Caspase-8 and p38MAPK in DATS-induced apoptosis of human CNE2 cells

Ji, Chunxiao; Feng-lian, Ren; Xu, Ming

doi:10.1590/s0100-879x2010007500084

Cited by 13 publications

(10 citation statements)

References 30 publications

(27 reference statements)

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“…MAPKs are comprised of the three parallel kinase modules, including p38-MAPK, ERK and JNK, especially the MAPK/ERK signaling pathway involved in cell survival and proliferation. Some active components from garlic have anti-cancer effects through the ERK1/2 and p38-MAPK signaling pathways (20,39,40). In the present study, the level of ERK phosphorylation was increased, and allicin-induced apoptosis was prevented by a pre-treatment with U0126, an ERK inhibitor (Fig.…”

Section: Discussionsupporting

confidence: 57%

Allicin inhibits cell growth and induces apoptosis in U87MG human glioblastoma cells through an ERK-dependent pathway

et al. 2012

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Abstract. Allicin, the main flavor compound in garlic, has anti-carcinogenic activities in a range of cancer cells, however, the underlying molecular mechanisms are not completely understood. This study examined the effect of allicin on the cell viability of U87MG human glioma cells along with its molecular mechanisms of induction of cell death. Apoptosis was determined by TUNEL and Hoechst 33258 staining as well as by western blot analysis. Allicin inhibited the cell viability of U87MG human glioma cells in a dose-and time-dependent manner. Allicin-induced inhibition of cell viability was due to apoptosis of cells. The mechanisms of apoptosis were found to involve the mitochondrial pathway of Bcl-2/Bax, the MAPK/ ERK signaling pathway and antioxidant enzyme systems. These results suggest that allicin can serve as a novel chemotherapeutic candidate for the treatment of glioblastoma multiforme.

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Section: Discussionsupporting

confidence: 57%

Allicin inhibits cell growth and induces apoptosis in U87MG human glioblastoma cells through an ERK-dependent pathway

et al. 2012

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“…And we verified the carcinogenic roles of BCAR1 via RNA interference (RNAi) in A549 lung adenocarcinoma cell line. Experiments in vivo and vitro demonstrated the closed correlation between BCAR1 expression and activation of p38 which is a crucial branch of the MAPK (mitogen-activated protein kinase) pathway [10], [11].…”

Section: Introductionmentioning

confidence: 99%

BCAR1 Protein Plays Important Roles in Carcinogenesis and Predicts Poor Prognosis in Non-Small-Cell Lung Cancer

et al. 2012

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ObjectiveOur previous study suggested the potential clinical implications of BCAR1 in non-small-cell lung cancer (NSCLC) (Mol Diagn Ther. 2011. 15(1): 31–40). Herein, we aim to evaluate the predictive power of BCAR1 as a marker for poor prognosis in NSCLC cases, verify the carcinogenic roles of BCAR1 in the A549 lung adenocarcinoma cell line, and testify to the BCAR1/phospho-p38 axis.MethodsBetween January 2006 and June 2010, there were a total of 182 patients with NSCLC (151 cases with available follow up data, and 31 cases lost to follow-up due to the invalid contact information). We inspected BCAR1, phospho-BCAR1(Tyr410), phospho-p38(Thr180/Tyr182) and p38 expression in NSCLC tissues and matched adjacent normal tissues by immunoblotting and IHC. After BCAR1 -RNA interference in A549 cells, we inspected the protein expression (BCAR1, phospho-BCAR1, phospho-p38 and p38) and performed cell biology experiments (cell growth, migration and cycle).ResultsBCAR1 was overexpressed in NSCLC tissues (177/182) and cell lines (A549 and Calu-3). However, it was not detected in the normal adjacent tissue in 161 of the 182 cases. Higher BCAR1 levels were strongly associated with more poorly differentiated NSCLC and predicted poorer prognosis. BCAR1 knockdown caused cell growth arrest, cell migration inhibition and cell cycle arrest of A549 cells. Overexpression of BCAR1 was associated with activation of p38 in NSCLC cases, and BCAR1 knockdown caused reduction of phospho-p38 levels in A549 cells.ConclusionOverexpression of BCAR1 is a predictor of poor prognosis in NSCLC and plays important carcinogenic roles in carcinogenesis, probably via activation of p38 MAPK. However, further investigations are required immediately.

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“…Among organosulfur compounds contained in garlic, S-allylcysteine significantly suppressed 7,12-dimethylbenz[a]anthracene induced buccal pouch carcinogenesis when administered to hamsters [44]. N-acetylcysteine had growth-inhibitory function in both "in vitro" and "in vivo" in human tongue squamous carcinoma cell lines and in a xenograft mouse model, and diallyl trisulfide induced apoptosis in human nasopharyngeal carcinoma cells [45]. Preclinical studies also showed anticancer effect of organosulfur compounds and flavonoids against esophageal SCC, as in esophageal squamous cell cancer lines diallyl disulfide induced apoptosis, and myricetin (a flavonoid mainly present in onions) induced apoptosis and inhibited proliferation and invasion [46].…”

Section: Discussionmentioning

confidence: 99%

Allium vegetables and upper aerodigestive tract cancers: a meta‐analysis of observational studies

Guercio

Turati

Vecchia

et al. 2015

Molecular Nutrition Food Res

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Caspase-8 and p38MAPK in DATS-induced apoptosis of human CNE2 cells

Cited by 13 publications

References 30 publications

Allicin inhibits cell growth and induces apoptosis in U87MG human glioblastoma cells through an ERK-dependent pathway

Allicin inhibits cell growth and induces apoptosis in U87MG human glioblastoma cells through an ERK-dependent pathway

BCAR1 Protein Plays Important Roles in Carcinogenesis and Predicts Poor Prognosis in Non-Small-Cell Lung Cancer

Allium vegetables and upper aerodigestive tract cancers: a meta‐analysis of observational studies

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