在皮肤癌中,IGF1R信号传导通过ITGAV诱导表皮层-介质细胞可塑性
Marta Lopez-Cerda1, Laura Lorenzo-Sanz2, Victoria da Silva-Diz2,3
1Oncobell Program, Bellvitge Biomedical Research Institute (IDIBELL), 08908, L'Hospitalet de Llobregat, Barcelona, Spain. mlopezc@idibell.cat.
Journal of experimental & clinical cancer research : CR
|July 29, 2024
概括
在上皮癌细胞中的整体αV (ITGAV) 表达促进皮肤状细胞癌 (cSCC) 的进展. ITGAV作为cSCC复发的预后生物标志物,有助于患者分层和确定治疗点.
科学领域:
- 在瘤学瘤学.
- 皮肤病学 皮肤病学
- 癌症生物学 癌症生物学
背景情况:
- 皮肤状细胞癌 (cSCC) 的进展涉及从上皮细胞转移到介质细胞的特征,与预后不佳相关.
- 目前用于预测cSCC临床过程的标志物是不理想的.
- 驱动cSCC进展的机制在很大程度上仍然不清楚.
研究的目的:
- 确定cSCC复发的新型预后生物标志物.
- 在cSCC中驱动表皮质-介质细胞可塑性 (EMP) 的解化机制.
- 评估ITGAV作为预后标志物和治疗目标.
主要方法:
- 使用cSCC进展的小鼠模型.
- 进行表达微阵列,免疫光和流细胞计.
- 通过遗传和药物抑制进行了蛋白质组分析和验证的途径.
主要成果:
- 在上皮癌细胞中识别了整合素αV (ITGAV) 表达,作为cSCC向介质细胞状态进展的驱动因素.
- 患者样本中的ITGAV表达预测了超出当前基因病理参数的cSCC复发风险.
- 证明胰岛素样生长因子-1受体 (IGF1R) 路径激活对于诱导EMP和ITGAV表达至关重要.
结论:
- ITGAV是一种有价值的预后生物标志物,用于改善cSCC患者分层.
- ITGAV与IGF1R合作,在上皮癌细胞中驱动EMP,促进cSCC的进展.
- 针对ITGAV-IGF1R轴是一个潜在的治疗策略,用于对抗先进的介质细胞cSCCs.
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