Pristimerin induces caspase-dependent apoptosis in MDA-MB-231 cells via direct effects on mitochondria

Wu, Chin Chung; Chan, Mei Ling; Chen, Wen Ying; Tsai, Cheng-Chia; Chang, Fang Rong; Wu, Yang Chang

doi:10.1158/1535-7163.mct-05-0027

Cited by 115 publications

(99 citation statements)

References 40 publications

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“…Furthermore, we found that treatment with pristimerin inhibited the migration and invasion of MDA-MB-231 cells in vitro in a dose-dependent manner and the growth and invasion of implanted breast tumors in vivo. These novel data extend previous findings (Wu et al, 2005;Yang et al, 2008;Tiedemann et al, 2009) and suggest that pristimerin may have broad antitumor activity.…”

Section: Discussionsupporting

confidence: 90%

“…Ideally, simultaneous 1 can inhibit tumor cell proliferation by inhibiting the NF-κB pathway and cell cycling (Boire et al, 2005;Costa et al, 2008;Yang et al, 2008;Byun et al, 2009;Tiedemann et al, 2009). In addition, prestimerin has been reported to induce caspase-dependent apoptosis of breast cancer cells (Wu et al, 2005) and prostate cancer cells in vitro (Yang et al, 2008). Recently, pristimerin is reported to be a potent natural triterpenoid inhibitor of 20s proteasome chymotrypsin-like activity in prostate cancer cells (Tiedemann et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

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Pristimerin Inhibits Breast Cancer Cell Migration by Up-regulating Regulator of G Protein Signaling 4 Expression

Mu¹,

Shi²,

Sun³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Background/Aim: Pristimerin isolated from Celastrus and Maytenus spp can inhibit proteasome activity. However, whether pristimerin can modulate cancer metastasis is unknown. Methods: The impacts of pristimerin on the purified and intracellular chymotrypsin proteasomal activity, the levels of regulator of G protein signaling 4 (RGS 4) expression and breast cancer cell lamellipodia formation, and the migration and invasion were determined by enzymatic, Western blot, immunofluorescent, and transwell assays, respectively. Results: We found that pristimerin inhibited human chymotrypsin proteasomal activity in MDA-MB-231 cells in a dose-dependent manner. Pristimerin also inhibited breast cancer cell lamellipodia formation, migration, and invasion in vitro by up-regulating RGS4 expression. Thus, knockdown of RGS4 attenuated pristimerin-mediated inhibition of breast cancer cell migration and invasion. Furthermore, pristimerin inhibited growth and invasion of implanted breast tumors in mice. Conclusion: Pristmerin inhibits proteasomal activity and increases the levels of RGS4, inhibiting the migration and invasion of breast cancer cells.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Pristimerin Inhibits Breast Cancer Cell Migration by Up-regulating Regulator of G Protein Signaling 4 Expression

Mu¹,

Shi²,

Sun³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…Accumulating evidence indicates that mitochondria play a pivotal role in the apoptotic process in mammalian cells (22)(23)(24). Disruption of mitochondrial ∆Ψm is considered to be an indicator of mitochondria damage and is generally defined as an early stage of apoptosis, preceding efflux of small molecules from the mitochondria (including cytochrome c, apoptosis-inducing factor) and followed by caspase-9/-3 cascade activation (25)(26)(27)(28). In the present study, we found the marked decrease of pro-caspases (pro-caspase-3 and -9) by 7-PEC after the breakdown of ∆Ψm, suggesting that the mitochondria-mediated pathway is involved in 7-PEC-triggered apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Induction of apoptosis by 7-piperazinethylchrysin in HCT-116 human colon cancer cells

