AKT signalling and mitochondrial pathways are involved in mushroom polysaccharide-induced apoptosis and G1 or S phase arrest in human hepatoma cells

OuYang, Fengju; Wang, Guibin; Guo, Wei; Zhang, Yuanyuan; Xiang, Wenhua; Zhao, Min

doi:10.1016/j.foodchem.2012.10.047

Cited by 40 publications

(19 citation statements)

References 27 publications

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“…Akt, also known as protein kinase B, is a primary downstream effector of the PI3K signal transduction pathway, with crucial functions in regulating cell proliferation and survival (29,30). Furthermore, it has been reported that the Akt signaling pathway is particularly important in preventing apoptosis (31,32) and inhibiting the activation of Akt may induce apoptosis (33). ERK and JNK are members of the mitogen-activated protein kinase (MAPK) family, and have been shown to be key in cell proliferation, differentiation, development and programmed cell death (34).…”

Section: Discussionmentioning

confidence: 99%

Effects of Saikosaponin D on apoptosis in human U87 glioblastoma cells

Cai

Zhang

et al. 2017

Molecular Medicine Reports

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Saikosaponin D (SSd) is a type of Saponin derivative, which is a component extracted from Bupleurum falactum. SSd has been reported to exert anticancer activities. However, the effects of SSd on gliomas have not been elucidated. The aim of the present study was to investigate the pharmacological functions and potential molecular mechanisms of SSd in human U87 glioblastoma cells. The cells were treated with SSd at various concentrations for 48 h, the cell viability was assessed with 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyltetrazolium assay, and the activation of Akt, extracellular signal‑regulated kinases (ERK), c‑Jun N‑terminal kinases (JNK) and caspase‑3 was assessed by western blotting. In addition, apoptosis levels were analyzed with Hoechst 33258 and Annexin V staining. The results demonstrated that treatment of the U87 glioma cells with SSd markedly suppressed cell proliferation in a dose‑dependent manner. Meanwhile, SSd treatment enhanced apoptosis in the U87 cells. Furthermore, SSd significantly inhibited the phosphorylation of Akt and ERK, and promoted phosphorylated‑JNK and cleaved caspase‑3 expression. The present study revealed the potential therapeutic effects of SSd in the treatment of gliomas, and the cytotoxic effects of SSd in U87 cells were at least partly attributed to the depression of phosphatidylinositol 3‑kinase/Akt and ERK protein expression levels, and activation of JNK and caspase-3 expression.

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Section: Discussionmentioning

confidence: 99%

Effects of Saikosaponin D on apoptosis in human U87 glioblastoma cells

Cai

Zhang

et al. 2017

Molecular Medicine Reports

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“…Numerous reports have pointed out that apoptosis can be divided into the caspase and mitochondria associations after agents (including anticancer drugs) stimulate the cancer cells (Zhang et al, ; Ou Yang et al, ). Results from Figure (C) showed that CERP promoted TRAIL and Fas expression indicating that CERP induced cell apoptosis through the death receptor and subsequent caspase activation.…”

Section: Discussionmentioning

confidence: 99%

Crude extract of Rheum palmatum L. Induces cell cycle arrest S phase and apoptosis through mitochondrial‐dependent pathways in U‐2 OS human osteosarcoma cells

Lin

Lee

Lin

et al. 2015

Environmental Toxicology

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Cancer is the second cause of death in children. Osteosarcoma is the most common primary malignancy of solid bone cancer primarily affecting adolescents and young adults. In the Chinese population, the crude extract of Rheum palmatum L. (CERP) has been used for treating different diseases, including SARS, rheumatoid arthritis, coxsackievirus B3, and human colon cancer cell, pancreatic cancer. There are no reports on CERP and human osteosarcoma cells. The present study examined effects of CERP on cytotoxicity including cell cycle distribution and cell death (apoptosis) in U-2 OS human osteosarcoma cells. CERP significantly induced S phase arrest in U-2 OS cells in a dose-dependent. CERP produced DNA damage and DNA condensation. Other effects of CERP were stimulation of ROS and Ca(2+) , mitochondria impairment, and activation of caspase-3, -8, and -9. CERP increased the levels of Bax, Bak, Bad, cyclin B, Fas, PARP, GRP78, GADD153, AIF, Endo G, Calpain-2, p21, and p27, but decreased the levels of Bcl-2, BCL-X, XIAP, Akt, CDC25A, CDK2, Cyclin A, and Cyclin E of U-2 OS cells. It was also observed that CERP promoted the expression of AIF, Endo G, GADD153, and cytochrome c. These results indicate that CERP has anticancer effects in vitro and provide the foundation for in vivo studies of animal models of osteosarcoma. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 957-969, 2016.

