Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glibenclamide, a blocker of ATP-sensitive potassium (K(ATP)) channels, can suppress progression of many cancers, but the involved mechanism is unclear. Herein we reported that MGC-803 cells expressed the K(ATP) channels composed of Kir6.2 and SUR1 subunits. Glibenclamide induced cellular viability decline, coupled with cell apoptosis and reactive oxygen species (ROS) generation in MGC-803 cells. Meanwhile, glibenclamide increased NADPH oxidase catalytic subunit gp91(phox) expression and superoxide anion (O2-) generation, and caused mitochondrial respiration dysfunction in MGC-803 cells, suggesting that glibenclamide induced an increase of ROS derived from NADPH oxidase and mitochondria. Glibenclamide could also lead to loss of mitochondrial membrane potential, release of cytochrome c and apoptosis-inducing factor (AIF), and activation of c-jun NH2-terminal kinase (JNK) in MGC-803 cells. Pretreatment with antioxidant N-acetyl-l-cysteine (NAC) prevented glibenclamide-induced JNK activation, apoptosis and cellular viability decline. Furthermore, glibenclamide greatly decreased the cellular viability, induced apoptosis and inhibited Akt activation in wild-type mouse embryonic fibroblast (MEF) cells but not in JNK1-/- or JNK2-/- MEF cells. Taken together, our study reveals that glibenclamide exerts an antitumor activity in MGC-803 cells by activating ROS-dependent, JNK-driven cell apoptosis. These findings provide insights into the use of glibenclamide in the treatment of human gastric cancer.
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PMID:Glibenclamide exerts an antitumor activity through reactive oxygen species-c-jun NH2-terminal kinase pathway in human gastric cancer cell line MGC-803. 1884 Apr 12

E2F-1 plays a critical role in cell cycle regulation and other biological processes in cells. E2F-1 mediates apoptosis and suppresses tumorigenesis in many tissue types, but there are few data available on E2F-1 expression and its relationship to tumor kinetics in gastric cancer. To gain better insight into the involvement of E2F-1 in the biological characteristics of gastric tumors, we investigated the effect of E2F-1 overexpression on the progression of gastric carcinoma cells. A gastric cancer cell line stably overexpressing E2F-1 (MGC-803/E2F-1) was established. The influence of E2F-1 overexpression on in vitro cell growth was assessed by measuring cell survival, colony formation, and cell cycle progression. The results clearly show that overexpression of E2F-1 significantly inhibits cell growth and proliferation, blocking entry into the S-phase of the cell cycle. MGC-803/E2F-1 cells also had a higher apoptotic rate than control cells. In addition, E2F-1 reduced the motility and invasion of gastric cancer cells.
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PMID:Overexpression of E2F-1 inhibits progression of gastric cancer in vitro. 1928 76

Gastric cancer is the third most common cancer in China. The sustained overexpression of E2F-1 is a characteristic feature of gastric cancer. RNA interference (RNAi), which has been proven to be a powerful tool for suppressing gene expression, may provide a promising way forward in gastric cancer therapy. In this study, we constructed the recombinant Psilencer 4.1- E2F-1 siRNA plasmids and transfected them into gastric cancer MGC-803 cells in vitro. Our data demonstrated that E2F-1 siRNA led to inhibition of endogenous E2F-1 mRNA and protein expression as determined by real-time quantitative RT-PCR and Western blotting. Furthermore, simultaneous silencing of E2F-1 resulted in a reduction of tumor cell proliferation activity and a higher percentage of apoptotic cells. The inhibition of migration and invasion potential of tumor cells was investigated in vitro. In summary, siRNA targeting of E2F-1 can effectively inhibit gastric cancer progression and may be used as a potent therapy.
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PMID:Short interfering RNA directed against the E2F-1 gene suppressing gastric cancer progression in vitro. 1936 Mar 13

2',4'-Dihydroxychalcone (TFC), one of the main components in Herba Oxytropis, belongs to the flavonoid group, which is known to have anti-tumor activity in vitro. In this study, the authors examined the effects of TFC on cell proliferation and apoptosis in human gastric cancer MGC-803 cells. The MTT assay results showed that TFC was able to induce cytotoxicity in MGC-803 cells in a concentration- and time-dependent manner. Acridine orange/ethidium bromide (AO/EB) staining analysis indicated that the cytotoxicity induced by TFC was mediated by apoptosis, and flow cytometry analysis indicated an increase in apoptotic cells after treatment with TFC. Furthermore, typical apoptotic morphology such as condensed chromatin, irregular nuclei, vacuoles, and dispersed granular material in the nuclear compartment were also observed using a transmission electron microscope. These results suggested that TFC can inhibit the growth of MGC-803 cells and induce apoptosis. However, further studies are necessary to investigate the possible mechanism.
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PMID:Preliminary studies on anti-tumor activity of 2',4'-dihydroxychalcone isolated from Herba Oxytropis in human gastric cancer MGC-803 cells. 1945 54

