Corosolic acid induces apoptosis through mitochondrial pathway and caspases activation in human cervix adenocarcinoma HeLa cells

Xu, Yanfeng; Ge, Ruowen; Du, Juan; Xin, Hailiang; Yi, Tingjiao; Sheng, Jiayu; Wang, Yongzi; Ling, Changquan

doi:10.1016/j.canlet.2009.04.028

Cited by 106 publications

(93 citation statements)

References 31 publications

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“…These findings provide evidence that the apoptosis induced by CRA in MG-63 cells is mediated by the mitochondrial pathway. Our observations regarding the caspase cascade-mediated apoptosis-inducing properties of CRA were in agreement with those from previous studies (1,34).…”

Section: Discussionsupporting

confidence: 93%

“…To confirm whether CRA-induced apoptosis involved caspase cascade activation, MG-63 cells were pretreated with 100 µM of z-VAD-FMK (Sigma-Aldrich; Merck Millipore), a general caspase inhibitor (34), for 1 h, prior to be treated with CRA. The colorimetric assay revealed that the increased activity of caspase-3 and -9 induced by CRA was significantly diminished in the presence of z-VAD-FMK (Fig.…”

Section: Cra Induces Loss Of Mitochondrial Membrane Potentialmentioning

confidence: 99%

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Corosolic acid inhibits the proliferation of osteosarcoma cells by inducing apoptosis

Jia¹,

Yuan²,

Shan³

et al. 2016

Oncology Letters

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Abstract. Corosolic acid (CRA), a pentacyclic triterpene isolated from medicinal herbs, has been reported to exhibit anticancer properties in several cancers. However, the anticancer activity of CRA in osteosarcoma cells is still unclear. In the present study, the inhibitory effect of CRA in osteosarcoma MG-63 cells was investigated, and the results revealed that CRA significantly inhibited the viability of MG-63 cells in a dose-and time-dependent manner. A typical apoptotic hallmark such as DNA ladder was detected by agarose gel electrophoresis following treatment with CRA. Further experiments demonstrated that CRA induced apoptosis of MG-63 cells by flow cytometry using propidium iodide and annexin V staining. In addition, it was observed that the apoptosis of MG-63 cells induced by CRA was closely associated with activation of caspase-3 and caspase-9, loss of mitochondrial membrane potential, and release of cytochrome c from mitochondria, suggesting that CRA may trigger the activation of the mitochondria-mediated apoptosis pathway. In addition, the inhibition of caspase activity attenuated the CRA-induced apoptosis of MG-63 cells, which further confirmed the role of the mitochondrial pathway in CRA-induced apoptosis. These results indicated that CRA could induce the apoptosis of osteosarcoma cells through activating the mitochondrial pathway, which provides an evidence that CRA may be a useful chemotherapeutic agent for osteosarcoma.

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Section: Discussionsupporting

confidence: 93%

Section: Cra Induces Loss Of Mitochondrial Membrane Potentialmentioning

confidence: 99%

Corosolic acid inhibits the proliferation of osteosarcoma cells by inducing apoptosis

Jia¹,

Yuan²,

Shan³

et al. 2016

Oncology Letters

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“…Cancer cells are characterized by uncontrolled proliferation and reduced apoptosis. Thus, activation of apoptotic pathways is a key mechanism by which cytotoxic drugs kill cancer cells (Xu et al, 2009). The Bcl-2 protein family is a critical regulator of apoptotic pathways.…”

Section: Resultsmentioning

confidence: 99%

Evaluation on Anticancer Effect Against HL-60 Cells and Toxicity in vitro and in vivo of the Phenethyl Acetate Isolated from a Marine Bacterium Streptomyces griseus

Lee¹,

Zhang²,

Ko³

et al. 2015

Fisheries and aquatic sciences

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We previously identified Streptomyces griseus as an anti-cancer agent . In this study, we isolated compounds from S. griseus and evaluated their anticancer effect and toxicity in vitro and in vivo. Preparative centrifugal partition chromatography (CPC) was used to obtain three compounds, cyclo, cyclo( L -Phe-trans-4-hydroxy-L -Pro) and phenethyl acetate (PA). We chose PA, which had the highest anticancer activity, as a target compound for further experiments. PA induced the formation of apoptotic bodies, DNA fragmentation, DNA accumulation in G 0 /G 1 phase, and reactive oxygen species (ROS) formation. Furthermore, PA treatment increased Bax/Bcl-xL expression, activated caspase-3, and cleaved poly-ADP-ribose polymerase (PARP) in HL-60 cells. Simultaneous evaluation in vitro and in vivo, revealed that PA exhibited no toxicity in Vero cells and zebrafish embryos. We revealed, for the first time, that PA generates ROS, and that this ROS accumulation induced the Bcl signaling pathway.

