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首页> 外文期刊>Cell communication & adhesion >Altered Tumor Biology and Tumorigenesis in Irradiated and Chemical Carcinogen-Treated Single and Combined Connexin32/p27Kip1-Deficient Mice
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Altered Tumor Biology and Tumorigenesis in Irradiated and Chemical Carcinogen-Treated Single and Combined Connexin32/p27Kip1-Deficient Mice

机译：辐照和化学致癌物治疗的单和联合Connexin32 / p27Kip1缺陷小鼠的肿瘤生物学和肿瘤发生改变。

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摘要

Connexin32 knockout mice (Cx32-KO) exhibit increased chemical and radiation-induced liver and lung tumorigenesis. This increased tumor incidence is associated with altered tumor biology including enhanced tumor progression and an increased percent of MAPK-active tumors. Likewise, mice lacking the tumor suppressor/cell cycle regulator p27Kip1 exhibit increased tumorigenesis in a variety of tissues following chemical and radiation induction. Interestingly, in a double-deficient mouse model (DKO), additional loss of p27Kip1 in a Cx32-KO background results in attenuation of liver and lung tumorigenesis as well as MAPK activation profiles, suggesting pathway interaction. While these mouse strains exhibit altered liver and lung tumor susceptibility following both chemical (DEN) and radiation (X-ray) induction protocols, comparisons of the resulting tumor incidence, multiplicity, tumor progression, and MAPK activation in response to these two distinct carcinogens underscores the separate influence of each individual gene on both tumor formation and activation of specific oncogenic pathways. Furthermore, these studies demonstrate that different carcinogens interact disparately with Cx32/p27Kip1 genotypic backgrounds in situ resulting in varied tumorigenic response.
机译：连接蛋白32基因敲除小鼠（Cx32-KO）表现出增加的化学和辐射诱导的肝和肺肿瘤发生。这种增加的肿瘤发生率与改变的肿瘤生物学有关，包括增强的肿瘤进展和增加的MAPK活性肿瘤百分数。同样，缺乏肿瘤抑制因子/细胞周期调节因子p27Kip1的小鼠在化学和放射诱导后，在各种组织中的肿瘤发生增加。有趣的是，在双缺陷小鼠模型（DKO）中，Cx32-KO背景中p27Kip1的额外丧失导致肝脏和肺部肿瘤的发生以及MAPK激活谱的减弱，提示途径相互作用。虽然这些小鼠品系在化学（DEN）和放射（X射线）诱导方案后均表现出改变的肝和肺肿瘤易感性，但对这两种不同的致癌物的反应所产生的肿瘤发生率，多重性，肿瘤进展和MAPK活化的比较强调了每个单独基因对肿瘤形成和特定致癌途径激活的独立影响。此外，这些研究表明，不同的致癌物与Cx32 / p27Kip1基因型背景原位相互作用完全不同，从而导致多种致瘤反应。

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