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“…PIP3 is essential for the phosphorylation and activation of the serine/threonine kinase Akt, a key media tor of the PI3K/Akt‐signaling pathway [Blanco‐Aparicio et al, ]. Although some studies show that PTEN/Akt signaling affects cell proliferation via regulating p27 kip1 expression in cancer cells [van Duijn and Trapman, ; Lee et al, ; OuYang et al, ], its possible connection with the abnormalities of SLE BM‐MSCs has not been explored.…”

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confidence: 99%

PTEN/Akt‐p27^kip1 Signaling Promote the BM‐MSCs Senescence and Apoptosis in SLE Patients

Tan

Shen

et al. 2015

J of Cellular Biochemistry

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Recent studies showed that allogeneic bone marrow (BM)-mesenchymal stem cells transplantation (MSCT) was effective in systemic lupus erythematosus (SLE) patients and lupus-prone mice. However, syngeneic BM-MSCT was ineffective. Previous studies, including ours, revealed that BM-MSCs from SLE patients exhibited early signs of senescence and apoptosis such as slow proliferation, increasing senescence-associated β-galactosidase (SA-β-gal)-positive cells and Annexin V-positive cells, and caspase cascade activation. The abnormalities of BM-MSCs might be associated with the pathogenesis of SLE. In this study, we aimed to determine the molecular mechanism of senescent BM-MSCs from SLE patients. We found that the expression of protein 27 kinase inhibition protein 1(p27(kip1) ) increased significantly, which was regulated by phosphatase and tensin homology deleted on chromosome 10 (PTEN)/protein kinase B (Akt) signaling in SLE BM-MSCs. Knockdown of PTEN or p27(kip1) could reverse the senescent features of BM-MSCs via down-regulating p27(kip1) expression. When purified CD4(+) T cells were incubated with PTEN or p27(kip1) -silenced SLE BM-MSCs, the ratio of regulatory T (Treg)/T helper type 17 (Th17) cells increased significantly by enhancing regulatory cytokines (IL-10 and TGF-β) and reducing pro-inflammatory cytokines (IL-17 and IL-6). Taken together, we demonstrated that PTEN/Akt signaling played an essential role in the senescent and apoptotic BM-MSCs from SLE patients by up-regulating p27(kip1) expression.

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AKT signalling and mitochondrial pathways are involved in mushroom polysaccharide-induced apoptosis and G1 or S phase arrest in human hepatoma cells

Cited by 40 publications

References 27 publications

Effects of Saikosaponin D on apoptosis in human U87 glioblastoma cells

Effects of Saikosaponin D on apoptosis in human U87 glioblastoma cells

Crude extract of Rheum palmatum L. Induces cell cycle arrest S phase and apoptosis through mitochondrial‐dependent pathways in U‐2 OS human osteosarcoma cells

PTEN/Akt‐p27^kip1 Signaling Promote the BM‐MSCs Senescence and Apoptosis in SLE Patients

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AKT signalling and mitochondrial pathways are involved in mushroom polysaccharide-induced apoptosis and G1 or S phase arrest in human hepatoma cells

Cited by 40 publications

References 27 publications

Effects of Saikosaponin D on apoptosis in human U87 glioblastoma cells

Effects of Saikosaponin D on apoptosis in human U87 glioblastoma cells

Crude extract of Rheum palmatum L. Induces cell cycle arrest S phase and apoptosis through mitochondrial‐dependent pathways in U‐2 OS human osteosarcoma cells

PTEN/Akt‐p27kip1 Signaling Promote the BM‐MSCs Senescence and Apoptosis in SLE Patients

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PTEN/Akt‐p27^kip1 Signaling Promote the BM‐MSCs Senescence and Apoptosis in SLE Patients