et al. 2012

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Abstract. The antitumor activity of 7-piperazinethylchrysin (7-PEC) was investigated in HCT-116 human colon cancer cells. MTT assay revealed that the IC 50 of 7-PEC in HCT-116 cells was 1.5 µM after 72 h of treatment, much lower than that of chrysin (>100 µM). The data showed that 7-PEC was able to inhibit the growth of HCT-116 cells in a concentration-and time-dependent manner. Topical morphological changes of apoptotic body formation after 7-PEC treatment were observed by Hoechst 33258 staining. 7-PEC reduced mitochondrial membrane potential (∆Ψm) of cells in a concentration-dependent manner and increased the production of intracellular reactive oxygen species (ROS). After treatment with 7-PEC, a significant increase of Bax protein expression and decrease of Bcl-2 protein expression were observed at the same time. These events paralleled with activation of p53, caspase-3 and -9 and the release of cytochrome c (cyt-c), as well as poly(ADPribose) polymerase-1 (PARP1) cleavage and downregulation of p-Akt. However, the apoptosis induced by 7-PEC was blocked by Ac-DEVD-CHO, a caspase-3 inhibitor. These results demonstrate that 7-PEC-induced mitochondrial dysfunction in HCT-116 human colon cancer cells triggers events responsible for caspase-dependent apoptosis pathways, and the elevated ratio of Bax/Bcl-2 is likely involved in this effect.

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“…In addition, it has been reported that pristimerin has promising clinical potential as both a therapeutic and chemopreventive agent for various types of cancer such as pancreatic cancer, glioma, leukemia, cervical cancer, prostate cancer and breast cancer (6)(7)(8)(9)(10)(11). Pristimerin has been shown to induce cell death via a number of several mechanisms, including proteosome inhibition, caspase activation, inhibition of cell cycle progression, and suppression of antiapoptotic nuclear factor kappa B (NF-κB) and Akt signaling pathways (6,9).…”

Section: Introductionmentioning

confidence: 99%

“…Pristimerin has been shown to induce cell death via a number of several mechanisms, including proteosome inhibition, caspase activation, inhibition of cell cycle progression, and suppression of antiapoptotic nuclear factor kappa B (NF-κB) and Akt signaling pathways (6,9). In breast cancer, it has been reported that pristimeirin induces apoptotic cell death in MDA-MB-231 breast cancer cells in a caspase-dependent manner (11). In addition, prestimerin has been demonstrated to inhibit the migration and invasion of breast cancer cells (12).…”

Section: Introductionmentioning

confidence: 99%

Pristimerin overcomes adriamycin resistance in breast cancer cells through suppressing Akt signaling

Xie

Liang

et al. 2016

Oncology Letters

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Abstract. Breast cancer remains a major public health problem worldwide. Chemotherapy serves an important role in the treatment of breast cancer. However, resistance to chemotherapeutic agents, in particular, multi-drug resistance (MDR), is a major cause of treatment failure in cancer. Agents that can either enhance the effects of chemotherapeutics or overcome chemoresistance are urgently needed for the treatment of breast cancer. Pristimerin, a quinonemethide triterpenoid compound isolated from Celastraceae and Hippocrateaceae, has been shown to possess antitumor, anti-inflammatory, antioxidant and insecticidal properties. The aim of the present study was to investigate whether pristimerin can override chemoresistance in MCF-7/adriamycin (ADR)-resistant human breast cancer cells. The results demonstrated that pristimerin indeed displayed potent cytocidal effect on multidrug-resistant MCF-7/ADR breast cancer cells, and that these effects occurred through the suppression of Akt signaling, which in turn led to the downregulation of antiapoptotic effectors and increased apoptosis. These findings indicate that use of pristimerin may represent a potentially promising approach for the treatment of ADR-resistant breast cancer.

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Pristimerin induces caspase-dependent apoptosis in MDA-MB-231 cells via direct effects on mitochondria

Abstract: Pristimerin, a naturally occurring triterpenoid, has been shown to cause cytotoxicity in several cancer cell lines.

Cited by 115 publications

References 40 publications

Pristimerin Inhibits Breast Cancer Cell Migration by Up-regulating Regulator of G Protein Signaling 4 Expression

Pristimerin Inhibits Breast Cancer Cell Migration by Up-regulating Regulator of G Protein Signaling 4 Expression

Induction of apoptosis by 7-piperazinethylchrysin in HCT-116 human colon cancer cells

Pristimerin overcomes adriamycin resistance in breast cancer cells through suppressing Akt signaling

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