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科林林通过向Pim-3抑制食道状细胞癌的生长

Yunshu Shi¹, Qiang Yuan¹, Yingying Chen²

¹The Pathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450000, China; China-US (Henan) Hormel Cancer Institute, Zhengzhou 450000, China; Tianjian Laboratory for Advanced Biomedical Sciences, Zhengzhou, Henan 450052, China.

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概括

马洛尼小鼠白血病病毒3 (Pim-3) 的预病毒整合部位驱动食道状细胞癌 (ESCC) 的生长. 科林林通过向Pim-3有效地抑制ESCC进展,提供了潜在的新疗法.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
药物发现药物发现药物发现

背景情况:

食道状细胞癌 (ESCC) 是一种具有很低生存率的高度侵袭性癌症.
目前对ESCC的治疗方法经常遇到抗药性,这凸显了对新型治疗点的需求.
确定关键的致癌驱动因素和有效的抑制剂对于推进ESCC治疗至关重要.

研究的目的:

在ESCC中调查马洛尼小鼠白血病病毒3 (Pim-3) 的前病毒整合部位的作用.
评估科林林作为一种潜在的治疗药物,在ESCC中准Pim-3.
为了阐明可林林抑制ESCC进展的分子机制.

主要方法:

免疫组织化学被用来评估ESCC组织中的Pim-3蛋白水平.
细胞增殖试验 (MTT,殖民地形成) 用于研究Pim-3的功能.
生物化学试验 (计算机对接,拉下,CTSA,激酶试验) 证实了科林林林-Pim-3的相互作用和抑制.
西方涂抹和患者衍生的异种移植模型被用于探索抑制机制.

主要成果:

发现Pim-3在ESCC中表达高,促进细胞增殖和瘤发育.
皮姆-3通过酸化基因激活蛋白激酶1 (MAPK1) 来增强ESCC的生长.
科林林直接与Pim-3结合,抑制其激酶活性并抑制ESCC的生长,从而导致亡.

结论:

皮姆-3是ESCC进展的重要推动者.
科林林通过向Pim-3来抑制ESCC的有效性.
针对Pim-3使用诸如科里诺林之类的药物代表了ESCC的一种有前途的治疗策略.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.科里诺林 (Corynoline) 是一种食道状细胞癌的癌症.核武器的扩散马洛尼小鼠白血病病毒3的Proviral整合部位

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