Lycium barbarum polysaccharide (LBP) is extracted from the traditional Chinese herb Lycium barbarum, and has potential anticancer activity. However, the detailed mechanisms are largely unknown. The purpose of this study was to observe the anticancer effect of LBP on human gastric cancer, and its possible mechanisms. Human gastric cancer MGC-803 and SGC-7901 cells were treated with various concentrations of LBP for 1-5 days, and cell growth was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay. Distribution of the cell cycle was analyzed by flow cytometry. Western blotting was used to indicate changes in the level of cyclins and cyclin-dependent kinases (CDKs). LBP treatment inhibited growth of MGC-803 and SGC-7901 cells, with cell-cycle arrest at the G0/G1 and S phase, respectively. We believe that this is the first study to show that LBP arrested different cell lines from the same types of cancer at different phases. The changes in cell-cycle-associated protein, cyclins, and CDKs were consistent with the changes in cell-cycle distribution. This study suggests that induction of cell-cycle arrest participates in the anticancer activity of LBP on gastric cancer cells.
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PMID:Growth inhibition and cell-cycle arrest of human gastric cancer cells by Lycium barbarum polysaccharide. 1966 55

TWIST, a basic helix-loop-helix transcription factor, has been recently reported to play an important role in tumorigenesis of human cancer through converting the early stage tumors into invasive malignancies. Upregulation of TWIST is often found in cancer patients, especially those with shorter survival period and poor response to chemotherapy. Here we studied the functions of TWIST on regulating migration rate, apoptosis, and gene expression in gastric cancer cells. TWIST expression is elevated in MGC-803 and HGC-27 cells that exhibit high invasive potential; whereas it is reduced in BGC-823 and SGC-7901 cells that possess relatively low invasive content. To evaluate functional consequences of TWIST induction, we examined the effect of TWIST on cell migration and apoptosis. Overexpression of TWIST in BGC-823 cells resulted in increased migration content and decreased sensitivity to the arsenic oxide-induced cell death. Moreover, small interference RNA-mediated TWIST ablation in MGC-803 and HGC-27 cells showed suppressed migration ability, increased induction of apoptosis in response to arsenic oxide, and elevated cell cycle arrest. Furthermore, we found a negative correlation between the TWIST level and p53 level, probably due to transcriptional regulation. Our results have identified TWIST as a critical regulator of gastric cancer cell proliferation and migration, suggesting a potential therapeutic approach to inhibit the growth and metastasis of gastric cancer through inactivation of TWIST.
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PMID:Metastasis-induction and apoptosis-protection by TWIST in gastric cancer cells. 1980 64

Cladosporol was isolated from the fermentation broth of Alternaria alternata var. monosporus obtained from the inner bark of the yew tree and mutated for many generations. We investigated the antitumor effects of cladosporol in vitro and in vivo. The growth-inhibitory effects of cladosporol in vitro against six human cancer cell lines were examined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method. The results showed that cladosporol selectively killed cancer cells and had a significant inhibitory effect on the human gastric carcinoma cell line MGC-803 in a concentration- and time-dependent manner. In vivo, cladosporol also showed antitumor activity in nude mice bearing MGC-803 gastric cancer xenografts. These findings suggest that cladosporol has potentially useful growth inhibitory effects on human gastric carcinoma cell lines.
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PMID:Inhibition of human gastric carcinoma cell growth in vitro and in vivo by cladosporol isolated from the paclitaxel-producing strain Alternaria alternata var. monosporus. 1995 32

