Plumbagin induces apoptotic and autophagic cell death through inhibition of the PI3K/Akt/mTOR pathway in human non-small cell lung cancer cells

Yan Cong Li; Shu Ming He; Zhi Xu He; Minghua Li; Yinxue Yang; Jian Xin Pang; Xueji Zhang; Kevin Chow; Qingyu Zhou; Wei Duan; Zhi Wei Zhou; Tianxin Yang; Gui Hua Huang; Aibing Liu; Jia Xuan Qiu; Jun Ping Liu; Shu Feng Zhou

doi:10.1016/j.canlet.2013.11.001

Plumbagin induces apoptotic and autophagic cell death through inhibition of the PI3K/Akt/mTOR pathway in human non-small cell lung cancer cells

Yan Cong Li, Shu Ming He, Zhi Xu He, Minghua Li, Yinxue Yang, Jian Xin Pang, Xueji Zhang, Kevin Chow, Qingyu Zhou, Wei Duan, Zhi Wei Zhou, Tianxin Yang, Gui Hua Huang, Aibing Liu, Jia Xuan Qiu, Jun Ping Liu, Shu Feng Zhou

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

135 Scopus citations

Abstract

Plumbagin (PLB) has shown anti-cancer activity but the mechanism is unclear. This study has found that PLB has a potent pro-apoptotic and pro-autophagic effect on A549 and H23 cells. PLB arrests cells in G2/M phase, and increases the intracellular level of reactive oxygen species in both cell lines. PLB dose-dependently induces autophagy through inhibition of PI3K/Akt/mTOR pathway as indicated by reduced phosphorylation of Akt and mTOR. Inhibition or induction of autophagy enhances PLB-induced apoptosis. There is crosstalk between PLB-induced apoptosis and autophagy. These findings indicate that PLB initiates both apoptosis and autophagy in NSCLC cells through coordinated pathways.

Original language	English (US)
Pages (from-to)	239-259
Number of pages	21
Journal	Cancer Letters
Volume	344
Issue number	2
DOIs	https://doi.org/10.1016/j.canlet.2013.11.001
State	Published - Mar 28 2014
Externally published	Yes

Keywords

Apoptosis
Autophagy
Non-small-cell lung cancer
PI3K/Akt/mTOR
Plumbagin

ASJC Scopus subject areas

Oncology
Cancer Research

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10.1016/j.canlet.2013.11.001

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Li, Y. C., He, S. M., He, Z. X., Li, M., Yang, Y., Pang, J. X., Zhang, X., Chow, K., Zhou, Q., Duan, W., Zhou, Z. W., Yang, T., Huang, G. H., Liu, A., Qiu, J. X., Liu, J. P., & Zhou, S. F. (2014). Plumbagin induces apoptotic and autophagic cell death through inhibition of the PI3K/Akt/mTOR pathway in human non-small cell lung cancer cells. Cancer Letters, 344(2), 239-259. https://doi.org/10.1016/j.canlet.2013.11.001

Li, YC, He, SM, He, ZX, Li, M, Yang, Y, Pang, JX, Zhang, X, Chow, K, Zhou, Q, Duan, W, Zhou, ZW, Yang, T, Huang, GH, Liu, A, Qiu, JX, Liu, JP & Zhou, SF 2014, 'Plumbagin induces apoptotic and autophagic cell death through inhibition of the PI3K/Akt/mTOR pathway in human non-small cell lung cancer cells', Cancer Letters, vol. 344, no. 2, pp. 239-259. https://doi.org/10.1016/j.canlet.2013.11.001

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title = "Plumbagin induces apoptotic and autophagic cell death through inhibition of the PI3K/Akt/mTOR pathway in human non-small cell lung cancer cells",

abstract = "Plumbagin (PLB) has shown anti-cancer activity but the mechanism is unclear. This study has found that PLB has a potent pro-apoptotic and pro-autophagic effect on A549 and H23 cells. PLB arrests cells in G2/M phase, and increases the intracellular level of reactive oxygen species in both cell lines. PLB dose-dependently induces autophagy through inhibition of PI3K/Akt/mTOR pathway as indicated by reduced phosphorylation of Akt and mTOR. Inhibition or induction of autophagy enhances PLB-induced apoptosis. There is crosstalk between PLB-induced apoptosis and autophagy. These findings indicate that PLB initiates both apoptosis and autophagy in NSCLC cells through coordinated pathways.",

keywords = "Apoptosis, Autophagy, Non-small-cell lung cancer, PI3K/Akt/mTOR, Plumbagin",

author = "Li, {Yan Cong} and He, {Shu Ming} and He, {Zhi Xu} and Minghua Li and Yinxue Yang and Pang, {Jian Xin} and Xueji Zhang and Kevin Chow and Qingyu Zhou and Wei Duan and Zhou, {Zhi Wei} and Tianxin Yang and Huang, {Gui Hua} and Aibing Liu and Qiu, {Jia Xuan} and Liu, {Jun Ping} and Zhou, {Shu Feng}",

year = "2014",

month = mar,

day = "28",

doi = "10.1016/j.canlet.2013.11.001",

language = "English (US)",

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pages = "239--259",

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AU - Li, Yan Cong

AU - He, Shu Ming

AU - He, Zhi Xu

AU - Li, Minghua

AU - Yang, Yinxue

AU - Pang, Jian Xin

AU - Zhang, Xueji

AU - Chow, Kevin

AU - Zhou, Qingyu

AU - Duan, Wei

AU - Zhou, Zhi Wei

AU - Yang, Tianxin

AU - Huang, Gui Hua

AU - Liu, Aibing

AU - Qiu, Jia Xuan

AU - Liu, Jun Ping

AU - Zhou, Shu Feng

PY - 2014/3/28

Y1 - 2014/3/28

N2 - Plumbagin (PLB) has shown anti-cancer activity but the mechanism is unclear. This study has found that PLB has a potent pro-apoptotic and pro-autophagic effect on A549 and H23 cells. PLB arrests cells in G2/M phase, and increases the intracellular level of reactive oxygen species in both cell lines. PLB dose-dependently induces autophagy through inhibition of PI3K/Akt/mTOR pathway as indicated by reduced phosphorylation of Akt and mTOR. Inhibition or induction of autophagy enhances PLB-induced apoptosis. There is crosstalk between PLB-induced apoptosis and autophagy. These findings indicate that PLB initiates both apoptosis and autophagy in NSCLC cells through coordinated pathways.

AB - Plumbagin (PLB) has shown anti-cancer activity but the mechanism is unclear. This study has found that PLB has a potent pro-apoptotic and pro-autophagic effect on A549 and H23 cells. PLB arrests cells in G2/M phase, and increases the intracellular level of reactive oxygen species in both cell lines. PLB dose-dependently induces autophagy through inhibition of PI3K/Akt/mTOR pathway as indicated by reduced phosphorylation of Akt and mTOR. Inhibition or induction of autophagy enhances PLB-induced apoptosis. There is crosstalk between PLB-induced apoptosis and autophagy. These findings indicate that PLB initiates both apoptosis and autophagy in NSCLC cells through coordinated pathways.

KW - Apoptosis

KW - Autophagy

KW - Non-small-cell lung cancer

KW - PI3K/Akt/mTOR

KW - Plumbagin

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JO - Cancer Letters

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ER -

Plumbagin induces apoptotic and autophagic cell death through inhibition of the PI3K/Akt/mTOR pathway in human non-small cell lung cancer cells

Abstract

Keywords

ASJC Scopus subject areas

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