IDH-Inhibiting Small Molecule DTDQ Inhibits Migration and Invasion of A549 Human Non-Small-Cell Lung Cancer Cells via Sequential Inactivation Of ERK and P38 Signaling Pathways
- Authors
- Park, Soonchan; Lee, Jongsung; Lee, Sang Yeol
- Issue Date
- Jun-2018
- Publisher
- HUMANA PRESS INC
- Keywords
- 6,7-dimethyl-4-(3,4,5-trimethoxyphenyl)-3,4-dihydroquinolin-2(1H)-one; IDH; Human lung cancer; Metastasis; Matrix metalloproteinases; MAPK
- Citation
- CELL BIOCHEMISTRY AND BIOPHYSICS, v.76, no.1-2, pp.255 - 263
- Journal Title
- CELL BIOCHEMISTRY AND BIOPHYSICS
- Volume
- 76
- Number
- 1-2
- Start Page
- 255
- End Page
- 263
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/3672
- DOI
- 10.1007/s12013-017-0789-2
- ISSN
- 1085-9195
- Abstract
- Migration and invasion are two core processes during cancer metastasis, and several signaling pathways have been shown to be involved. A key regulator of metastasis is the mitogen-activated protein kinase signaling pathway. Here, we report that the small molecule, 6,7-dimethyl-4-(3,4,5-trimethoxyphenyl)-3,4-dihydroquinolin-2(1H)-one, inhibited isocitrate dehydrogenase activity and had anti-metastatic effects in A549 human non-small-cell lung cancer cells. 6,7-dimethyl-4-(3,4,5-trimethoxyphenyl)-3,4-dihydroquinolin-2(1H)-one induced sequential inactivation of the extracellular signal-regulated kinases and p38 signaling pathways, both representative mitogen-activated protein kinase family members. We also found that 6,7-dimethyl-4-(3,4,5-trimethoxyphenyl)-3,4-dihydroquinolin-2(1H)-one suppressed the transcription factor c-Myc, a regulator of cancer metastasis. This led to selective attenuation of matrix metalloproteinase-2 and subsequent suppression of migration and invasion in A549 non-small-cell lung cancer cells. 6,7-dimethyl-4-(3,4,5-trimethoxyphenyl)-3,4-dihydroquinolin-2(1H)-one also suppressed metastasis in H1299 non-small-cell lung cancer cells, suggesting that the effects of 6,7-dimethyl-4-(3,4,5-trimethoxyphenyl)-3,4-dihydroquinolin-2(1H)-one are not limited to A549 non-small-cell lung cancer cells. We therefore propose that the antimetastatic effects of 6,7-dimethyl-4-(3,4,5-trimethoxyphenyl)-3,4-dihydroquinolin-2(1H)-one are due to sequential inactivation of the extracellular signal-regulated kinases and p38 signaling pathways.
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