Glaucocalyxin A induces apoptosis in human leukemia HL-60 cells through mitochondria-mediated death pathway

Gao, Li; Zhang, Jian; Yang, Wen; Wang, Bin; Wang, Jian Wen

doi:10.1016/j.tiv.2010.09.006

Cited by 61 publications

(40 citation statements)

References 49 publications

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“…Many studies have demonstrated that GLA exerted a potent cytotoxic activity and had a significantly inhibitory effect on several tumor cells, such as leukemia HL60 cell (Gao et al, 2011;Yang et al, 2013). Our results revealed that a marked anti-proliferative activity was observed in MCF-7 and Hs578T cells with IC50 value of 1 μM and 4 μM after treatment of GLA for 72 h, respectively ( Figure 1).…”

Section: Gla Suppressed the Viability And Growth Of Cells Through G2/mentioning

confidence: 49%

Glaucocalyxin A Activates FasL and Induces Apoptosis Through Activation of the JNK Pathway in Human Breast Cancer Cells

Jiang²,

Z³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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This study was conducted to analyze the molecular mechanisms responsible for anti-proliferation effects of glaucocalyxin A in cultured MCF-7 and Hs578T breast cancer cells. The concentration that reduced cell viability to 50% (IC50) after 72 h treatment was derived and potential molecular mechanisms of anti-proliferation using the IC50 were investigated as changes in cell cycle arrest and apoptosis. Gene and protein expression changes related to apoptosis were investigated by semi-quantitative RT-PCR and western blotting, respectively. Involvement of phosphorylated mitogen-activated protein kinases and JNK signaling in regulation of these molecules was characterized by western blotting. Cell viability decreased in a concentration-dependent manner and the IC50 was determined as 1 μΜ in MCF-7 and 4 μΜ in Hs578T cell. Subsequently, we demonstrated that the GLA-induced MCF-7 and Hst578T cell death was due to cell cycle arrest at the G2/M transition and was associated with activation of the c-jun N-terminal kinase (JNK) pathway. We conclude that GLA has the potential to inhibit the proliferation of human breast cancer cells through the JNK pathway and suggest its application forthe effective therapy for patients with breast cancer.

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Section: Gla Suppressed the Viability And Growth Of Cells Through G2/mentioning

confidence: 49%

Glaucocalyxin A Activates FasL and Induces Apoptosis Through Activation of the JNK Pathway in Human Breast Cancer Cells

Jiang²,

Z³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…HepG-2 cells were seeded at an initial concentration of 1x10 6 /l in a 6-well plate. After culturing for 24 h, cells were treated with 50 or 100 µmol/l TTF1.…”

Section: Methodsmentioning

confidence: 99%

“…The apoptosome complex dimer then activates caspase-9 and further activates caspase-3, which may next degrade centrosome DNA by DNase activity to induce apoptosis (1)(2)(3). Finding a component in Chinese herbal medicine which can effectively induce apoptosis is an important area in anti-tumor research within Chinese medicine (4)(5)(6). Sorbaria sorbifolia (SS) is rosaceous plant which grows extensively in Changbai Mountain in Yunnan, Guizhou, Sichuan, Hubei, Gansu and Ningxia Provinces.…”

Section: Introductionmentioning

confidence: 99%

TTF1-induced apoptosis of HepG-2 cells through a mitochondrial pathway

Bian²,

Cui³

et al. 2011

Oncol Rep

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Abstract. The Chinese medicinal herb Sorbaria sorbifolia, native to Changbai Mountain, can induce apoptosis in HepG-2 cells. We studied the mechanism by which 5, 2' , 4'-trihydroxy-6,7, 5'-trimethoxyflavone (TTF1) isolated from acetic ether extracts of Sorbaria sorbifolia induces apoptosis in HepG-2 cells. The results showed that TTF1 both inhibited cell growth and induced apoptosis. RT-PCR and Western blot analysis showed that TTF1 treatment led to decreased transcription and protein expression of bcl-2 and an increase in bax, . These results together suggest that TTF1 may induce apoptosis of HepG-2 cells through a mitochondrial pathway.

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“…1), also termed leukamenin F or (5β,7α,9β,10α)-7,14-dihydroxy kaur-16-ene-3,15-dione, is a chemical form of ent-kaurene diterpenoids that demonstrates a wide range of biological activities. GLA has been reported to attenuate lipopolysaccharide-stimulated neuroinflammation (11), inhibit protein kinase B phosphorylation in human-derived malignant glioma U87MG cells (12), cause a marked increase of platelet cyclic adenosine monophosphate levels (13), inhibit H 2 O 2 -induced H9c2 cardiomyocyte injury (14), and induce apoptosis in a radical oxygen species-dependent mitochondrial dysfunction pathway (15). Furthermore, the intracellular glutathione-redox system is important in regulating the GLA-induced cytotoxicity on HL-60 cells (16).…”

Section: Introductionmentioning

confidence: 99%

Glaucocalyxin A inhibits the growth of liver cancer Focus and SMMC-7721 cells

Tang

Jin

et al. 2015

Oncology Letters

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Abstract. Liver cancer is one of the most common types of cancer, and hepatoma demonstrates a poor long-term prognosis. The present study reports that glaucocalyxin A (GLA), a natural product isolated from Rabdosia umbrosa, inhibits the growth of the liver cancer Focus and SMMC-7721 cell lines in a dose-and time-dependent manner. The present study revealed that GLA arrested the liver cancer cells at the G2/M stage of the cell cycle and led to decreased expression of caspase 3 and the cleavage of poly(adenosine diphosphate-ribose) polymerase.Overall, the present study demonstrated that GLA inhibits the growth of liver cancer cells by G2/M stage cell-cycle arrest and cell apoptosis.

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Glaucocalyxin A induces apoptosis in human leukemia HL-60 cells through mitochondria-mediated death pathway

Cited by 61 publications

References 49 publications

Glaucocalyxin A Activates FasL and Induces Apoptosis Through Activation of the JNK Pathway in Human Breast Cancer Cells

Glaucocalyxin A Activates FasL and Induces Apoptosis Through Activation of the JNK Pathway in Human Breast Cancer Cells

TTF1-induced apoptosis of HepG-2 cells through a mitochondrial pathway

Glaucocalyxin A inhibits the growth of liver cancer Focus and SMMC-7721 cells

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