Gambogic acid induces apoptosis by regulating the expression of Bax and Bcl‐2 and enhancing caspase‐3 activity in human malignant melanoma A375 cells

Xu, Xiaoyuan; Liu, Yeqiang; Wang, Ling; He, Jun; Zhang, Hongfeng; Chen, Xinxiang; Li, Yan; Yang, Jinqiang; Tao, Juan

doi:10.1111/j.1365-4632.2009.03946.x

Cited by 57 publications

(31 citation statements)

References 24 publications

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“…this result is consistent with previous findings that GA induces apoptosis in some other tumor cells by up-regulating the Bax/Bcl-2 ratio (9,10,26,27).…”

Section: Discussionsupporting

confidence: 83%

Gambogic acid inhibits the growth of osteosarcoma cells in vitro by inducing apoptosis and cell cycle arrest

Zhao

Zhou²,

Zhang³

et al. 2011

Oncol Rep

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Abstract. the natural product gambogic acid (gA) has been demonstrated to be a promising chemotherapeutic drug for some cancers because of its ability to induce apoptosis and cell cycle arrest. Until now, no studies have looked at the role of gA in osteosarcoma. In this study, we observed the effects of gA on the growth and apoptosis of osteosarcoma cells in vitro. We found that gA treatment inhibits the proliferation of osteosarcoma cells by inducing cell cycle arrest. Moreover, we found that gA induces apoptosis in Mg63, Hos and U2os cells. Furthermore, we showed that gA treatment elevates the Bax/Bcl-2 ratio. gA mediated the g0/g1 phase arrest in U2os cells; this arrest was associated with a decrease in phospho-gsK3-ß (ser9) and the expression of cyclin D1. similarly, in Mg63 cells, gA mediated g2/M cell cycle arrest, which was associated with a decrease in phospho-cdc2 (Thr 161) and cdc25B. Overall, our findings suggest that gA may be an effective anti-osteosarcoma drug because of its capability to inhibit proliferation and induce apoptosis of osteosarcoma cells.

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“…this result is consistent with previous findings that GA induces apoptosis in some other tumor cells by up-regulating the Bax/Bcl-2 ratio (9,10,26,27).…”

Section: Discussionsupporting

confidence: 83%

Gambogic acid inhibits the growth of osteosarcoma cells in vitro by inducing apoptosis and cell cycle arrest

Zhao

Zhou²,

Zhang³

et al. 2011

Oncol Rep

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“…Previous studies have shown that GA can induce apoptosis in some tumor cells 13,33,34) . Our results suggested that the antiproliferative effect of GA was not due to apoptosis or necrosis (Fig.…”

Section: Discussionmentioning

confidence: 99%

Gambogic Acid Induces G0/G1 Cell Cycle Arrest and Cell Migration Inhibition Via Suppressing PDGF Receptor β Tyrosine Phosphorylation and Rac1 Activity in Rat Aortic Smooth Muscle Cells

Liu

et al. 2010

J Atheroscler Thromb

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Aim: Gambogic acid (GA) is the major active compound of Gamboge, a brownish or orange resin exuded from Garcinia hanburryi tree in Southeast Asia. Previous studies have demonstrated that GA exhibits potent anticancer effects by inducing cell cycle arrest or apoptosis in many types of cancer cell lines and blocking angiogenesis via inhibition of vascular endothelial cell proliferation and migration. Proliferation and migration of vascular smooth muscle cells (VSMCs) are critical steps in the progress of atherosclerosis and restenosis after angioplasty. In the present study, we investigated whether GA has an inhibitory effect on the proliferation and migration of VSMCs and its possible mechanism. Methods: The inhibitory effect of GA on the proliferation induced by PDGF-BB and EGF was measured by using Cell number counting assay and [

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“…1) is the main active ingredient of gamboges secreted from the Garcinia hanburryi tree, which mainly grows in Southeast Asia. GA is known to have extensive antitumor activities in certain solid tumors (3,4). Over the last decade, our group has confirmed that GA exhibits cytotoxicity in various types of hematological malignancy (5,6).…”

Section: Introductionmentioning

confidence: 59%

“…The effect of GA on the proliferation of RPMI-8226 cells was analyzed using the MTT assay. Briefly, cells (2x10 4 ) were seeded in a 96-well plate and treated with 0.5, 1.0, 1.5, 2.0 or 2.5 µM GA for 12 h. Following incubation, 20 µl MTT (5 mg/ml) was added to each well and the cells were incubated for a further 3 h at 37˚C. The supernatant was discarded, 150 µl DMSO was added and the plate was gently agitated until the blue crystals were dissolved.…”

