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作为一种通过ERK-c-Myc路径抑制CRC进展的策略,打击UBQLN1功能
Ruoxuan Ni1,2,3, Jianwei Jiang4, Mei Zhao1,2,3
1Department of Etiology and Carcinogenesis, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.
Cancers
|June 28, 2023
概括
乌比基林-1 (UBQLN1) 在结直肠癌 (CRC) 中表达高,促进瘤生长. 通过向ERK-c-Myc通路,抑制UBQLN1可能为CRC提供一种新的治疗策略.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
背景情况:
- 大肠直肠癌 (CRC) 往往呈现晚期诊断,导致高死亡率.
- 乌比基林-1 (UBQLN1) 涉及各种生物过程,但其在CRC进展中的作用尚不清楚.
研究的目的:
- 研究UBQLN1在结直肠癌进展中的作用.
- 阐明UBQLN1在CRC中的作用的基础分子机制.
主要方法:
- 在CRC和正常组织中对UBQLN1表达的比较分析.
- 在体外测试评估细胞增殖,殖民地形成和上皮-介质细胞过渡 (EMT).
- 使用裸体小鼠进行体内研究,以评估UBQLN1敲击后的瘤发生和转移.
- 研究ERK-MAPK通路和c-Myc表达水平.
主要成果:
- 在CRC组织中,UBQLN1表达显著升高.
- 在体外,UBQLN1促进了CRC细胞的增殖,殖民地形成和EMT.
- 击败UBQLN1抑制了CRC细胞瘤发生和体内转移.
- 通过降低ERK-MAPK通路的调节,UBQLN1敲击降低了c-Myc表达.
- 恢复c-Myc表达恢复了UBQLN1缺乏细胞中的增殖缺陷.
结论:
- 通过向ERK-c-Myc通路,UBQLN1的淘汰抑制了CRC的进展.
- UBQLN1可能成为结直肠癌的潜在预后生物标志物和治疗点.
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