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(E)-2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one (BCI) induces apoptosis via the intrinsic pathway in H1299 lung cancer cells

Jong-Woon Shin, Sae-Bom Kwon, Yesol Bak, Sangku Lee, Do-Young Yoon
doi: https://doi.org/10.1101/131045
Jong-Woon Shin
aDepartment of Bioscience and Biotechnology, Konkuk University, Seoul, Korea
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Sae-Bom Kwon
aDepartment of Bioscience and Biotechnology, Konkuk University, Seoul, Korea
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Yesol Bak
aDepartment of Bioscience and Biotechnology, Konkuk University, Seoul, Korea
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Sangku Lee
bTargeted Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Korea
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Do-Young Yoon
aDepartment of Bioscience and Biotechnology, Konkuk University, Seoul, Korea
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  • For correspondence: ydy4218@konkuk.ac.kr
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Abstract

(E)-2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one (BCI) is known as a dual specific phosphatase 1/6 or MAPK inhibitor. However, its precise anti-lung cancer mechanism remains unknown. In this study, the effects of BCI on cell viability were investigated in the non-small cell lung cancer cell lines NCI-H1299, A549, and NCI-H460. We confirmed that BCI significantly inhibited the cell viability of NCI-H1299 compared to those of NCI-H460 and A549 cells. The anti-cancer effects of BCI were evaluated by MTS assay, annexin V-fluorescein isothiocyanate/propidium iodide staining, cell cycle analysis, reverse transcription-PCR, western blotting, and JC-1 staining in NCI-H1299 cells. BCI induced cellular morphological changes and inhibited viability of NCI-H1299 cells in a dose-dependent manner. BCI enhanced Bax expression and induced processing of caspase-9, caspase-3, and poly (ADP-ribose) polymerase as well as the release of cytochrome c from the mitochondria into the cytosol. BCI also down-regulated Bcl-2 expression but enhanced Bax expression in a dose-dependent manner in NCI-H1299 cells. In addition, BCI did not modulate death receptor expression or the extrinsic factor caspase-8 and Bid, a linker between the intrinsic and extrinsic apoptotic pathways in NCI-H1299 cells. On the basis of these results, we conclude that BCI induces apoptosis through a mediated intrinsic pathway, but not extrinsic pathway in NCI-H1299 cells. These results suggest that BCI can be used as a therapeutic agent in lung cancer.

Footnotes

  • Abbreviations: PARP: poly (ADP-ribose) polymerase; MMP: Mitochondria Membrane Potential; DISC: death-inducing signaling complex; BCI: (E)-2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one; PS: phosphatidylserine; FADD: Fas associated protein with death domain

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Posted April 26, 2017.
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(E)-2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one (BCI) induces apoptosis via the intrinsic pathway in H1299 lung cancer cells
Jong-Woon Shin, Sae-Bom Kwon, Yesol Bak, Sangku Lee, Do-Young Yoon
bioRxiv 131045; doi: https://doi.org/10.1101/131045
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(E)-2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one (BCI) induces apoptosis via the intrinsic pathway in H1299 lung cancer cells
Jong-Woon Shin, Sae-Bom Kwon, Yesol Bak, Sangku Lee, Do-Young Yoon
bioRxiv 131045; doi: https://doi.org/10.1101/131045

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