Gene silencing of TKTL1 by RNAi inhibits cell proliferation in human hepatoma cells

Zhang, Song; Yang, Juhong; Guo, Chang-Kai; Cai, Peng

doi:10.1016/j.canlet.2007.01.010

Cited by 86 publications

(68 citation statements)

References 18 publications

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“…The role of the mitochondria in both apoptotic and necrotic cell death has received considerable attention, and an increase of mitochondrial membrane permeability is considered one of the key events in apoptosis (37,40). In our study, an adverse effect of farnesol on the mitochondria was indicated by the downregulation of several proteins involved in mitochondrial electron transport and respiration (Table 2).…”

Section: Discussionmentioning

confidence: 75%

“…ROS can damage almost every essential cellular component, resulting in enzyme inactivation, membrane disruption, and mutations, and ultimately in cell death (2,20). Studies have revealed that perturbations in mitochondrion respiration occur early in the apoptotic process and that the mitochondrion itself serves as a control switch for apoptosis (40). We have previously shown that the farnesol-induced apoptosis in human tumor cells was mediated by mitochondria and the generation of ROS (33).…”

Section: Discussionmentioning

confidence: 99%

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Farnesol-Induced Apoptosis in Candida albicans

Shirtliff

Krom

Meijering

et al. 2009

Antimicrob Agents Chemother

213

185

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Farnesol, a precursor in the isoprenoid/sterol pathway, was recently identified as a quorum-sensing molecule produced by the fungal pathogen Candida albicans. Farnesol is involved in the inhibition of germination and biofilm formation by C. albicans and can be cytotoxic at certain concentrations. In addition, we have shown that farnesol can trigger apoptosis in mammalian cells via the classical apoptotic pathways. In order to elucidate the mechanism behind farnesol cytotoxicity in C. albicans, the response to farnesol was investigated, using proteomic analysis. Global protein expression profiles demonstrated significant changes in protein expression resulting from farnesol exposure. Among the downregulated proteins were those involved in metabolism, glycolysis, protein synthesis, and mitochondrial electron transport and the respiratory chain, whereas proteins involved in folding, protection against environmental and oxidative stress, actin cytoskeleton reorganization, and apoptosis were upregulated. Cellular changes that accompany apoptosis (regulated cell death) were further analyzed using fluorescent microscopy and gene expression analysis. The results indicated reactive oxygen species accumulation, mitochondrial degradation, and positive terminal deoxynucleotidyltransferasemediated dUTP-biotin nick end labeling (TUNEL) in the farnesol-exposed cells concurrent with increased expression of antioxidant-encoding and drug response genes. More importantly, the results demonstrated farnesol-induced upregulation of the caspase gene MCA1 and the intracellular presence of activated caspases.In conclusion, this study demonstrated that farnesol promotes apoptosis in C. albicans through caspase activation, implying an important physiological role for farnesol in the fungal cell life cycle with important implications for adaptation and survival.

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Section: Discussionmentioning

confidence: 75%

Section: Discussionmentioning

confidence: 99%

Farnesol-Induced Apoptosis in Candida albicans

Shirtliff

Krom

Meijering

et al. 2009

Antimicrob Agents Chemother

213

185

View full text Add to dashboard Cite

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“…The high transketolase expression in HCC may imply a strong activation of this alternate pathway to glycolysis in the utilization of cellular glucose. The in vitro suppression of the transketolase gene by using a silencing approach effectively arrested cellular growth in human hepatoma cells (HepG2), suggesting a possible role in HCC development (14). The metabolic control of the non-oxidative pentose phosphate pathway by inhibition of transketolase may constitute a promising novel pharmacological target to be explored.…”

Section: Discussionmentioning

confidence: 99%

Differential proteomic analysis of hepatocellular carcinoma

Corona¹,

Lorenzo²,

Elia³

et al. 2009

Int J Oncol

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Abstract. The principal aim of the present study consisted in the identification of the disregulated proteins associated with the development of hepatocellular carcinoma (HCC). The differences in protein expression between hepatocellular carcinoma (HCC) and the corresponding non-HCC liver tissues were investigated in a cohort of 20 patients using twodimensional fluorescence difference in gel electrophoresis (2D-DIGE) coupled with mass spectrometry (MS). The upand down-regulated protein spots that exhibited 1.5-fold difference signal intensity with statistical significance (p<0.05, t-test, confidence intervals 95%) were excised from the gel and identified by peptide mass fingerprinting using matrix assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). Thirty-six protein spots corresponding to 29 different disregulated proteins, belonging to heterogeneous metabolic pathways, have been identified. Down-regulated proteins (n=23) were found superior in number than the up-regulated proteins (n=6). Detoxification, carbohydrate metabolism and amino acid biotrasformation represented the main disregulated pathways in HCC. Upregulation of aldo-keto reductase 1C2, thioredoxin and transketolase, involved in metabolic and regulatory cellular processes including proliferation, differentiation and carcinogenesis were remarkable. These proteins could represent useful biomarkers to provide new insights into global pathophysiologic changes of HCC and for the development of new pharmacological approaches to HCC therapy.

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“…In most studies, the silencing of critical gene products by RNAi technology has generated significant antiproliferative and/or proapoptotic effects in cell-culture systems or in preclinical animal models (Castanotto and Rossi, 2009). Moreover, the advantage of RNAi technology is that it can be used to target a large number of different genes involving a number of distinct cellular pathways (Zhang et al, 2007). This is particularly important for a disease as complex as cancer.…”

Section: Introductionmentioning

confidence: 99%

Suppression of Cellular Apoptosis Susceptibility (CSE1L) Inhibits Proliferation and Induces Apoptosis in Colorectal Cancer Cells

Zhu

Hong²,

Song³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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The cellular apoptosis susceptibility (CSE1L) gene has been demonstrated to regulate multiple cellular mechanisms including the mitotic spindle check point as well as proliferation and apoptosis. However, the importance of CSE1L in human colon cancer is largely unknown. In the present study, we examined expression levels of CSE1L mRNA by semiquantitative RT-PCR. A lentivirus-mediated small interfering RNA (siRNA) was used to knock down CSE1L expression in the human colon cancer cell line RKO. Changes in CSE1L target gene expression were determined by RT-PCR. Cell proliferation was examined by a high content screening assay. In vitro tumorigenesis was measured by colony-formation assay. Cell cycle distribution and apoptosis were detected by flow cytometric analysis. We found CSE1L mRNA to be expressed in human colon cancer cells. Using a lentivirus based RNAi approach, CSE1L expression was significantly inhibited in RKO cells, causing cell cycle arrest in the G2/M and S phases and a delay in cell proliferation, as well as induction of apoptosis and an inhibition of colony growth capacity. Collectively, the results suggest that silencing of CSE1L may be a potential therapeutic approach for colon cancer.

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Gene silencing of TKTL1 by RNAi inhibits cell proliferation in human hepatoma cells

Cited by 86 publications

References 18 publications

Farnesol-Induced Apoptosis in Candida albicans

Farnesol-Induced Apoptosis in Candida albicans

Differential proteomic analysis of hepatocellular carcinoma

Suppression of Cellular Apoptosis Susceptibility (CSE1L) Inhibits Proliferation and Induces Apoptosis in Colorectal Cancer Cells

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