Department of Pharmacology, Nanjing Medical University, Nanjing, China.
Cancer Invest. 2010 Feb;28(2):146-55. doi: 10.3109/07357900903179617.
Previously, we found the activation of corticotropin-releasing factor receptor 2 (CRFR2) could inhibit tumor growth via an anti-angiogenic pathway, implying CRFR2 may be a tumor therapeutic target. Here, CRFR2 expression in human neuroendocrine small cell lung carcinoma (SCLC) tissues and cell lines NCI-H446 and NCI-H1688 were detected. Meanwhile, UCNs could directly inhibit the proliferation and promote the apoptosis of SCLC cells via CRFR2. It was also shown that the activation of CRFR2 could inhibit p38 and Akt phosphorylation to suppress the secretion of VEGF in SCLC cells. These observations implied CRFR2 might be a therapeutic target in human SCLC.
此前，我们发现促肾上腺皮质素释放因子受体 2（CRFR2）的激活可以通过抗血管生成途径抑制肿瘤生长，这意味着 CRFR2 可能是肿瘤治疗的靶点。在这里，检测了人类神经内分泌小细胞肺癌（SCLC）组织和细胞系 NCI-H446 和 NCI-H1688 中的 CRFR2 表达。同时，UCNs 可以通过 CRFR2 直接抑制 SCLC 细胞的增殖并促进其凋亡。还表明，CRFR2 的激活可以抑制 p38 和 Akt 的磷酸化，从而抑制 SCLC 细胞中 VEGF 的分泌。这些观察结果表明 CRFR2 可能是人类 SCLC 的治疗靶点。