Section: Introductionmentioning

confidence: 99%

Effects of gambogic acid on the activation of caspase-3 and downregulation of SIRT1 in RPMI-8226 multiple myeloma cells via the accumulation of ROS

Yang

Chen

et al. 2012

Oncology Letters

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Abstract. Multiple myeloma (MM) is the second most commonly diagnosed hematologic malignancy. Although new drugs, including bortezomib and lenalidomide, have improved the treatment landscape for MM patients, MM remains incurable. Therefore, screening for novel anti-myeloma drugs is necessary. Gambogic acid (GA), the main active ingredient of gamboges secreted from the Garcinia hanburryi tree, has been reported to exhibit potent anticancer activity in certain solid tumors and hematological malignancies, while there are few studies that are available concerning its effects on MM cells. In the present study, we investigated the anticancer activity of GA on the MM RPMI-8226 cells and further studied the underlying mechanisms by which GA affected the cells. RPMI-8226 cells were cultured and the effect of GA on cell proliferation was analyzed using MTT assay. Hoechst 33258 staining was used to visualize nuclear fragmentation, and reactive oxygen species (ROS) levels were detected. GA was found to have a significant, dose-dependent effect on growth inhibition and apoptosis induction in RPMI-8226 cells. This activity is associated with the accumulation of ROS, which contributes to the activation of caspase-3 and the cleavage of poly (ADP-ribose) polymerase (PARP), accompanied with apoptosis in RPMI-8226 cells treated with GA. Mammalian SIRT1, as the closest homolog of the yeast Sir2, was extensively involved in regulating cell processes, including cell senescence, aging and neuronal protection, as well as having anti-apoptotic properties. Moreover, SIRT1 overexpression has been shown to protect cancer cells from chemotherapy and ionizing radiation. In the present study, we demonstrated that GA has the potential to downregulate the expression of SIRT1 via ROS accumulation. In conclusion, our study found that GA is able to induce apoptosis in RPMI-8226 cells via ROS accumulation followed by caspase-3 activation, PARP cleavage and SIRT1 downregulation. These results suggest that GA may have the potential to not only induce apoptosis in MM cells, but also to decrease the relapse rate of MM.

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Gambogic acid induces apoptosis by regulating the expression of Bax and Bcl‐2 and enhancing caspase‐3 activity in human malignant melanoma A375 cells

Abstract: GA can inhibit the proliferation of A375 cells and induce their apoptosis, which may be related to the up-regulation of the Bax/Bcl-2 ratio and caspase-3 activity.

Cited by 57 publications

References 24 publications

Gambogic acid inhibits the growth of osteosarcoma cells in vitro by inducing apoptosis and cell cycle arrest

Gambogic acid inhibits the growth of osteosarcoma cells in vitro by inducing apoptosis and cell cycle arrest

Gambogic Acid Induces G0/G1 Cell Cycle Arrest and Cell Migration Inhibition Via Suppressing PDGF Receptor β Tyrosine Phosphorylation and Rac1 Activity in Rat Aortic Smooth Muscle Cells

Effects of gambogic acid on the activation of caspase-3 and downregulation of SIRT1 in RPMI-8226 multiple myeloma cells via the accumulation of ROS

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Gambogic acid induces apoptosis by regulating the expression of Bax and Bcl‐2 and enhancing caspase‐3 activity in human malignant melanoma A375 cells

Abstract: GA can inhibit the proliferation of A375 cells and induce their apoptosis, which may be related to the up-regulation of the Bax/Bcl-2 ratio and caspase-3 activity.

Cited by 57 publications

References 24 publications

Gambogic acid inhibits the growth of osteosarcoma cells in vitro by inducing apoptosis and cell cycle arrest

Gambogic acid inhibits the growth of osteosarcoma cells in vitro by inducing apoptosis and cell cycle arrest

Gambogic Acid Induces G0/G1 Cell Cycle Arrest and Cell Migration Inhibition Via Suppressing PDGF Receptor &beta; Tyrosine Phosphorylation and Rac1 Activity in Rat Aortic Smooth Muscle Cells

Effects of gambogic acid on the activation of caspase-3 and downregulation of SIRT1 in RPMI-8226 multiple myeloma cells via the accumulation of ROS

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Gambogic Acid Induces G0/G1 Cell Cycle Arrest and Cell Migration Inhibition Via Suppressing PDGF Receptor β Tyrosine Phosphorylation and Rac1 Activity in Rat Aortic Smooth Muscle Cells