Quantitative proteomic analysis of the inhibitory effects of CIL-102 on viability and invasiveness in human glioma cells

Teng, Chiao-Fang; Kuo, Hsing Chun; Sze, Chun I.

doi:10.1016/j.taap.2013.07.009

Cited by 13 publications

(17 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The protein pellets were re-solubilized in rehydration solution and kept at -80°C until further analysis. The chemicals and reagents used for two-dimensional gel electrophoresis have been previously described [21]. The total amount of protein was determined using the Bradford assay with bovine serum albumin as the standard sample for normalization; following cell lysis, the total cell protein was precipitated with 10% trichloroacetate in acetone.…”

Section: Methodsmentioning

confidence: 99%

“…Protein identification required detection of unique peptides, and proteins with more than two spectral counts were selected for further analysis based on their molecular mass and photoionization values. Proteins identified with a higher Mascot score in the bovine database than in the human database were considered to be serum contamination and removed [21, 22]. …”

Section: Methodsmentioning

confidence: 99%

“…The data were analysed using the SAS statistical package “SigmaPlot” version 9.0 (SAS Institute Inc., Cary, NC, USA) [21]. …”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Comparative Proteomic Identification of Protein Disulphide Isomerase A6 Associated with Tert-Butylhydroperoxide-Induced Liver Injury in Rat Hepatocytes

Shen

Tung

Huang

et al. 2018

Cell Physiol Biochem

Self Cite

View full text Add to dashboard Cite

Background/Aims: Oxidants are important human toxicants. They have been implicated in the occurrence and development of liver diseases. Increased intracellular tert-butylhydroperoxide (t-BHP) may be critical for oxidant toxicity, and is commonly used for evaluating mechanisms involving oxidative stress, but the method remains controversial. Methods: Primary cultures of hepatocytes as well as human Hep G2 and mouse FL83B liver cells were obtained. Cell viability was measured by annexin V–FITC/propidium iodide and DAPI staining to determine the effects of t-BHP treatment on acute liver injury. A proteomic assay provided information that was used to identify the differentially expressed proteins following t-BHP treatment; immunohistochemistry and western blotting were performed to detect the expression of PDIA6 activity in apoptotic and endoplasmic reticulum (ER) stress pathways. Results: Our results demonstrate that t-BHP treatment of liver cells increased cell cytotoxicity and the generation of reactive oxygen species. This treatment also increased the level of PDIA6; this was validated in vitro and in vivo based on a comparison of t-BHP-treated and -untreated groups. Treatment of mouse liver FL83B cells with t-BHP activated caspase 3, increased the expression of apoptotic molecules, caused cytochrome c release, and induced Bcl-2, Bax and IRE1α/TRAF2 complex formation. t-BHP-dependent induction of apoptosis was accompanied by sustained phosphorylation of the IRE1α/ASK1/JNK1/2/p38 pathways and PDIA6 expression. Furthermore, t-BHP induced liver FL83B cell viability and apoptosis by upregulating the levels of PDIA6; this process could be involved in the activation of the IRE1α/ASK1/JNK1/2/p38 signalling pathways. Conclusions: We conclude that t-BHP induced an apoptosis cascade and ER stress in hepatocytes by upregulation of PDIA6, providing a new mechanism underlying the effects of t-BHP on liver injury.

show abstract

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Comparative Proteomic Identification of Protein Disulphide Isomerase A6 Associated with Tert-Butylhydroperoxide-Induced Liver Injury in Rat Hepatocytes

Shen

Tung

Huang

et al. 2018

Cell Physiol Biochem

Self Cite

View full text Add to dashboard Cite

show abstract

“…Here, tubeimoside-1 was found to induced cell cycle arrest at G2/M phase, presumably by inhibiting the expression levels of selected cyclins, as well as interfering with the post-translational modifications (Xu et al, 2011). On the other hand, CIL-102 (an alkaloid derivative) was linked specifically to inhibit cancer cells proliferation by up-regulating the N-terminal kinases (JNK1/2) and mTOR signaling pathways (Teng et al, 2013). The functional roles of JNK are complex and different among carcinomas (Bubici and Papa, 2014), with implication in multi-drug resistance during chemotherapy (Zhan et al, 2013).…”

