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低调LPAR1促使皮质甲状腺癌细胞的侵入性行为
Zahra Bokaii Hosseini1, Fatemeh Rajabi2, Reza Morovatshoar3
1Faculty of Pharmacy, Zanjan University of Medical Sciences, Zanjan, Iran.
Cancer informatics
|September 10, 2024
概括
lysophosphatidic 酸受体 1 (LPAR1) 通过调节表皮-介质细胞转换 (EMT) 抑制皮质甲状腺癌 (PTC) 的转移. 较低的LPAR1表达和较高的miR-221-5p表明它有可能成为PTC的诊断和治疗点.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 基因组学就是基因组学.
背景情况:
- Lysophosphatidic 酸受体 1 (LPAR1) 是各种癌症中已知的生物标志物.
- 它在乳头甲状腺癌 (PTC) 中的特定生物作用以前没有被阐明.
研究的目的:
- 为了研究LPAR1在乳头甲状腺癌 (PTC) 中的功能.
- 确定LPAR1是否在PTC上皮质-介质细胞过渡 (EMT) 和转移中发挥作用.
- 探索LPAR1作为潜在的PTC生物标志物和治疗点.
主要方法:
- 对TCGA和GEO数据集的生物信息学分析,以确定PTC中EMT的关键监管者.
- 蛋白与蛋白相互作用 (PPI) 分析和与免疫透物相关联.
- 在PTC细胞系中使用Gepia2,GTEx和定量实时聚合酶链反应 (qRT-PCR) 评估LPAR1表达.
- 使用多MiR.miRNA目标基因预测.
主要成果:
- LPAR1被确定为PTC中EMT的关键调节者,与正常组织相比,有1081个基因被上调和544个基因被下调.
- LPAR1表达与CD4+ T细胞,巨细胞,中性粒细胞和髓状树突细胞正相关,但与B细胞负相关.
- 预计miR-221-5p将准LPAR1,实验数据显示LPAR1在PTC细胞系中明显表达不足,与正常甲状腺细胞系相比 (P < .01).
结论:
- LPAR1抑制转移,并且与PTC中的EMT有关.
- 减少LPAR1表达和增加PTC中的miR-221-5p表明LPAR1在疾病进展中的作用.
- LPAR1具有作为PTC中EMT的诊断生物标志物,预后指标和治疗点的潜力.
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