Blackshear Pamela E, Pandiri Arun R, Ton Thai-Vu T, Clayton Natasha P, Shockley Keith R, Peddada Shyamal D, Gerrish Kevin E, Sills Robert C, Hoenerhoff Mark J
Integrated Laboratory Systems, Inc., Research Triangle Park, North Carolina, USA.
Experimental Pathology Laboratories, Inc., Research Triangle Park, North Carolina, USA.
Toxicol Pathol. 2014 Jul;42(5):863-76. doi: 10.1177/0192623313501894. Epub 2013 Aug 26.
Aged male Fischer 344/N rats are prone to developing spontaneous peritoneal mesotheliomas that arise predominantly from the tunica vaginalis of the testes. A definitive cause for the predominance of this neoplasm in F344/N rats is unknown. Investigation of the molecular alterations that occur in spontaneous rat mesotheliomas may provide insight into their pathogenesis as well enable a better understanding regarding the mechanisms underlying chemically induced mesothelioma in rodents. Mesothelial cell function represents a complex interplay of pathways related to host defense mechanisms and maintenance of cellular homeostasis. Global gene expression profiles of spontaneous mesotheliomas from vehicle control male F344/N rats from 2-year National Toxicology Program carcinogenicity bioassays were analyzed to determine the molecular features of these tumors and elucidate tumor-specific gene expression profiles. The resulting gene expression pattern showed that spontaneous mesotheliomas are associated with upregulation of various growth factors, oncogenes, cytokines, pattern recognition response receptors, and pathogen-associated molecular patterns receptors, and the production of reactive oxygen and nitrogen species, as well as downregulation of apoptosis pathways. Alterations in these pathways in turn trigger molecular responses that stimulate cell proliferation and promote tumor survival and progression.
老年雄性Fischer 344/N大鼠容易发生自发性腹膜间皮瘤,这些肿瘤主要起源于睾丸鞘膜。F344/N大鼠中这种肿瘤占优势的确切原因尚不清楚。对自发性大鼠间皮瘤中发生的分子改变进行研究,可能有助于深入了解其发病机制,也能更好地理解啮齿动物化学诱导间皮瘤的潜在机制。间皮细胞功能代表了与宿主防御机制和细胞内稳态维持相关的复杂途径相互作用。分析了来自两年期国家毒理学计划致癌性生物测定中载体对照雄性F344/N大鼠自发性间皮瘤的全基因组表达谱,以确定这些肿瘤的分子特征并阐明肿瘤特异性基因表达谱。所得的基因表达模式表明,自发性间皮瘤与多种生长因子、癌基因、细胞因子、模式识别反应受体和病原体相关分子模式受体的上调,以及活性氧和氮物种的产生有关,同时凋亡途径下调。这些途径的改变反过来触发刺激细胞增殖、促进肿瘤存活和进展的分子反应。