达。免疫组化染色是基于四级量表进行半定量评估的。基于免疫反应性的程度和强度的组合，确定每个样品的免疫染色评分（0-300）。在5例正常结肠组织和癌标本中分别使用Western blot和逆转录聚合酶链反应（RT-PCR）检测了Epo和EpoR蛋白及mRNA的表达。结果：正常结肠粘膜（8.3±5.6，平均值±SEM），腺瘤（26.4±9.1），原发癌（96.1±12.8）和转移性癌（122±51.3）中的Epo表达依次增加。在正常结肠粘膜（22.3±11.8），腺瘤（108.7±24.2），原发癌（178.7±16.6）和转移性癌（220±58.3）中，EpoR表达也依次增加（所有结果均P <0.05）。 Epo和EpoR在邻近缺血/坏死的区域表达增强。 Western blot和RT-PCR分析显示，与正常粘膜结肠标本相比，癌组织中EpoR蛋白和mRNA水平增加。局灶性基质Epo和EpoR免疫反应分别存在于10例和12例中。结论：Epo和EpoR的表达沿结肠肿瘤序列一致增加，并且缺血/坏死区域进一步增加，表明Epo信号通路是结肠癌发生过程中重要的组成部分，包括可能的上皮-基质相互作用。

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