TTC13表达和STAT3激活可能形成一个积极的反循环,以促进ccRCC进展
Lingling Xie1, Yu Fang2, Jianping Chen1
1Department of Laboratory Medicine, Affiliated Hospital of Nantong University, Nantong, China.
PeerJ
|November 6, 2023
概括
通过STAT3途径增强增殖和抑制亡,TTC13促进清细胞细胞癌 (ccRCC) 的进展. 这一发现为ccRCC治疗提供了潜在的治疗点.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 癌症研究 癌症研究
背景情况:
- 清细胞细胞癌 (ccRCC) 是一种具有不良预后的侵袭性癌亚型.
- 了解ccRCC进展机制对于识别诊断和预后生物标志物至关重要.
- 需要阐明TC13在ccRCC发病过程中的作用.
研究的目的:
- 调查TTC13在ccRCC发展和进展中的作用.
- 在ccRCC中探索TTC13和STAT3之间的监管关系.
- 为了确定ccRCC的潜在治疗点.
主要方法:
- 使用RT-PCR,西部斑点和IHC.用TTC13mRNA和蛋白质水平的量化.
- 使用CCK-8,流细胞计和其他测试,评估细胞增殖,细胞亡和自.
- 通过 luciferase reporter 和 ChIP 试验研究 STAT3 与 TTC13 促进体的结合,并分析 STAT3 核转位.
主要成果:
- 在ccRCC组织中,TTC13表达是上调的.
- TTC13促进了ccRCC细胞的增殖,并抑制了细胞亡和自.
- 在ccRCC中,TTC13影响免疫透和免疫治疗反应.
- STAT3 直接激活了 TTC13 的转录.
结论:
- STAT3和TTC13形成一个积极的反循环,促进ccRCC细胞的增殖,抑制细胞亡和自.
- 针对STAT3-TTC13轴为ccRCC提供了一个潜在的治疗策略.
- 这些发现有助于制定ccRCC的个性化治疗策略.
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