Andrographolide enhances 5-fluorouracil-induced apoptosis via caspase-8-dependent mitochondrial pathway involving p53 participation in hepatocellular carcinoma (SMMC-7721) cells

Yang, Lu; Wu, Dazhi; Luo, Ke-Wang; Wu, Shuai; Wu, Ping

doi:10.1016/j.canlet.2008.11.015

Cited by 96 publications

(57 citation statements)

References 43 publications

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“…It induces mitochondrial-mediated apoptosis in lymphoma cells through caspase cascades . Yang et al (2009) showed that andrographolide enhances 5-fluorouracil-induced apoptosis via caspase-8-dependent mitochondrial pathway involving p53 participation in hepatocellular carcinoma cells. Notably, we found that andrographolide at concentrations of >20 μM caused apoptotic death in RAFLSs.…”

Section: Discussionmentioning

confidence: 99%

Andrographolide induces cell cycle arrest and apoptosis in human rheumatoid arthritis fibroblast-like synoviocytes

Yan

Yang

et al. 2011

Cell Biol Toxicol

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The pseudo-tumoral expansion of fibroblast-like synoviocytes is a hallmark of rheumatoid arthritis (RA), and targeting rheumatoid arthritis fibroblast-like synoviocytes (RAFLSs) may have therapeutic potentials in this disease. Andrographolide, a diterpenoid compound isolated from the herb Andrographis paniculata, has been reported to have potent anti-inflammatory activity. In the present study, we aimed to investigate the effects of andrographolide on human RAFLSs and the underlying molecular mechanism(s). RAFLSs were isolated from patients with RA and treated with or without various concentrations (i.e., 10, 20, and 30 μM) of andrographolide for 48 h. 3-[4,5-Dimethyl-2-yl]-2,5-diphenyl tetrazolium bromide assay revealed that andrographolide treatment decreased the proliferation of RAFLSs in a dose-dependent manner. Cell cycle analysis using propidium iodide (PI) staining showed a G0/G1 cell cycle arrest in andrographolide-treated RAFLSs. Immunoblotting analysis of key cell cycle regulators demonstrated that andrographolide treatment caused a dose-dependent increase in the expression of cell-cycle inhibitors p21 and p27 and a concomitant reduction of cyclin-dependent kinase 4. Exposure to andrographolide-induced apoptosis of RAFLSs measured by annexin V/PI double staining, which was coupled with promotion of cytochrome C release from mitochondria and activation of caspase-3. Moreover, andrographolide-treated RAFLSs displayed a significant decrease in the Bcl-2/Bax ratio compared to untreated cells. In conclusion, our data demonstrate that andrographolide exerts anti-growth and pro-apoptotic effects on RAFLSs, thus may have therapeutic potential for the treatment of RA.

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Section: Discussionmentioning

confidence: 99%

Andrographolide induces cell cycle arrest and apoptosis in human rheumatoid arthritis fibroblast-like synoviocytes

Yan

Yang

et al. 2011

Cell Biol Toxicol

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“…p53 can induce both the intrinsic and extrinsic apoptotic pathways [11]. It has been reported to be involved in the caspase-8-dependent intrinsic pathway [12]. In addition to direct activation of Bax, p53 can trigger caspase-8-dependent Bid cleavage, which results in Bax conformation and induces cytochrome c release into the cytosol from mitochondria [13].…”

Section: Introductionmentioning

confidence: 99%

Apoptosis: Reprogramming and the Fate of Mature Cells

2012

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Apoptosis is essential for embryogenesis, organ metamorphosis, and tissue homeostasis. In embryonic stem cells, self-renewal is balanced with proliferative potential, inhibition of differentiation, and prevention of senescence and apoptosis. Growing evidence supports the role of apoptosis in self-renewal, differentiation of pluripotent stem cells, and dedifferentiation (reprogramming) of somatic cells. In this paper we discuss the multiple roles of apoptosis in embryonic stem cells (ESCs) and reprogramming of differentiated cells to pluripotency. The role of caspases and p53 as key effectors in controlling the generation of iPSC is emphasized. Remarkably, the complication of apoptosis arising during reprogramming may provide insights into technical improvements for derivation of iPSC from senescent cells as a tool for modeling aging-related diseases.

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“…25) Although A549 cell line is not sensitive to 5-FU, we have found that 5-FU combined with GNA has a synergistic effect unexpectedly. It also has precedents that 5-FU was used for lung cancer, 26,27) although 5-FU is not the first choice.…”

Section: Cell Viability and Combination Index Of Two-drugmentioning

confidence: 64%

Synergistic Effects of 5-Fluorouracil and Gambogenic Acid on A549 Cells: Activation of Cell Death Caused by Apoptotic and Necroptotic Mechanisms <i>via</i> the ROS-Mitochondria Pathway

Cheng

Zhang

et al. 2014

Biological & Pharmaceutical Bulletin

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Andrographolide enhances 5-fluorouracil-induced apoptosis via caspase-8-dependent mitochondrial pathway involving p53 participation in hepatocellular carcinoma (SMMC-7721) cells

Cited by 96 publications

References 43 publications

Andrographolide induces cell cycle arrest and apoptosis in human rheumatoid arthritis fibroblast-like synoviocytes

Andrographolide induces cell cycle arrest and apoptosis in human rheumatoid arthritis fibroblast-like synoviocytes

Apoptosis: Reprogramming and the Fate of Mature Cells

Synergistic Effects of 5-Fluorouracil and Gambogenic Acid on A549 Cells: Activation of Cell Death Caused by Apoptotic and Necroptotic Mechanisms <i>via</i> the ROS-Mitochondria Pathway

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