Targeted uptake of nanoscale controlled release polymer micelles encapsulated with drugs represents a potential powerful therapeutic technology. Herein we reported the development of anti-HIF-1alpha antibody-conjugated unimolecular polymer nano micelles filled with Paclitaxel for cancer targeting therapy. Pluronic triblock copolymers(Poly(ethylene glycol)-block-poly(propylene glycol)-block-poly(ethylene glycol), PEO-block-PPO-block-PEO) P123 were functionalized with terminal carboxylic groups, and were characterized by infrared (IR) spectroscopy, nuclear magnetic resonance (NMR), thermogravimetric analysis (TGA), and differential scanning calorimetric (DSC). The amphiphilic copolymer nano micelles encapsulated with Paclitaxel were fabricated by self-assembly means, and then were conjugated with anti-HIF-1alpha antibody, the resultant anti-HIF-1alpha conjugated nano micelles filled with PTX (anti-HIF-1alpha-NMs-PTX nanocomposites) were characterized by dynamic light scattering (DLS) and transmission electron microscopy (TEM), and incubated with stomach cancer MGC-803 cells and HDF fibroblast cells, these treated cells were analyzed by MTT and cell-ELISA. The nanocomposites composed of anti-HIF-1alpha conjugated nano micelles filled with CdTe quantum dots were also prepared, and incubated with stomach cancer MGC-803 cells and HDF fibroblast cells for 24 h, then were observed by fluorescent microscope. Results showed that the anti-HIF-1alpha-NMs-PTX nanocomposites were successfully prepared, bound with stomach cancer MGC-803 cells specifically, were internalized, and released PTX inside cancer cells, and selectively killed cancer cells. In conclusion, unique anti-HIF-1alpha antibody-conjugated nano micelles filled with Paclitaxel can target and selectively kill cancer cells with over-expression of HIF-1alpha, and has great potential in clinical tumor targeting imaging and therapy.
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PMID:Anti-HIF-1alpha antibody-conjugated pluronic triblock copolymers encapsulated with Paclitaxel for tumor targeting therapy. 2000 70

The caudal-type homeobox gene Cdx2 encodes a transcription factor which in adult mammals is expressed in the cells of the intestinal epithelium and is thought to play an important role in their proliferation and differentiation. Cdx2 mediates apoptosis and suppresses tumorigenesis in many tissue types, but there are few data available on Cdx2 expression and its relationship to tumor kinetics in gastric cancer. To gain better insight into the involvement of Cdx2 in the biological characteristics of gastric cancer, we investigated the effect of Cdx2 overexpression on the progression of gastric carcinoma cells. A gastric cancer cell line stably overexpressing Cdx2 (MGC-803/Cdx2) was established. The influence of Cdx2 overexpression on in vitro cell growth was assessed by measuring cell survival, colony formation and cell cycle progression. The results clearly showed that overexpression of Cdx2 significantly inhibited cell growth and proliferation, blocking entry into the S phase of the cell cycle. MGC-803/Cdx2 cells also had a higher apoptotic rate than control cells. In addition, Cdx2 reduced the motility and invasion of gastric cancer cells. In summary, Cdx2 overexpression can effectively inhibit gastric cancer progression and may be used as a potent therapy.
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PMID:Overexpression of Cdx2 inhibits progression of gastric cancer in vitro. 2004 87

Cimetidine, a histamine-2 (H2) receptor antagonist, has been demonstrated to have anticancer effects on various types of malignancies. However, the mechanisms of its action on gastric cancer are not completely understood. This study was designed to investigate its antitumor effect and underlying mechanisms in human gastric cancer SGC-7901 and MGC-803 cells. The MTT assay was used to evaluate cell viability, and flow cytometry, acridine orange staining and transmission electron microscopy were used to detect apoptosis, for cultured cells. The protein expression in cells was evaluated by Western blot analysis and colorimetric assay. Gastric tumors were established by subcutaneous injection of SGC-7901 cells in nude BALB/c mice, and cimetidine was administered to the mice. The size of tumors was monitored and the weight of tumors was examined. The exposure of gastric cancer cells to cimetidine resulted in growth inhibition and the induction of apoptosis in a dose-dependent manner. Activation of the caspase cascade for both the extrinsic and intrinsic pathways were demonstrated in vitro, including caspase-8, -9 and -3. We also found that the expression of Bcl-2 protein decreased and the expression of Bax protein increased which lead to an increase of the Bax/Bcl-2 ratio. In mice bearing SGC-7901 xenograft tumors, administration of cimetidine showed a significant decrease of tumor volumes and tumor weight compared with the control. Our results showed that cimetidine exhibited antitumor effects in gastric cancer cells with an induction of apoptosis.
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PMID:Cimetidine induces apoptosis in gastric cancer cells in vitro and inhibits tumor growth in vivo. 2012 8


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