Deciphering the role of paclitaxel in the SKGT4 human esophageal adenocarcinoma cell line

Kim, Seo Ju; Chung, Myoung Ja; Kim, Jong‐Suk; Kim, Bumseok; Park, Woo Hyun; Kim, Suhn Hee; Kim, Sung Zoo; Lee, Ju Seog; Kim, Soo Mi

doi:10.3892/ijo.2011.1135

Cited by 6 publications

(11 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The effect of DIM on cell proliferation was determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay as described previously (38). Briefly, cells were plated in 96-well plates (SPL, Seoul, Korea) at 1x10 4 cells/well.…”

Section: Methodsmentioning

confidence: 99%

“…To determine the effect of DIM on the cell cycle, cells were incubated in 100-mm dishes and were treated for 24 h with various DIM concentrations. Subsequently, cells were washed with PBS and the nuclei were stained with propidium iodide (PI) (Sigma Chemical, St. Louis, MO, USA) as described previously (28,38). The percentage of cells in the different cell cycle phases was measured with a FACstar flow cytometer (Becton-Dickinson, San Jose, CA, USA) and analyzed using Becton-Dickinson software (Lysis II and CellFit).…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

3,3′-Diindolylmethane suppresses the growth of gastric cancer cells via activation of the Hippo signaling pathway

Park

et al. 2013

Oncology Reports

View full text Add to dashboard Cite

Abstract. Recent studies have revealed that 3,3-diindolylmethane (DIM) has antitumor effects in both in vivo and in vitro tumor models. However, the biological function of DIM in human gastric cancer cells is unknown. Genetic and biological studies have confirmed the importance of the novel Hippo tumor-suppressor pathway in regulating cell proliferation, apoptosis, organ size and tumorigenesis in mammals. Thus, the purpose of this study was to investigate the cytotoxic effects of DIM in human gastric cancer cells and to elucidate whether DIM induces cell death by activating the Hippo signaling pathway. Two human gastric cancer cell lines (SNU-1 and SNU-484) were used to investigate the DIM response. DIM significantly inhibited the proliferation of human gastric cancer cells in a dose-dependent manner. The percentage of G1 phase cells increased 24 h following DIM treatment. DIM reduced CDK2, CDK4, CDK6 and cyclin D1 protein levels, while increasing p53 protein levels. DIM induced the levels of cleaved poly(ADP-ribose) polymerase, cleaved-caspase-9, and diminished pro-caspase-3 protein production. In addition, DIM increased pLATS1, Mob1, pMob1, pYAP and Ras association domain family 1 (RASSF1) protein levels and reduced Yap protein production levels. DIM stimulated the binding of RASSF1 with the Mst1/2-LATS1-Mob1 complex, promoting an active Hippo signaling pathway and favoring YAP phosphorylation (pYAP) that inactivates cell proliferation. Furthermore, DIM inhibited the growth of human gastric tumors in a xenograft mouse model. These results indicate that DIM suppresses the growth of gastric cancer cells by activating the Hippo signaling pathway.

show abstract

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

3,3′-Diindolylmethane suppresses the growth of gastric cancer cells via activation of the Hippo signaling pathway

Park

et al. 2013

Oncology Reports

View full text Add to dashboard Cite

show abstract

“…The cells were treated for 48 h with various concentrations of DIM. After trypsinization, the nuclei were stained with propidum iodide (Sigma Chemical, St. Louis, MO, USA) as described previously (14,24). The percentage of cells in the different cell cycle phases was measured with a FACStar flow cytometer (Becton-Dickinson, San Jose, CA, USA) and analyzed using the Becton-Dickinson software (Lysis II, Cellfit).…”

Section: Reagentsmentioning

confidence: 99%

“…These effects may be due to reduced cyclin-dependent kinase (CDK) activity. (10,20,30,40,50 or 100 µM) for 72 h. Cell viability was assessed with the MTT assay as described previously (24). Experiments were conducted in triplicate, and viability assays were repeated three times to confirm results.…”

