Promoter methylation and downregulation of SLC22A18 are associated with the development and progression of human glioma

Chu, Sheng-Hua; Feng, Donghan; Ma, Yupo; Zhang, Hong; Zhu, Zhenan; Li, Zhiqiang; Jiang, Pu-cha

doi:10.1186/1479-5876-9-156

Cited by 34 publications

(33 citation statements)

References 21 publications

(30 reference statements)

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“…However, there are few studies on its effect on glioma cancer cells (6). Gliomas are the most primary prevalent and aggressive form of intracranial tumors affecting adults 40-60 years of age (7,8). Despite multidisciplinary treatments including surgery, chemotherapy and radiotherapy, it has a poor prognosis with a median survival of less than 15 months (9).…”

Section: Introductionmentioning

confidence: 99%

Salinomycin induces endoplasmic reticulum stress-mediated autophagy and apoptosis through generation of reactive oxygen species in human glioma U87MG cells

Kim

et al. 2017

Oncology Reports

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Abstract. Salinomycin is a polyether ionophore antibiotic that has recently been shown to induce cell apoptosis in human cancer cells displaying multiple mechanisms of drug resistance. In the present study, we explored the impact of salinomycin on the apoptosis and autophagy as well as the correlation between those effects and endoplasmic reticulum (ER) stress molecular mechanisms in human glioma U87MG cells. Apoptosis, autophagy and reactive oxygen species (ROS) were analyzed using flow cytometry. In addition, expression levels of apoptosis-, autophagy-and ER stress-related proteins were determined by western blotting. The results showed that salinomycin induced apoptosis, ER stress and autophagy in glioma cancer cell lines. In addition, salinomycin also induced ROS generation, and the ROS scavenger N-acetyl-L-cysteine was found to inhibit the salinomycin-induced apoptosis, ER stress and autophagy. The inhibition of ER stress with 4-phenylbutyric acid depressed salinomycin-induced apoptosis and autophagy. Salinomycin increased the expression of autophagy marker protein, LC3B, and accumulation of acidic vesicular organelles. Furthermore, pre-treatment with the autophagy inhibitor 3-methyladenine showed potential in increasing the apoptosis rate induced by salinomycin in the U87MG cells. Taken together, these results revealed that salinomycin induced apoptosis and autophagy via ER stress mediated by ROS, suggesting that ER stress by salinomycin plays a dual function in both promoting and suppressing cell death.

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Section: Introductionmentioning

confidence: 99%

Salinomycin induces endoplasmic reticulum stress-mediated autophagy and apoptosis through generation of reactive oxygen species in human glioma U87MG cells

Kim

et al. 2017

Oncology Reports

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“…In recent years, great progress has been made in diagnosing and treating glioma, but its recurrence after resection still makes long-term prognosis unsatisfactory. [1][2][3] Looking for new treatments and further studying its mechanism remain very important. With the development of nanotechnology, a new inorganic material, 1 nanoparticles (nano-HAPs), was found capable of inhibiting the proliferation of tumor cells.…”

Section: Introductionmentioning

confidence: 99%

“…[22][23][24][25] Recently, we have found that SLC22A18 downregulation via promoter methylation was associated with the development and progression of glioma, that it represented a candidate biomarker, and that the elevated expression of SLC22A18 increased the sensitivity of U251 glioma cells to BCNU. 1,2,26 In recent years, SATB1 has attracted considerable attention because of its high expression in tumor tissues as a variety of malignancies, which suggests its important role in promoting tumor growth, invasion, and metastasis; it may also have potential value as a candidate for cancer therapy. [27][28][29] Our results showed that the expression of c-Met, SATB1, and Ki-67 protein decreased and that SLC22A18 protein in glioma U251 and SHG44 cells increased after the cells were treated with various concentrations of hydroxyapatite nanoparticles in vitro.…”

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confidence: 99%

Hydroxyapatite nanoparticles inhibit the growth of human glioma cells in vitro and in vivo

Chu¹,

Feng²,

Ma³

et al. 2012

IJN

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Hydroxyapatite nanoparticles (nano-HAPs) have been reported to exhibit antitumor effects on various human cancers, but the effects of nano-HAPs on human glioma cells remain unclear. The aim of this study was to explore the inhibitory effect of nano-HAPs on the growth of human glioma U251 and SHG44 cells in vitro and in vivo. Nano-HAPs could inhibit the growth of U251 and SHG44 cells in a dose-and time-dependent manner, according to methyl thiazoletetrazolium assay and flow cytometry. Treated with 120 mg/L and 240 mg/L nano-HAPs for 48 hours, typical apoptotic morphological changes were noted under Hoechst staining and transmission electron microscopy. The tumor growth of cells was inhibited after the injection in vivo, and the related side effects significantly decreased in the nano-HAP-and-drug combination group. Because of the function of nano-HAPs, the expression of c-Met, SATB1, Ki-67, and bcl-2 protein decreased, and the expression of SLC22A18 and caspase-3 protein decreased noticeably. The findings indicate that nano-HAPs have an evident inhibitory action and induce apoptosis of human glioma cells in vitro and in vivo. In a drug combination, they can significantly reduce the adverse reaction related to the chemotherapeutic drug 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU).

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“…PLAGL1 is thought to be a transcriptional regulator and has been associated with pheochromocytoma, a tumor of the adrenal grand [26]. SLC22A18 is a transporter of organic cations, and has been associated with glioma and breast cancer progression and survival [27,28]. WT1 plays an important role in normal development of the urogenital system, and is named after its association with Wilms’ tumor development [29].…”

Section: Discussionmentioning

confidence: 99%

Dysregulated methylation at imprinted genes in prostate tumor tissue detected by methylation microarray

Jacobs

Mao

et al. 2013

BMC Urol

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BackgroundImprinting is an important epigenetic regulator of gene expression that is often disrupted in cancer. While loss of imprinting (LOI) has been reported for two genes in prostate cancer (IGF2 and TFPI2), disease-related changes in methylation across all imprinted gene regions has not been investigated.MethodsUsing an Illumina Infinium Methylation Assay, we analyzed methylation of 396 CpG sites in the promoter regions of 56 genes in a pooled sample of 12 pairs of prostate tumor and adjacent normal tissue. Selected LOI identified from the array was validated using the Sequenom EpiTYPER assay for individual samples and further confirmed by expression data from publicly available datasets.ResultsMethylation significantly increased in 52 sites and significantly decreased in 17 sites across 28 unique genes (P < 0.05), and the strongest evidence for loss of imprinting was demonstrated in tumor suppressor genes DLK1, PLAGL1, SLC22A18, TP73, and WT1. Differential expression of these five genes in prostate tumor versus normal tissue using array data from a publicly available database were consistent with the observed LOI patterns, and WT1 hypermethylation was confirmed using quantitative DNA methylation analysis.ConclusionsTogether, these findings suggest a more widespread dysregulation of genetic imprinting in prostate cancer than previously reported and warrant further investigation.

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Promoter methylation and downregulation of SLC22A18 are associated with the development and progression of human glioma

Cited by 34 publications

References 21 publications

Salinomycin induces endoplasmic reticulum stress-mediated autophagy and apoptosis through generation of reactive oxygen species in human glioma U87MG cells

Salinomycin induces endoplasmic reticulum stress-mediated autophagy and apoptosis through generation of reactive oxygen species in human glioma U87MG cells

Hydroxyapatite nanoparticles inhibit the growth of human glioma cells in vitro and in vivo

Dysregulated methylation at imprinted genes in prostate tumor tissue detected by methylation microarray

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