Activation of corticotropin-releasing factor receptor 2 inhibits the growth of human small cell lung carcinoma cells.
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.
Wang
Juejin
J
Department of Pharmacology, Nanjing Medical University, Nanjing, China.
Jin
Lai
L
Chen
Jie
J
Li
Shengnan
S
D017209:Apoptosis / Q000187:drug effects; D045744:Cell Line, Tumor; D006801:Humans; D008175:Lung Neoplasms / Q000378:metabolism* / Q000473:pathology*; D020929:Mitogen-Activated Protein Kinase Kinases / Q000378:metabolism; D051058:Oncogene Protein v-akt / Q000378:metabolism; D010766:Phosphorylation; D018019:Receptors, Corticotropin-Releasing Hormone / Q000037:antagonists & inhibitors / Q000378:metabolism*; D055752:Small Cell Lung Carcinoma / Q000378:metabolism* / Q000473:pathology*; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*
C101531:CRF receptor type 2; D018019:Receptors, Corticotropin-Releasing Hormone; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D051058:Oncogene Protein v-akt; D020929:Mitogen-Activated Protein Kinase Kinases