지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2017.1
- 수록면
- 581 - 591 (11page)
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Purpose: c-Met and its ligand, hepatocyte growth factor (HGF), play a critical role in oncogenesis and metastatic progression. The aim of this study was to identify inhibited enzymogram and to test the antitumor activity of SIM-89 (a c-Met receptor tyrosine kinaseinhibitor) in non-small cell lung cancer.
Materials and Methods: Z’-LYTE kinase assay was employed to screen the kinase enzymogram, and mechanism of action (MOA) analysis was used to identify the inhibited kinases. Cell proliferation was then analyzed by CCK8 assay, and cell migration was determinedby transwell assay. The gene expression and the phosphorylation of c-Met were examined by realtime-PCR and western blotting, respectively. Finally, the secretion of HGF was detected by ELISA assay.
Results: c-Met, activated protein kinase (AMPK), and tyrosine kinase A (TRKA) were inhibited by SIM-89 with the IC50 values of 297 nmol/L, 1.31 μmol/L, and 150.2 nmol/L, respectively. SIM-89 exerted adenosine triphosphate (ATP) competitive inhibition on c-Met. Moreover, the expressions of STAT1, JAK1, and c-Met in H460 cells were decreased by SIM-89 treatment, and c-Met phosphorylationwas suppressed in A549, H441, H1299, and B16F10 cells by the treatment. In addition, SIM-89 treatment significantly decreased the level of HGF, which accounted for the activation of c-Met receptor tyrosine kinase. Finally, we showed cell proliferationinhibition and cell migration suppression in H460 and H1299 cells after SIM-89 treatment.
Conclusion: In conclusion, SIM-89 inhibits tumor cell proliferation, migration and HGF autocrine, suggesting it’s potential antitumoractivity.
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참고문헌 (29)
참고문헌 신청
Tretiakova M / 2011 / MET and phosphorylated MET as potential biomarkers in lung cancer / J Environ Pathol Toxicol Oncol 30:341~354
Ferraro D / 2006 / Pro-metastatic signaling by c-Met through RAC-1 and reactive oxygen species (ROS) / Oncogene 25:3689~3698
Navab R / 2009 / Co-overexpression of Met and hepatocyte growth factor promotes systemic metastasis in NCI-H460 non-small cell lung carcinoma cells / Neoplasia 11:1292~1300
Ravichandran K / 2011 / Interleukin-1beta-induced iNOS expression in human lung carcinoma A549 cells: involvement of STAT and MAPK pathways / Indian J Exp Biol 49:840~847
Birchmeier C / 2003 / Met, metastasis, motility and more / Nat Rev Mol Cell Biol 4 : 915 ~ 925
Ferraro D / 2006 / Pro-metastatic signaling by c-Met through RAC-1 and reactive oxygen species (ROS) / Oncogene 25:3689~3698
Navab R / 2009 / Co-overexpression of Met and hepatocyte growth factor promotes systemic metastasis in NCI-H460 non-small cell lung carcinoma cells / Neoplasia 11:1292~1300
Ravichandran K / 2011 / Interleukin-1beta-induced iNOS expression in human lung carcinoma A549 cells: involvement of STAT and MAPK pathways / Indian J Exp Biol 49:840~847
Birchmeier C / 2003 / Met, metastasis, motility and more / Nat Rev Mol Cell Biol 4 : 915 ~ 925
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