Identification of genes related to a synergistic effect of taxane and suberoylanilide hydroxamic acid combination treatment in gastric cancer cells

Chang, Hyun; Rha, Sun Young; Jeung, Hei Cheul; Jung, Jae Jun; Kim, Tae Soo; Kwon, Ho Jeong; Kim, Byung Soo; Chung, Hyun Cheol

doi:10.1007/s00432-010-0849-0

Cited by 28 publications

(23 citation statements)

References 38 publications

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“…Although treatments involving combinations of docetaxel and sirtuin inhibitors have not been reported, combinations of docetaxel and other HDAC inhibitors such as trichostatin A and suberoylanilide hydroxamic acid (SAHA) have been reported to have synergistic effects related to caspase activation or tubulin acetylation in several cancer cell lines [48]–[50]. In our study, it remains unclear if the tubulin acetylation by tenovin-6 always affected the antitumor effect, because the tubulin acetylation was shown only in one cell line.…”

Section: Discussionmentioning

confidence: 74%

Antitumor Effects of a Sirtuin Inhibitor, Tenovin-6, against Gastric Cancer Cells via Death Receptor 5 Up-Regulation

et al. 2014

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Up-regulated sirtuin 1 (SIRT1), an NAD+-dependent class III histone deacetylase, deacetylates p53 and inhibits its transcriptional activity, leading to cell survival. SIRT1 overexpression has been reported to predict poor survival in some malignancies, including gastric cancer. However, the antitumor effect of SIRT1 inhibition remains elusive in gastric cancer. Here, we investigated the antitumor mechanisms of a sirtuin inhibitor, tenovin-6, in seven human gastric cancer cell lines (four cell lines with wild-type TP53, two with mutant-type TP53, and one with null TP53). Interestingly, tenovin-6 induced apoptosis in all cell lines, not only those with wild-type TP53, but also mutant-type and null versions, accompanied by up-regulation of death receptor 5 (DR5). In the KatoIII cell line (TP53-null), DR5 silencing markedly attenuated tenovin-6-induced apoptosis, suggesting that the pivotal mechanism behind its antitumor effects is based on activation of the death receptor signal pathway. Although endoplasmic reticulum stress caused by sirtuin inhibitors was reported to induce DR5 up-regulation in other cancer cell lines, we could not find marked activation of its related molecules, such as ATF6, PERK, and CHOP, in gastric cancer cells treated with tenovin-6. Tenovin-6 in combination with docetaxel or SN-38 exerted a slight to moderate synergistic cytotoxicity against gastric cancer cells. In conclusion, tenovin-6 has potent antitumor activity against human gastric cancer cells via DR5 up-regulation. Our results should be helpful for the future clinical development of sirtuin inhibitors.

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Section: Discussionmentioning

confidence: 74%

Antitumor Effects of a Sirtuin Inhibitor, Tenovin-6, against Gastric Cancer Cells via Death Receptor 5 Up-Regulation

et al. 2014

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“…FBLN4 promoter methylation has frequently been found in lung cancers43 and melanoma cells 44. Other studies have reported that FBLN4 is overexpressed in tumors of the digestive system45–47 and in gynecological tumors;48–50 FBLN4 overexpression correlates with tumor progression and poor prognosis in these studies. In contrast, FBLN4 is downregulated in prostate cancer 51.…”

Section: Discussionmentioning

confidence: 50%

<em>FBLN4</em> as candidate gene associated with long-term and short-term survival with primary glioblastoma

