在小鼠结肠癌发生的化学诱导模型中,Panx1淘汰赛促进了 preneoplastic aberrant crypt foci 的发展
Sara Gomes Espírito Santo1, Tereza Cristina Da Silva2, Bruno Cogliati2
1Botucatu Medical School, Experimental Research Unit (UNIPEX), Multimodel Drug Screening Platform - Laboratory of Chemically Induced and Experimental Carcinogenesis (MDSP-LCQE), São Paulo State University (UNESP), Botucatu, São Paulo State, Brazil.
International journal of experimental pathology
|August 18, 2023
概括
在化学诱导的结肠癌模型中,Pannexin 1 (Panx1) 淘汰赛小鼠在化学诱导的结肠癌模型中显示了增加的 preneoplastic aberrant crypt foci (ACF) 发育,这表明Panx1在早期结肠癌发生过程中起着保护作用.
科学领域:
- 在瘤学瘤学.
- 细胞生物学 细胞生物学
- 分子致癌症的产生.
背景情况:
- 大肠直肠癌 (CRC) 是癌症死亡的主要原因.
- 异常密室焦点 (ACF) 是CRC中早期的前瘤病变.
- 素1 (Panx1) 在结肠癌发生中的作用尚不清楚.
研究的目的:
- 为了研究Panx1淘汰对小鼠化学诱导的结肠癌发生的影响.
- 为了评估Pax1在早期前瘤事件中的作用.
主要方法:
- 野生型 (WT) 和Panx1淘汰赛 (Panx1-/-) 雌性小鼠接受了1,2-二甲基氨酸 (DMH),用于化学诱导的结肠癌发生.
- 在DMH后7周 (亚急性毒性) 和37周 (ACF负担) 分析了小鼠.
- 评估了基因毒性,氧化应激,亡和ACF的发展.
主要成果:
- 在第7周,Panx1淘汰赛增加了DMH诱导的基因毒性,结肠恶性甲和亡.
- 在第37周,Panx1淘汰赛小鼠表现出明显更高的异常密码 (AC),ACF数量和ACF多重性.
- 具体来说,AC增加了56%,ACF数量增加了57%,ACF多重性增加了20%.
结论:
- 潘克斯1基因切除促进了在结肠癌发生的小鼠模型中前性ACF的发展.
- 这些发现表明,Panx1在结肠癌发展的早期阶段可能起着保护作用.
- 需要进一步的研究来阐明Panx1在结肠癌发生过程中的机制.
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