Capsaicin induced apoptosis of B16-F10 melanoma cells through down-regulation of Bcl-2

Hye Seung Jun; Taesun Park; Chang Ki Lee; Mi Kyung Kang; Mi Sun Park; Ho Il Kang; Young Joon Surh; Ok Hee Kim

doi:10.1016/j.fct.2006.10.011

Capsaicin induced apoptosis of B16-F10 melanoma cells through down-regulation of Bcl-2

Hye Seung Jun, Taesun Park, Chang Ki Lee, Mi Kyung Kang, Mi Sun Park, Ho Il Kang, Young Joon Surh, Ok Hee Kim

Department of Food and Nutrition

Research output: Contribution to journal › Article › peer-review

56 Citations (Scopus)

Abstract

Capsaicin (8-methyl-N-vanillyl-6-nonenamide), a pungent ingredient of hot chili peppers, has been reported to possess substantial anticarcinogenic and antimutagenic activities. In the present study, we investigated the effect of capsaicin on induction of apoptosis in highly metastatic B16-F10 murine melanoma cells. Capsaicin inhibited growth of B16-F10 cells in a concentration-dependent manner. Proapoptotic effect of capsaicin was evidenced by nuclear condensation, internucleosomal DNA fragmentation, in situ terminal nick-end labeling of fragmented DNA (TUNEL), and an increased sub G1 fraction. Treatment of B16-F10 cells with capsaicin caused release of mitochondrial cytochrome c, activation of caspase-3, and cleavage of poly (ADP-ribose) polymerase in a dose-dependent manner. Furthermore, Bcl-2 expression in the B16-F10 cells was slightly down-regulated by capsaicin treatment. In contrast, there were no alterations in the levels of Bax in capsaicin-treated cells. Collectively, these findings indicate that capsaicin-induces apoptosis of B16-F10 melanoma cells via down-regulation the Bcl-2.

Original language	English
Pages (from-to)	708-715
Number of pages	8
Journal	Food and Chemical Toxicology
Volume	45
Issue number	5
DOIs	https://doi.org/10.1016/j.fct.2006.10.011
Publication status	Published - 2007 May

Bibliographical note

Funding Information:
This work was supported by the Grants from National Institute of Toxicological Research, KFDA and the Brain Korea 21 Project, Yonsei University.

All Science Journal Classification (ASJC) codes

Food Science
Toxicology

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10.1016/j.fct.2006.10.011

Cite this

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title = "Capsaicin induced apoptosis of B16-F10 melanoma cells through down-regulation of Bcl-2",

abstract = "Capsaicin (8-methyl-N-vanillyl-6-nonenamide), a pungent ingredient of hot chili peppers, has been reported to possess substantial anticarcinogenic and antimutagenic activities. In the present study, we investigated the effect of capsaicin on induction of apoptosis in highly metastatic B16-F10 murine melanoma cells. Capsaicin inhibited growth of B16-F10 cells in a concentration-dependent manner. Proapoptotic effect of capsaicin was evidenced by nuclear condensation, internucleosomal DNA fragmentation, in situ terminal nick-end labeling of fragmented DNA (TUNEL), and an increased sub G1 fraction. Treatment of B16-F10 cells with capsaicin caused release of mitochondrial cytochrome c, activation of caspase-3, and cleavage of poly (ADP-ribose) polymerase in a dose-dependent manner. Furthermore, Bcl-2 expression in the B16-F10 cells was slightly down-regulated by capsaicin treatment. In contrast, there were no alterations in the levels of Bax in capsaicin-treated cells. Collectively, these findings indicate that capsaicin-induces apoptosis of B16-F10 melanoma cells via down-regulation the Bcl-2.",

author = "Jun, {Hye Seung} and Taesun Park and Lee, {Chang Ki} and Kang, {Mi Kyung} and Park, {Mi Sun} and Kang, {Ho Il} and Surh, {Young Joon} and Kim, {Ok Hee}",

note = "Funding Information: This work was supported by the Grants from National Institute of Toxicological Research, KFDA and the Brain Korea 21 Project, Yonsei University.",

year = "2007",

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AU - Jun, Hye Seung

AU - Park, Taesun

AU - Lee, Chang Ki

AU - Kang, Mi Kyung

AU - Park, Mi Sun

AU - Kang, Ho Il

AU - Surh, Young Joon

AU - Kim, Ok Hee

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PY - 2007/5

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N2 - Capsaicin (8-methyl-N-vanillyl-6-nonenamide), a pungent ingredient of hot chili peppers, has been reported to possess substantial anticarcinogenic and antimutagenic activities. In the present study, we investigated the effect of capsaicin on induction of apoptosis in highly metastatic B16-F10 murine melanoma cells. Capsaicin inhibited growth of B16-F10 cells in a concentration-dependent manner. Proapoptotic effect of capsaicin was evidenced by nuclear condensation, internucleosomal DNA fragmentation, in situ terminal nick-end labeling of fragmented DNA (TUNEL), and an increased sub G1 fraction. Treatment of B16-F10 cells with capsaicin caused release of mitochondrial cytochrome c, activation of caspase-3, and cleavage of poly (ADP-ribose) polymerase in a dose-dependent manner. Furthermore, Bcl-2 expression in the B16-F10 cells was slightly down-regulated by capsaicin treatment. In contrast, there were no alterations in the levels of Bax in capsaicin-treated cells. Collectively, these findings indicate that capsaicin-induces apoptosis of B16-F10 melanoma cells via down-regulation the Bcl-2.

AB - Capsaicin (8-methyl-N-vanillyl-6-nonenamide), a pungent ingredient of hot chili peppers, has been reported to possess substantial anticarcinogenic and antimutagenic activities. In the present study, we investigated the effect of capsaicin on induction of apoptosis in highly metastatic B16-F10 murine melanoma cells. Capsaicin inhibited growth of B16-F10 cells in a concentration-dependent manner. Proapoptotic effect of capsaicin was evidenced by nuclear condensation, internucleosomal DNA fragmentation, in situ terminal nick-end labeling of fragmented DNA (TUNEL), and an increased sub G1 fraction. Treatment of B16-F10 cells with capsaicin caused release of mitochondrial cytochrome c, activation of caspase-3, and cleavage of poly (ADP-ribose) polymerase in a dose-dependent manner. Furthermore, Bcl-2 expression in the B16-F10 cells was slightly down-regulated by capsaicin treatment. In contrast, there were no alterations in the levels of Bax in capsaicin-treated cells. Collectively, these findings indicate that capsaicin-induces apoptosis of B16-F10 melanoma cells via down-regulation the Bcl-2.

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Capsaicin induced apoptosis of B16-F10 melanoma cells through down-regulation of Bcl-2

Abstract

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