Curcumin induces apoptosis through the mitochondria-mediated apoptotic pathway in HT-29 cells

Wang, Jinbo; Li, Qi; Zheng, Shui-di; Wu, Tingfeng

doi:10.1631/jzus.b0820238

Cited by 97 publications

(57 citation statements)

References 38 publications

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“…colorectal cancer is one of the leading causes of cancer-related death in Western countries, and its incidence is increasing rapidly in asia (1,2). Surgical resection followed by adjuvant chemotherapy has been considered the optimal treatment approach for patients with colon cancer (3,4).…”

Section: Introductionmentioning

confidence: 99%

20(S)-Ginsenoside Rg3-induced apoptosis in HT-29 colon cancer cells is associated with AMPK signaling pathway

Chung¹

2010

Mol Med Rep

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Abstract. 20(S)-ginsenoside rg3 [20(S)-rg3)], one of the main constituents isolated from Panax ginseng, has been shown to have an anti-cancer effect and to induce apoptosis by interfering with several signaling pathways. However, the molecular mechanisms of aMP-activated protein kinase (aMPK) associated with apoptosis in HT-29 colon cancer cells remain unclear. in the present study, we investigated whether 20(S)-rg3 exerts an anti-proliferative effect and induces apoptosis by modulating the aMPK signaling pathway in HT-29 cells. 20(S)-rg3-treated cells displayed several apoptotic features, including dna fragmentation, proteolytic cleavage of poly (adP-ribose) polymerase (ParP) and morphological changes. 20(S)-rg3 downregulated the expression of anti-apoptotic protein B-cell cll/lymphoma 2 (Bcl2), up-regulated the expression of pro-apoptotic protein of p53 and Bcl-2-associated X protein (Bax), and caused the release of mitochondrial cytochrome c, ParP, caspase-9 and caspase-3. However, 20(S)-rg3-induced apoptosis was completely abolished in the presence of compound c (aMPK inhibitor) or small interfering rna for aMPK (siaMPK). in addition, STo-609 (caMKKβ inhibitor) attenuated 20(S)-rg3-induced aMPK activation and apoptosis. These results suggest that 20(S)-rg3-induced apoptosis in HT-29 cells is mediated via the aMPK signaling pathway, and that 20(S)-rg3 is capable of inducing apoptosis in colon cancer.

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Section: Introductionmentioning

confidence: 99%

20(S)-Ginsenoside Rg3-induced apoptosis in HT-29 colon cancer cells is associated with AMPK signaling pathway

Chung¹

2010

Mol Med Rep

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“…Bcl-2 and Bcl-xl inhibit apoptosis while Bax and Bad promote apoptosis (32). It is reported that a number of traditional Chinese medicines exhibit their antitumor effects by simultaneous upregulation of Bax and Bad and downregulation of Bcl-2 and Bcl-xl (33)(34)(35).…”

Section: Discussionmentioning

confidence: 99%

Role of pseudolaric acid B in A549 lung cancer cell proliferation and apoptosis

Guan

Yang

2013

Molecular Medicine Reports

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Abstract. Recently, traditional Chinese medicine has gained attention for its potential use as a chemotherapeutic agent. Pseudolaric acid B (PAB) is a diterpene acid isolated from Pseudolarix kaempferi and possesses antifungal, antimicrobial, antifertility and antiangiogenic properties. It was also reported that PAB may inhibit proliferation and induce apoptosis in various types of cancer. However, its effects on A549 lung cancer cells remain to be determined. The present study aimed to determine the potential roles of PAB in the proliferation and apoptosis of A549 cells. The results showed that PAB inhibited A549 cell proliferation in a time-and dose-dependent manner. Fluorescence microscopy results showed that cells treated with 20 µmol/l PAB for 24 h exhibited karyorrhexis and apoptotic body formation. In addition, A549 cells were treated with 5, 10, 20, 40 or 80 µmol/l PAB for 24 h and apoptosis was analyzed using Annexin-V/propidium iodide kit. The apoptosis rates were 8. 95, 18.71, 24.66, 35.02 and 43.64%, respectively, in PAB-treated cells and 0.80% in the control group. Furthermore, western blot analysis showed that PAB treatment upregulated the protein levels of Bax, Bad and downregulated Bcl-2 and Bcl-xl expression. In conclusion, PAB may serve as a potent chemotherapeutic agent against human lung cancer.

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“…The transformation of fibroblasts into myofibroblasts is stimulated by TGFβ1, which is found in high levels in burns and scalds (Heng 2011, Tredget et al 2006. The formation of myofibroblasts is also enhanced by wound tension, infection, deep wounds (Dunkin et al 2007, Wang et al 2008) and an inherited keloidal tendency (Lee et al 1999, Abdou et al 2011, Heng 2011. It is noteworthy that hypertrophic scarring is usually not observed in embryos and fetuses , Martin 1997, Ferguson and O'Kane 2004, in whom TGFβ1 is only expressed transiently and at low levels (Martin et al 1993, Martin 1997, Whitby and Ferguson 1991 with resulting absence of myofibroblast conversion (Estes et al 1994, Armstrong andFerguson 1995).…”

Section: Role Of Fibroblasts and Myofibroblasts In Hypertrophic Scarringmentioning

confidence: 99%

Phosphorylase Kinase Inhibition Therapy in Burns and Scalds

Heng¹

2017

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Severe burns and scalds almost always result in unsightly hypertrophic scarring. Among the important processes involved in scarring are fibroblast formation and transformation of fibroblasts into myofibroblasts. Myofibroblasts contain α-smooth muscle actin which has contractile properties and can lead to wound contraction and hypertrophic scarring. Phosphorylase kinase (PhK), expressed within 5 mins of injury, is among the earliest enzymes released after tissue damage. It is responsible for activation of NF-kB, which in turn activates over 200 different genes related to inflammation, fibroblastic proliferation, myofibroblast conversion, and eventual scar tissue formation. The sequence and approximate timing of events following injury include the following: activation of PhK (5 mins), followed by appearance of neutrophils (30 mins), macrophages (hours to days), fibroblasts (1 week) and myofibroblasts (2 weeks). Cytokines and growth factors secreted by macrophages include fibroblast growth factor (FGF) and transforming growth factors α and β (TGFα and TGFβ). Fibroblast growth factor is responsible for fibroblastic proliferation, and TGFβ1 for conversion of fibroblasts into myofibroblasts. After thermal injury, the use of topical curcumin, a non-competitive, selective PhK inhibitor that blocks PhK activity upstream of NF-kB activation, was found to be associated with more rapid and improved skin healing, as well as less severe or absent scarring. ‡

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Curcumin induces apoptosis through the mitochondria-mediated apoptotic pathway in HT-29 cells

Cited by 97 publications

References 38 publications

20(S)-Ginsenoside Rg3-induced apoptosis in HT-29 colon cancer cells is associated with AMPK signaling pathway

20(S)-Ginsenoside Rg3-induced apoptosis in HT-29 colon cancer cells is associated with AMPK signaling pathway

Role of pseudolaric acid B in A549 lung cancer cell proliferation and apoptosis

Phosphorylase Kinase Inhibition Therapy in Burns and Scalds

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