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Mol. Cells 2011; 32(5): 451-457

Published online November 11, 2011

https://doi.org/10.1007/s10059-011-0137-0

© The Korean Society for Molecular and Cellular Biology

Jolkinolide B from Euphorbia fischeriana Steud Induces Apoptosis in Human Leukemic U937 Cells through PI3K/Akt and XIAP Pathways

Jia-He Wang*, Yi-Jun Zhou1, Xue Bai, and Ping He

Department of Geriatrics, Shengjing Hospital of China Medical University, Shenyang, 110004, P.R. China, 1Department of Endocrinology and Metabolism, the fourth affiliated hospital of China Medical University, Shenyang, 110004, P.R. China

Correspondence to : *Correspondence: wangjh1@sj-hospital.org

Received: June 26, 2011; Revised: September 5, 2011; Accepted: September 7, 2011

Abstract

Jolkinolide B, a bioactive diterpene isolated from the roots of Euphorbia fischeriana Steud, is known to induce apoptosis in cancer cells. However, the molecular mecha-nism of its anti-cancer activity have not been fully eluci-dated. In the present study, we found that Jolkinolide B reduced cell viability and induced apoptosis in a dose- and time-dependent manner in human leukemic U937. The induction of apoptosis was also accompanied by the downregulation of PI3K/Akt and the inhibitor of apoptosis protein (IAP) family proteins. Moreover, we observed that Jolkinolide B treatment resulted in activation of caspase-3 and -9, which may partly explain the anti-cancer activity of Jolkinolide B. Taken together, our study for the first time suggest that Jolkinolide B is able to enhance apoptosis of U937 cells, at least in part, through downregulation of PI3K/Akt and IAP family proteins. Moreover, the triggering of caspase-3 and -9 activation mediated apoptotic induction.

Keywords apoptosis, caspase, Euphorbia fischeriana Steud, Jolkinolide B, U937

Article

Research Article

Mol. Cells 2011; 32(5): 451-457

Published online November 30, 2011 https://doi.org/10.1007/s10059-011-0137-0

Copyright © The Korean Society for Molecular and Cellular Biology.

Jolkinolide B from Euphorbia fischeriana Steud Induces Apoptosis in Human Leukemic U937 Cells through PI3K/Akt and XIAP Pathways

Jia-He Wang*, Yi-Jun Zhou1, Xue Bai, and Ping He

Department of Geriatrics, Shengjing Hospital of China Medical University, Shenyang, 110004, P.R. China, 1Department of Endocrinology and Metabolism, the fourth affiliated hospital of China Medical University, Shenyang, 110004, P.R. China

Correspondence to:*Correspondence: wangjh1@sj-hospital.org

Received: June 26, 2011; Revised: September 5, 2011; Accepted: September 7, 2011

Abstract

Jolkinolide B, a bioactive diterpene isolated from the roots of Euphorbia fischeriana Steud, is known to induce apoptosis in cancer cells. However, the molecular mecha-nism of its anti-cancer activity have not been fully eluci-dated. In the present study, we found that Jolkinolide B reduced cell viability and induced apoptosis in a dose- and time-dependent manner in human leukemic U937. The induction of apoptosis was also accompanied by the downregulation of PI3K/Akt and the inhibitor of apoptosis protein (IAP) family proteins. Moreover, we observed that Jolkinolide B treatment resulted in activation of caspase-3 and -9, which may partly explain the anti-cancer activity of Jolkinolide B. Taken together, our study for the first time suggest that Jolkinolide B is able to enhance apoptosis of U937 cells, at least in part, through downregulation of PI3K/Akt and IAP family proteins. Moreover, the triggering of caspase-3 and -9 activation mediated apoptotic induction.

Keywords: apoptosis, caspase, Euphorbia fischeriana Steud, Jolkinolide B, U937

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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