Induction of apoptotic cell death by ursolic acid through mitochondrial death pathway and extrinsic death receptor pathway in MDA-MB-231 cells

Kim, Kyung Hun; Seo, Hye Sook; Choi, Han Seok; Choi, In-Hwa; Shin, Yong Cheol; Ko, Seong‐Gyu

doi:10.1007/s12272-011-0817-5

Cited by 99 publications

(72 citation statements)

References 48 publications

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“…Caspases are essential proteins for the execution of cell death induced by apoptotic stimuli (Kim et al, 2011). The activity of proteolytic caspase-9 and downstream effector caspase-3 promoted subsequent cellular destruction.…”

Section: Discussionmentioning

confidence: 99%

Triptolide Inhibits Proliferation and Induces Apoptosis of Human Melanoma A375 Cells

Tao¹,

Zhang²,

Ma³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Triptolide, a diterpenoid obtained from Tripteryglum wilfordii Hook.f, has attracted interest for its antitumor activities against human tumor cell lines in recent years. This report focuses on anti-proliferative and pro-apoptotic activities in human melanoma A375 cells assessed by CCK8 assay, Hoechst 33258 staining and flow cytometry. In addition, triptolide-induced arrest in the S phase was also observed. Caspase assays showed the apoptosis induced by triptolide was caspase-dependent and probably through intrinsic apoptotic pathways. Furthermore, expression of NF-kB (p65) and its downstream factors such as Bcl-2, Bcl-X L was down-regulated. Taken together, the data indicate that triptolide inhibits A375 cells proliferation and induces apoptosis by a caspase-dependent pathway and through a NF-kB-mediated mechanism.

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Section: Discussionmentioning

confidence: 99%

Triptolide Inhibits Proliferation and Induces Apoptosis of Human Melanoma A375 Cells

Tao¹,

Zhang²,

Ma³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…Previous studies have shown that the LCR extract improves insulin resistance and lipid metabolism in obesediabetic rats (10). Since it has been known that LCR contains a variety of physiologically active compounds such as apigenin, luteolin, kaempferol, quercetin, oleanolic acid, and urosolic acid (11,12) which may have anticancer activities (13)(14)(15), LCR may exert an inhibitory effect on tumor growth. However, little information is available regarding the effect of LCR on cancer cell growth.…”

Section: Introductionmentioning

confidence: 99%

Lycii cortex radicis extract inhibits glioma tumor growth in vitro and in vivo through downregulation of the Akt/ERK pathway

Jeong

Kim²,

Kim³

et al. 2012

Oncol Rep

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Abstract. Lycii cortex radicis (LCR) is a traditional Korean medicinal herb. The present study was undertaken to examine the effect of an LCR extract on glioma cell growth and to determine its molecular mechanism in U87MG human glioma cells. The LCR extract resulted in apoptotic cell death in a dose-and time-dependent manner. The LCR extract-induced cell death was associated with generation of reactive oxygen species (ROS). Western blot analysis showed that the LCR extract caused downregulation of Akt and ERK. The LCR-induced cell death was prevented by transfection with the constitutively active forms of Akt and MEK. Oral administration of LCR extracts in subcutaneous U87MG xenograft models reduced glioma tumor volume. Taken together, these findings suggest that the LCR extract results in human glioma cell death through mechanisms involving ROS generation, downregulation of Akt and ERK, and caspase activation in vitro and reduces glioma tumor growth in vivo. These data suggest that the LCR extract may serve as a potential therapeutic agent for malignant human glioblastomas.

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“…9 Ursolic acid (UA), a natural pentacyclic triterpenoid carboxylic acid, is a potent anticancer agent. It has been shown to prevent tumorigenesis, inhibit tumor growth 10,11 and suppress angiogenesis. 12 UA was shown to sensitize cancer cells to chemotherapeutic agents, to induce cancer cell apoptosis and to inhibit the growth of DU145 cells in nude mice.…”

mentioning

confidence: 99%

Ursolic acid promotes cancer cell death by inducing Atg5‐dependent autophagy

Leng

Hao

et al. 2013

Intl Journal of Cancer

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Ursolic acid (UA) has been reported to possess anticancer activities. Although some of the anticancer activities of UA have been explained by its apoptosis-inducing properties, the mechanisms underlying its anticancer actions are largely unknown. We have found that UA-activated autophagy induced cytotoxicity and reduced tumor growth of cervical cancer cells TC-1 in a concentration-dependent manner. UA did not induce apoptosis of TC-1 cells in vitro as determined by annexin V/propidium iodide staining, DNA fragmentation, and Western blot analysis of the apoptosis-related proteins. We found that UA increased punctate staining of light chain 3 (LC3), which is an autophagy marker. LC3II, the processed form of LC3I which is formed during the formation of double membranes, was induced by UA treatment. These results were further confirmed by transmission electron microscopy. Wortmannin, an inhibitor of autophagy, and a small interfering RNA (siRNA) for autophagy-related genes (Atg5) reduced LC3II and simultaneously increased the survival of TC-1 cells treated with UA. We also found that LC3II was significantly reduced and that survival was increased in Atg52/2 mouse embryonic fibroblast (MEF) cells compared to Atg51/1 MEF cells under UA treatment. However, silencing BECN1 by siRNA affected neither the expression of LC3II nor the survival of TC-1 cells under UA treatment. These results suggest that autophagy is a major mechanism by which UA kills TC-1 cells. It is Atg5 rather than BECN1 that plays a crucial role in UA-induced autophagic cell death in TC-1 cells. The activation of autophagy by UA may become a potential cancer therapeutic strategy complementing the apoptosis-based therapies. Furthermore, regulation of Atg5 may improve the efficacy of UA in cancer treatment.

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Induction of apoptotic cell death by ursolic acid through mitochondrial death pathway and extrinsic death receptor pathway in MDA-MB-231 cells

Cited by 99 publications

References 48 publications

Triptolide Inhibits Proliferation and Induces Apoptosis of Human Melanoma A375 Cells

Triptolide Inhibits Proliferation and Induces Apoptosis of Human Melanoma A375 Cells

Lycii cortex radicis extract inhibits glioma tumor growth in vitro and in vivo through downregulation of the Akt/ERK pathway

Ursolic acid promotes cancer cell death by inducing Atg5‐dependent autophagy

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