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“…Total saponin from the root of AVD inhibits the growth of several tumor cell lines in vitro and vivo Zheng et al, 2012). Corosolic acid, a natural triterpenoid derived from many traditional Chinese medicinal herbs, such as AVD and apple pomace, reportedly possesses cytotoxic activity against a variety of cell lines, including lung, cervix, gastric, ovarian, and colon cells (Xu et al, 2009;Lee et al, 2010;Fujiwara et al, 2013;Nho et al, 2013;Sung et al, 2014). Extract from the root of AVD, also known as Maorenshen in traditional Chinese medicine, has long been used to treat lung carcinoma, hepatoma, and myeloma .…”

Section: Preventive Effect Of Actinidia Valvatamentioning

confidence: 99%

Preventive Effect of Actinidia Valvata Dunn Extract on N-methyl-N'-nitro-N-nitrosoguanidine-induced Gastrointestinal Cancer in Rats

Wang¹,

Líu²,

Wang³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Asian Pac J Cancer Prev, 15 (15), [6363][6364][6365][6366][6367] Introduction Gastric cancer remains a major global problem. In 2008, 989,600 new stomach cancer cases and 738,000 deaths occurred, accounting for 8% of the total cases and 10% of total deaths, respectively (Jemal et al., 2011). Notwithstanding the global declining incidence of gastric cancer, mortality is continuously rising in Asian countries (Hu et al., 2004). Surgery is considered as the gold standard for localized gastric cancer, but most cases are diagnosed at an advanced stage. The five-year survival rate of patients with advanced gastric cancer for surgical treatment is less than 40% (Rasul et al., 2012). Recent primary prevention strategies for gastric cancer focus on behavior modification, including the eradication of Helicobacter pylori, reduction of salt intake, increase in food containing protective factors (fruit,vegetables, soybean products, non-fermented soy-foods,whole-grain) and vitamin C consumption, abolition of smoking, and chemoprevention (Tsugane et al., 2004 AbstractPurpose: This study was conducted to assess the preventive effect of Actinidia valvata Dunn (AVD) extract on an animal model of gastrointestinal carcinogenesis on the basis of changes in tumor incidence, cell proliferation, and apoptosis. Materials and Methods: Seventy-five male Wistar rats were divided into five different treatment groups with 15 rats in each group. Group I was given normal feed, whereas Groups II to IV were treated with 10% sodium chloride in the first six weeks and 100ug/mL of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in drinking water for 24 weeks. Group II was then given normal feed, whereas Group III was given AVD extract (0.24g/kg/day) for 12 weeks. Group IV was given AVD extract from the first week to the 36 th week, whereas Group V was treated with AVD extract alone for 36 weeks. All rats were sacrificed at the end of the 36-week experiment and assessed for the presence of gastrointestinal tumors. The occurrence of cancer was evaluated by histology. Bax, Bcl-2, Caspase-3, and cyclinD1 were determined by immunohistochemical staining and Western blotting. Results: The incidences of gastric cancer were 0% in Group I, 73.3% in Group II, 33.3% in Group III, 26.7% in Group IV, and 0% in Group V. Bcl-2 and cyclinD1 expression was decreased in AVD extract treated groups, whereas Bax and Caspase-3 expression was increased. Comparison with group II revealed significant differences (p<0.01). Conclusions: AVD extract exhibits an obvious preventive effect on gastrointestinal carcinogenesis induced by MNNG in rats through the regulation of cell proliferation and apoptosis.

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Corosolic acid induces apoptosis through mitochondrial pathway and caspases activation in human cervix adenocarcinoma HeLa cells

Cited by 106 publications

References 31 publications

Corosolic acid inhibits the proliferation of osteosarcoma cells by inducing apoptosis

Corosolic acid inhibits the proliferation of osteosarcoma cells by inducing apoptosis

Evaluation on Anticancer Effect Against HL-60 Cells and Toxicity in vitro and in vivo of the Phenethyl Acetate Isolated from a Marine Bacterium Streptomyces griseus

Preventive Effect of Actinidia Valvata Dunn Extract on N-methyl-N'-nitro-N-nitrosoguanidine-induced Gastrointestinal Cancer in Rats

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