COX-2通过Snail通路调控胃癌细胞E-cadherin表达的作用及分子机制
基本信息
结项摘要
粘附功能异常导致浸润转移是恶性肿瘤致死的主要原因。以往研究证实，COX-2通过促进细胞增殖、抑制细胞凋亡、促进新生血管形成参与恶性肿瘤的发生发展进程。我们研究表明，COX-2还可能通过下调主要粘附分子之一的E-cadherin表达与恶性肿瘤侵袭转移关联，但COX-2调控E-cadherin表达的分子机制尚不清楚。提示COX-2可能通过Snail信号通路实现对E-cadherin表达的调控。本研究拟对COX-2表达不同水平的胃癌细胞系，利用siRNA、阻断剂等干预实验及免疫共沉淀、染色质免疫共沉淀等技术，进一步证实COX-2通过下调E-cadherin表达从而介导胃癌的侵袭转移；深入探讨COX-2调控E-cadherin表达的相关信号通路及作用机制。揭示COX-2在胃癌发生发展中的生物学功能以及在胃癌侵袭转移过程中的分子机制，为胃癌侵袭转移的预防和治疗以及未来的靶向治疗提供新的理论依据。
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数据更新时间：2023-05-31
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