Section: Phytochemical-mediated Cancer Protein Targetsmentioning

confidence: 99%

Phytochemical-mediated Protein Expression Profiling and the Potential Applications in Therapeutic Drug Target Identifications

Wong

Tan

Chai

2015

Critical Reviews in Food Science and Nutrition

View full text Add to dashboard Cite

Many phytochemicals derived from edible medicinal plants have been investigated intensively for their various bioactivities. However, the detailed mechanism and their corresponding molecular targets frequently remain elusive. In this review, we present a summary of the research works done on phytochemical-mediated molecular targets, identified via proteomic approach. Concurrently, we also highlighted some pharmaceutical drugs which could be traced back to their origins in phytochemicals. For ease of presentation, these identified protein targets were categorized into two important healthcare-related fields, namely anti-bacterial and anti-cancer research. Through this review, we hope to highlight the usefulness of comparative proteomic as a powerful tool in phytochemical-mediated protein target identifications. Likewise, we wish to inspire further investigations on some of these protein targets identified over the last few years. With contributions from all researchers, the accumulative efforts could eventually lead to the discovery of some target-specific, low-toxicity therapeutic agents.

show abstract

“…Numerous studies have suggested that it possesses anticancer and chemopreventive properties and inhibits the proliferation of tumor cells [23, 24]. Our recent study showed that CIL-102 inhibited the proliferation and the invasiveness property in glioma cells and altered the expression of genes related to cell cycle regulation by activating the ERK1/2 and Cdc25cSer 216 cell-cycle-related proteins and inducing ROS generation [23].…”

Section: Introductionmentioning

confidence: 99%

CIL-102-Induced Cell Cycle Arrest and Apoptosis in Colorectal Cancer Cells via Upregulation of p21 and GADD45

Huang

Kuo

et al. 2017

PLoS ONE

Self Cite

View full text Add to dashboard Cite

CIL-102 (1-[4-(furo[2,3-b]quinolin-4-ylamino)phenyl]ethanone) is a well-known, major active agent of the alkaloid derivative of Camptotheca acuminata with valuable biological properties, including anti-tumorigenic activity. In this study, we investigated the molecular mechanisms by which CIL-102 mediated the induction of cell death, and we performed cell cycle G2/M arrest to clarify molecular changes in colorectal cancer cells (CRC). Treatment of DLD-1 cells with CIL-102 resulted in triggering the extrinsic apoptosis pathway through the activation of Fas-L, caspase-8 and the induction of Bid cleavage and cytochrome c release in a time-dependent manner. In addition, CIL-102 mediated apoptosis and G2/M arrest by phosphorylation of the Jun N-terminus kinase (JNK1/2) signaling pathway. This resulted in the expression of NFκB p50, p300 and CREB-binding protein (CBP) levels, and in the induction of p21 and GADD45 as well as the decreased association of cdc2/cyclin B. Furthermore, treatment with the JNK1/2 (SP600125), NFκB (PDTI) or the p300/CBP (C646) inhibitors abolished CIL-102-induced cell cycle G2/M arrest and reversed the association of cdc2 with cyclin B. Therefore, we demonstrated that there was an increase in the cellular levels of p21 and GADD45 by CIL-102 reduction in cell viability and cell cycle arrest via the activation of the JNK1/2, NFκB p50, p300 and CBP signaling modules. Collectively, our results demonstrated that CIL-102 induced cell cycle arrest and apoptosis of colon cancer cells by upregulating p21 and GADD45 expression and by activating JNK1/2, NFκB p50 and p300 to provide a new mechanism for CIL-102 treatment.

show abstract

Quantitative proteomic analysis of the inhibitory effects of CIL-102 on viability and invasiveness in human glioma cells

Cited by 13 publications

References 37 publications

Comparative Proteomic Identification of Protein Disulphide Isomerase A6 Associated with Tert-Butylhydroperoxide-Induced Liver Injury in Rat Hepatocytes

Comparative Proteomic Identification of Protein Disulphide Isomerase A6 Associated with Tert-Butylhydroperoxide-Induced Liver Injury in Rat Hepatocytes

Phytochemical-mediated Protein Expression Profiling and the Potential Applications in Therapeutic Drug Target Identifications

CIL-102-Induced Cell Cycle Arrest and Apoptosis in Colorectal Cancer Cells via Upregulation of p21 and GADD45

Contact Info

Product

Resources

About