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在Circ-LDLRAD3/miR-655-3p/MAPK1轴增强细胞迁移和侵入在乳头甲状腺癌的乳头甲状腺癌
Bingfei Zhang1, Yiquan Peng2, Lirong Zhou3
1Department of Endocrinology and Metabolism, Affiliated Sinopharm Dongfeng General Hospital, Hubei University of Medicine, Shiyan City, Hubei Province, 442008, China. zbf888716@sina.com.
Cellular and molecular biology (Noisy-le-Grand, France)
|March 2, 2024
概括
循环RNAcirc-LDLRAD3通过调节miR-655-3p和MAPK1.p来促进乳头甲状腺癌 (PTC). 抑制circ-LDLRAD3可能为甲状腺癌提供治疗策略.
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 是一个
背景情况:
- 乳头甲状腺癌 (PTC) 是一种常见的甲状腺癌亚型.
- 循环RNAs (circRNAs) 与癌症的发展有关.
- 循环RNAs的失调可能有助于PTC病原性.
研究的目的:
- 为了研究circ-LDLRAD3在乳头甲状腺癌中的作用和机制.
- 探索PTC细胞中circ-LDLRAD3,miR-655-3p和MAPK1之间的相互作用.
主要方法:
- 在PTC组织和细胞中量化测量circ-LDLRAD3,miR-655-3p和MAPK1.
- 用载体感染PTC细胞以调节circ-LDLRAD3,miR-655-3p或MAPK1.1的载体.
- 细胞增殖,细胞亡,迁移和入侵的评估.
- 生物信息预测和结合地点的实验验证.
主要成果:
- 在PTC样本中,环LDLRAD3和MAPK1的水平升高,miR-655-3p的水平降低.
- 对circ-LDLRAD3的下调或对miR-655-3p的上调抑制了PTC细胞生长和转移.
- circ-LDLRAD3直接针对miR-655-3p,影响MAPK1的表达.
- 过度表达MAPK1逆转了circ-LDLRAD3敲击的抑制作用.
结论:
- circ-LDLRAD3通过菌miR-655-3p和上调MAPK1.3来促进PTC进展.
- 环-LDLRAD3 / miR-655-3p / MAPK1轴是乳头甲状腺癌的一个关键驱动因素.
- circ-LDLRAD3代表了PTC的潜在治疗点.
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