Curcumin induces FasL-related apoptosis through p38 activation in human hepatocellular carcinoma Huh7 cells

Wang, Weizhang; Li, Li; Liu, Man-Yu; Jin, Xiaobao; Mao, Jianwen; Pu, Qiao-Hong; Mei, Meng; Chen, Xiaoguang; Zhu, Jianhua

doi:10.1016/j.lfs.2013.01.013

Cited by 47 publications

(40 citation statements)

References 24 publications

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“…The FASLG and its receptor (FAS) belong to the TNFa family, FAS and FASLG have been regarded as very important effectors of apoptosis in various biological conditions [20]. Previous studies demonstrated that FASLG down-regulated in many kinds of carcinomas such as hepatocellular, breast and colorectal cancer, and could regulate tumor cell apoptosis and proliferation [21][22][23]. Our results obtained from gain-offunction approaches confirmed that FASLG is a miR-21 0 s direct target gene.…”

Section: Discussionsupporting

confidence: 77%

MiR-21 up-regulation mediates glioblastoma cancer stem cells apoptosis and proliferation by targeting FASLG

et al. 2014

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To investigate whether miR-21 can affect the apoptosis and proliferation of glioblastoma cancer stem cells (GSCs) from down-regulating FASLG. The expression of miRNA-21 was detected by quantitative real-time PCR in normal brain tissue and glioblastoma samples, and the changes of miRNA-21 expression between GSCs and non-GSCs were also detected. The apoptosis and proliferation ability of miR-21 in GSCs were analyzed by MTT and flow cytometry assay after anti-miR-21 transfection. For the regulation mechanism analysis of miR-21, TargetScan, PicTar and microRNA were selected to predict some potential target genes of miR-21. The predicted gene was identified to be the direct and specific target gene of miR-21 by luciferase activities assay and western blot. RNA interference technology was used to confirm the apoptosis and proliferation effects of miR-21 were directly induced by FASLG. The expression of miR-21 increased significantly in glioblastoma contrast to normal brain tissue, and miR-21 up-regulated in GSCs remarkably. The proliferation of GSCs cell could be inhibited with high-expression of miR-21 and this effect could be restored by miR-21 knocked down. Mechanism analysis revealed that FASLG was a specific and direct target gene of miR-21. The advanced effects of anti-miR-21 on GSCs apoptosis and proliferation were mediated by expression of silenced FASLG. In summary, aberrantly expressed miR-21 regulates GSCs apoptosis and proliferation partly through directly down-regulating FASLG protein expression in GSCs and this might offer a new potential therapeutic stratagem for glioblastoma.

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Section: Discussionsupporting

confidence: 77%

MiR-21 up-regulation mediates glioblastoma cancer stem cells apoptosis and proliferation by targeting FASLG

et al. 2014

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“…According to our observations, survivin was positively expressed in nearly twice as many cystic-shaped and fusiform-shaped tissues compared with that in normal tissues, indicating that the upregulation of survivin may occur in the early stages of CCC development. The deregulation of apoptosis has emerged as a hallmark of human malignancies and carcinogenesis (Fuhrman et al, 1982;Wang et al, 2013;Uchida et al, 2013). In this regard, the IHC results of this study showed that there was a significantly higher positive expression rate of survivin in CCC tissues than that in normal tissues, which in turn provides evidence of the occurrence of apoptosis deregulation in CCC tissues, and strengthens the case for survivin to predict the existence of deregulated apoptosis.…”

Section: Discussionsupporting

confidence: 72%

Increased survivin expression and its association with clinical parameters of congenital choledochal cysts

et al. 2016

Genet. Mol. Res.

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ABSTRACT. The aim of the current study was to investigate survivin expression in congenital choledochal cysts (CCCs), and its associations with clinical parameters of CCCs. In total, 121 children with CCCs were included in this study as the case group, and their cysts were staged according to the Todani classification system. Additionally, 49 normal gallbladder specimens from healthy children were included as the control group. Survivin detection was conducted using immunohistochemical staining. Associations between positive survivin expression and clinical parameters of CCCs were then analyzed. Positive survivin expression was observed in the cytoplasm, and was seen as granular with yellow or dark brown staining. In the case group, positive survivin expression was detected in most tissues. Specifically, compared to that of normal tissues, the cystic-shaped and fusiform-shaped CCC tissues had significantly higher positive survivin expression rates (all P < 0.05). Importantly, positive survivin expression was also shown to be significantly associated with gender and histological type (both P < 0.05). In conclusion, increased survivin expression was observed in CCC tissues, and was correlated with certain clinical parameters of CCCs, suggesting a possible prognostic value of survivin for CCC progression.

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“…Chun et al showed that platycodin D induced growth inhibition and apoptosis in AGS human gastric cancer cells through the sustained activation of p38 [29] . Wang et al demonstrated that curcumin induced apoptosis through the p38-dependent up-regulation of FasL in Huh7 cells [30] . Recently, Hsieh et al reported that arctigenin induced the apoptosis of breast cancer MDA-MB-231 cells through the ROS/p38 pathway [31] .…”

Section: Discussionmentioning

confidence: 99%

β, β-Dimethylacrylshikonin induces mitochondria-dependent apoptosis of human lung adenocarcinoma cells in vitro via p38 pathway activation

Wang

2014

Acta Pharmacol Sin

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Curcumin induces FasL-related apoptosis through p38 activation in human hepatocellular carcinoma Huh7 cells

Cited by 47 publications

References 24 publications

MiR-21 up-regulation mediates glioblastoma cancer stem cells apoptosis and proliferation by targeting FASLG

MiR-21 up-regulation mediates glioblastoma cancer stem cells apoptosis and proliferation by targeting FASLG

Increased survivin expression and its association with clinical parameters of congenital choledochal cysts

β, β-Dimethylacrylshikonin induces mitochondria-dependent apoptosis of human lung adenocarcinoma cells in vitro via p38 pathway activation

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