Li¹,

Li²,

Zhang³

et al. 2017

OTT

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BackgroundGlioblastoma multiforme (GBM) is the most common malignant and lethal type of primary central nervous system tumor in humans. In spite of its high lethality, a small percentage of patients have a relatively good prognosis, with median survival times of 36 months or longer. The identification of clinical subsets of GBM associated with distinct molecular genetic profiles has made it possible to design therapies tailored to treat individual patients.MethodsWe compared microarray data sets from long-term survivors (LTSs) and short-term survivors (STSs) to screen for prognostic biomarkers in GBM patients using the WebArrayDB platform. We focused on FBLN4, IGFBP-2, and CHI3L1, all members of a group of 10 of the most promising, differentially regulated gene candidates. Using formalin-fixed paraffin-embedded GBM samples, we corroborated the relationship between these genes and patient outcomes using methylation-specific polymerase chain reaction (PCR) for MGMT methylation status and quantitative reverse transcription PCR for expression of these genes.ResultsExpression levels of the mRNAs of these 3 genes were higher in the GBM samples than in normal brain samples and these 3 genes were significantly upregulated in STSs compared to the levels in LTS samples (P<0.01). Furthermore, Kaplan–Meier analysis showed that the expression patterns of FBLN4 and IGFBP-2 serve as independent prognostic indicators for overall survival (P<0.01 and P<0.05, respectively).ConclusionTo our knowledge, this is the first report describing FBLN4 as a prognostic factor for GBM patient survival, demonstrating that increased GBM survival time correlates with decreased FBLN4 expression. Understanding FBLN4 expression patterns could aid in the creation of powerful tools to predict clinical prognoses of GBM patients.

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“…Reportedly, the combination of SAHA and XL184 synergistically induced cell apoptosis and inhibited tumor growth of prostate and lung cancer cells [19]. The similar results were observed in gastric [20] and hepatocellular [21] cancer cells, treated by oxaliplatin and SAHA. Therefore, they might be employed to treat the glioma if both hepatic and renal injuries are avoided and ameliorated in clinical practice.…”

Section: Discussionmentioning

confidence: 53%

SAHA and/or MG132 reverse the aggressive phenotypes of glioma cells: Anin vitroand vivo study

Zhao¹,

Liu²,

Yang

et al. 2016

Oncotarget

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To elucidate the anti-tumor effects and molecular mechanisms of SAHA (a histone deacetylase inhibitor) and MG132 (a proteasome inhibitor) on the aggressive phenotypes of glioma cells, we treated U87 and U251 cells with SAHA or/and MG132, and detected phenotypes’ assays with phenotype-related molecules examined. It was found that SAHA or/and MG132 treatment suppressed proliferation in both concentration- and time-dependent manners, inhibited energy metabolism, migration, invasion and lamellipodia formation, and induced G2 arrest and apoptosis in the glioma cells. The treatment with SAHA increased the expression of acetyl-histones 3 and 4, which were recruited to the promoters of p21, p27, Cyclin D1, c-myc and Nanog to down-regulate their transcriptional levels. Expression of acetyl-histones 3 and 4 was higher in gliomas than normal brain tissues. Both drugs’ exposure suppressed tumor growth in nude mice by inducing apoptosis and inhibiting proliferation, but increased serum aminotransferase and creatinine. These results indicated that SAHA and/or MG132 may suppress the aggressive phenotypes of glioma cells. They might be employed to treat the glioma if both hepatic and renal injuries are prevented.

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Identification of genes related to a synergistic effect of taxane and suberoylanilide hydroxamic acid combination treatment in gastric cancer cells

Abstract: The combination of taxane and SAHA could be efficacious for the treatment of gastric cancer. The genes that were related to the synergistic response to taxane and SAHA could serve as surrogate biomarkers to predict the therapeutic response in gastric cancer patients.

Cited by 28 publications

References 38 publications

Antitumor Effects of a Sirtuin Inhibitor, Tenovin-6, against Gastric Cancer Cells via Death Receptor 5 Up-Regulation

Antitumor Effects of a Sirtuin Inhibitor, Tenovin-6, against Gastric Cancer Cells via Death Receptor 5 Up-Regulation

<em>FBLN4</em> as candidate gene associated with long-term and short-term survival with primary glioblastoma

SAHA and/or MG132 reverse the aggressive phenotypes of glioma cells: Anin vitroand vivo study

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