Section: Introductionmentioning

confidence: 99%

3,3'-Diindolylmethane suppresses growth of human esophageal squamous cancer cells by G1 cell cycle arrest

2012

Self Cite

View full text Add to dashboard Cite

Abstract. 3,3'-Diindolylmethane (DIM), an active metabolite of indole-3-carbinol, is thought to have antitumor effects in experimental animals and induce apoptosis in various cancer cells. However, the biological functions of DIM in human esophageal cancer cells are unknown. Thus, the purpose of this study was to investigate the cytotoxic effects of DIM in human esophageal squamous cell carcinoma (ESCC) cells to elucidate the molecular mechanism of cell death. Three human ESCC cell lines (TT, TE-8 and TE-12) were used to test the response to DIM. MTT, cell cycle and western blot analyses were conducted. DIM significantly inhibited the proliferation of ESCC cells in a dose-and time-dependent manner. The percentage of G1 phase cells increased 48 h after being treated with DIM. DIM also reduced cyclin D1, cyclin E2, cyclin-dependent kinase (CDK) 4 and CDK 6 activities, and increased p15 and p27 levels. Additionally, DIM diminished pro-caspase-9 protein expression levels and induced increased cleaved poly (ADP-ribose) polymerase levels. These results indicate that DIM leads to G1 phase cell cycle arrest and induces apoptosis by activating caspase-9 in ESCC cells.

show abstract

“…Cell cycle regulation was measured as previously described [47]. Briefly, the cells were plated into 100 mm dishes at 1 × 10 6 cells in RPMI 1640.…”

Section: Methodsmentioning

confidence: 99%

Recombinant human bone morphogenetic protein-2 inhibits gastric cancer cell proliferation by inactivating Wnt signaling pathway via c-Myc with aurora kinases

Lee

Jin

et al. 2016

Oncotarget

View full text Add to dashboard Cite

The detailed molecular mechanisms and safety issues of recombinant human bone morphogenetic protein-2 (rhBMP-2) usage in bone graft substitution remain poorly understood. To investigate the molecular mechanisms underlying the function of rhBMP-2 in gastric cancer cells, we used microarrays to determine the gene expression patterns related to the effects of rhBMP-2. Based on a gene ontology analysis, several genes were upregulated during the regulation of the cell cycle and BMP signaling pathway. MYC was found to be significantly decreased along with its downstream target genes, the aurora kinases (AURKs), by rhBMP-2 in the network analysis. We further confirmed this finding with western blot data that rhBMP-2 inhibited c-Myc, AURKs, and β-catenin in SNU484 and SNU638 cells. An AURK inhibitor significantly decreased c-Myc expression in gastric cancer cells. Combination treatment with rhBMP-2 and AURK inhibitor resulted in significantly decreased c-Myc expression compared with gastric cancer cells treated with an rhBMP-2 or AURK inhibitor, respectively. Similar effects for decreased c-Myc expression were observed when we silenced β-catenin in gastric cancer cells. These results indicate that rhBMP-2 attenuated the growth of gastric cancer cells via the inactivation of β-catenin via c-Myc and AURKs. Therefore, our findings suggest that rhBMP-2 could be safely used with patients who undergo gastric or gastroesophageal cancer surgery.

show abstract

Deciphering the role of paclitaxel in the SKGT4 human esophageal adenocarcinoma cell line

Cited by 6 publications

References 26 publications

3,3′-Diindolylmethane suppresses the growth of gastric cancer cells via activation of the Hippo signaling pathway

3,3′-Diindolylmethane suppresses the growth of gastric cancer cells via activation of the Hippo signaling pathway

3,3'-Diindolylmethane suppresses growth of human esophageal squamous cancer cells by G1 cell cycle arrest

Recombinant human bone morphogenetic protein-2 inhibits gastric cancer cell proliferation by inactivating Wnt signaling pathway via c-Myc with aurora kinases

Contact Info

Product

Resources

About