Guibitang, a traditional herbal medicine, induces apoptotic death in A431 cells by regulating the activities of mitogen-activated protein kinases

Yim, Nam–Hui; Kim, Aeyung; Liang, Chun; Cho, Won‐Kyung; Yeul, Jin

doi:10.1186/1472-6882-14-344

Cited by 13 publications

(5 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been shown that the MAPK family, which includes p38 kinases, extracellular signal-regulated kinases (ERK), and JNK, all play important roles in cell death, differentiation, and survival. 19 JNK and p38 are activated in response to several stress signals, including tumor necrosis factor (TNF) and hyperosmotic conditions, and this activation is associated with induction of apoptosis. 20 ERK activation is induced by growth factors and oxidant injury and plays a major role in regulating cell growth and differentiation.…”

Section: Introductionmentioning

confidence: 99%

Effects of methylglyoxal and glyoxalase I inhibition on breast cancer cells proliferation, invasion, and apoptosis through modulation of MAPKs, MMP9, and Bcl-2

Guo

Zhang

Yang

et al. 2015

Cancer Biology & Therapy

View full text Add to dashboard Cite

Emerging evidence indicates that methylglyoxal (MG) can inhibit tumorigenesis. Glyoxalase I (GLOI), a MG degradation enzyme, is implicated in the progression of human malignancies. However, little is known about the roles of MG and GLOI in breast cancer. Our purpose was to investigate the anticancer effects of MG and inhibition of GLOI on breast cancer cells and the underlying mechanisms of these effects. Our findings demonstrate that cell viability, migration, invasion, colony formation, and tubule formation were significantly restrained by addition of MG or inhibition of GLOI, while apoptosis was significantly increased. Furthermore, the expression of p-JNK, p-ERK, and p-p38 was markedly upregulated by addition of MG or inhibition of GLOI, whereas MMP-9 and Bcl-2 expression levels were dramatically decreased. These effects were augmented by combined treatment with MG and inhibition of GLOI. Collectively, these data indicate that MG or inhibition of GLOI induces anticancer effects in breast cancer cells and that these effects are potentiated by combination of the 2. These effects were modulated by activation of the MAPK family and downregulation of Bcl-2 and MMP-9. These findings may provide a new approach for the treatment of breast cancer.

show abstract

Section: Introductionmentioning

confidence: 99%

Effects of methylglyoxal and glyoxalase I inhibition on breast cancer cells proliferation, invasion, and apoptosis through modulation of MAPKs, MMP9, and Bcl-2

Guo

Zhang

Yang

et al. 2015

Cancer Biology & Therapy

View full text Add to dashboard Cite

show abstract

“…Interestingly, cancer cells have self-renewal regulation mechanisms similar to stem cells, and show extensive proliferation properties. Therefore, in addition to their use for in vitro studies of cancer and anti-cancer therapies 14 15 , cancer cells are widely used for general in-vitro cell research and as a model for regenerative medicine 16 .…”

mentioning

confidence: 99%

In-vitro Optimization of Nanoparticle-Cell Labeling Protocols for In-vivo Cell Tracking Applications

Betzer

Meir

Dreifuss

et al. 2015

Sci Rep

View full text Add to dashboard Cite

Recent advances in theranostic nanomedicine can promote stem cell and immune cell-based therapy. Gold nanoparticles (GNPs) have been shown to be promising agents for in-vivo cell-tracking in cell-based therapy applications. Yet a crucial challenge is to develop a reliable protocol for cell upload with, on the one hand, sufficient nanoparticles to achieve maximum visibility of cells, while on the other hand, assuring minimal effect of particles on cell function and viability. Previous studies have demonstrated that the physicochemical parameters of GNPs have a critical impact on their efficient uptake by cells. In the current study we have examined possible variations in GNP uptake, resulting from different incubation period and concentrations in different cell-lines. We have found that GNPs effectively labeled three different cell-lines - stem, immune and cancer cells, with minimal impairment to cell viability and functionality. We further found that uptake efficiency of GNPs into cells stabilized after a short period of time, while GNP concentration had a significant impact on cellular uptake, revealing cell-dependent differences. Our results suggest that while heeding the slight variations within cell lines, modifying the loading time and concentration of GNPs, can promote cell visibility in various nanoparticle-dependent in-vivo cell tracking and imaging applications.

show abstract

“…Gleditsia sinensis thorn induced p38 MAPK, ERK1/2 and JNK phosphorylation in human colon cancer cells (26). Guibi-tang (GBT) treatment upregulated the expression of p38, ERK and JNK, which were retained during apoptosis in the A431 cells (27). Ponicin inhibited cell growth by arresting G1-cell cycle and inducing apoptosis in HT29 cells.…”

Section: Discussionmentioning

confidence: 99%

Rhus verniciflua Stokes extract induces inhibition of cell growth and apoptosis in human chronic myelogenous leukemia K562 cells

Lee

Jung

et al. 2018

Oncol Rep

View full text Add to dashboard Cite

Rhus verniciflua Stokes has been widely used as a traditional medicinal plant with a variety of pharmacological activities. We investigated the mechanisms involved in mediating the effects of Rhus verniciflua Strokes (R. verniciflua) extract in human chronic myelogenous leukemia K562 cells, including caspase-dependent apoptotic pathways related to cell-cycle arrest, as well as the inhibition of nuclear factor NF-κB activation and upregulation of the mitogen-activated protein kinase (MAPK) signaling pathway. R. verniciflua extract suppressed the abnormal cellular proliferation of K562 cells in a dose-and time-dependent manner and increased the quantitative proportions of cells involved in the early and late process of apoptosis. Furthermore, R. verniciflua extract significantly mediated the mRNA levels of pro-apoptotic and anti-apoptotic regulators, such as Bcl-2, Bax, Mcl-1 and survivin in apoptotic cells. Particularly, the treatment of K562 cells with R. verniciflua extract augmented the caspase-3 activity and increased the expression of caspase-3 protein, while co-treatment with R. verniciflua extract and the permeant pan-caspase inhibitor Z-VAD-FMK and caspase-3 inhibitor Z-DEVD-FMK inversely enhanced the proliferation of K562 cells. The extract of R. verniciflua inhibited the activation of NF-κB and the phosphorylation of ERK. Collectively, these results indicated that the extract of R. verniciflua inhibited the proliferation of human chronic myelogenous leukemia K562 cells by activating the apoptotic process via caspase-3 overexpression and the regulation of the NF-κB and MAPK signaling.

show abstract

Guibitang, a traditional herbal medicine, induces apoptotic death in A431 cells by regulating the activities of mitogen-activated protein kinases

Cited by 13 publications

References 29 publications

Effects of methylglyoxal and glyoxalase I inhibition on breast cancer cells proliferation, invasion, and apoptosis through modulation of MAPKs, MMP9, and Bcl-2

Effects of methylglyoxal and glyoxalase I inhibition on breast cancer cells proliferation, invasion, and apoptosis through modulation of MAPKs, MMP9, and Bcl-2

In-vitro Optimization of Nanoparticle-Cell Labeling Protocols for In-vivo Cell Tracking Applications

Rhus verniciflua Stokes extract induces inhibition of cell growth and apoptosis in human chronic myelogenous leukemia K562 cells

Contact Info

Product

Resources

About