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激活转录因子3在TP53突变的甲状腺癌细胞中调解了细胞亡和细胞循环停止
Abolfazl Kooti1, Haniyeh Abuei1, Alireza Jaafari2
1Division of Medical Biotechnology, Department of Medical Laboratory Sciences, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran.
Thyroid research
|July 31, 2024
概括
过度表达激活转录因子3 (ATF3) 抑制了突变型p53在形甲状腺癌 (ATC) 细胞中的活性. 这表明ATF3是p53-突变甲状腺癌的潜在治疗点.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 遗传学 遗传学是一种遗传学.
背景情况:
- 在甲状腺癌的进展中,p53功能的丧失至关重要,特别是在形甲状腺癌 (ATC) 中.
- 由于ATC的不良预后,由于化学抵抗,需要新的治疗点.
- 激活转录因子3 (ATF3) 抑制突变p53的致癌活性,并在TP53突变癌症中起到瘤抑制作用.
研究的目的:
- 为了研究外阴ATF3过度表达对具有突变p53 (R273C) 的化学耐药8305C甲状腺癌细胞的影响.
- 评估ATF3作为p53-突变甲状腺癌治疗点的潜力.
主要方法:
- 用pCMV6-ATF3等离子体感染8305C细胞.
- 使用MTT测定,光显微镜和流细胞计,评估细胞活力,细胞亡和细胞周期.
- 西部涂抹以评估p53蛋白水平和RT-qPCR用于TP53,TAp63,ΔNp63和SHARP1mRNA表达.
主要成果:
- 在8305C细胞中,ATF3过度表达显著降低了细胞活力,诱导了细胞亡和细胞循环停止.
- 在8305C细胞中,ATF3过度表达增加了突变的p53蛋白水平.
- 在ATF3表达细胞中观察到TAp63和SHARP1mRNA水平升高和ΔNp63mRNA水平降低.
结论:
- 异位ATF3表达抑制了抗癌突变p53在抗化疗甲状腺癌细胞中的活性.
- 针对ATF3表达或与突变p53相互作用的治疗策略显示出治疗p53-突变转移性甲状腺癌的前景.
关键词:
8305C5C8305C5C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8305C8 is the one who is the one who is the one who is the one who is the one who is the one who is the one在ATF3中使用ATF3.突变的 p53 变种在Sharp1中,可以使用Sharp1.这就是TAp63的原因.甲状腺癌是什么?甲状腺癌是什么?的 ΔNp63 的值.相关概念视频
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