Correlation of low SLC22A18 expression with poor prognosis in patients with glioma

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

doi:10.1016/j.jocn.2011.04.032

Cited by 37 publications

(25 citation statements)

References 7 publications

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“…A recent study has established a novel link between the transporter and fat accumulation [94], but the molecular basis of this interesting link is not known. Several reports have described the silencing of this gene by DNA methylation in glioma and breast cancer [95–100], and evaluation of the relationship between SLC22A18 expression and disease status has revealed that low expression of the transporter in tumours correlates with tumour progression, recurrence and poor survival in both cancer types [95,96,97,100]. Mutations in SLC22A18 are associated with Wilms tumour, adrenocortical carcinoma, rhabdomyosarcoma and Beckwith–Wiedemann syndrome, all pointing to potential function of the transporter as a tumour suppressor.…”

Section: Slc22a18mentioning

confidence: 99%

SLC transporters as a novel class of tumour suppressors: identity, function and molecular mechanisms

Bhutia

Babu

Ramachandran

et al. 2016

Biochemical Journal

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The role of plasma membrane transporters in cancer is receiving increasing attention in recent years. Several transporters for essential nutrients are up-regulated in cancer and serve as tumour promoters. Transporters could also function as tumour suppressors. To date, four transporters belonging to the SLC gene family have been identified as tumour suppressors. SLC5A8 is a Na+-coupled transporter for monocarboxylates. Among its substrates are the bacterial fermentation products butyrate and propionate and the ubiquitous metabolite pyruvate. The tumour-suppressive function of this transporter relates to the ability of butyrate, propionate and pyruvate to inhibit histone deacetylases (HDAC). SLC5A8 functions as a tumour suppressor in most tissues studied thus far, and provides a molecular link to Warburg effect, a characteristic feature in most cancers. It also links colonic bacteria and dietary fibre to the host. SLC26A3 as a tumour suppressor is restricted to colon; it is a Cl-/HCO3- exchanger, facilitating the efflux of HCO3-. The likely mechanism for the tumour-suppressive function of SLC26A3 is related to intracellular pH regulation. SLC39A1 is a Zn2+ transporter and its role in tumour suppression has been shown in prostate. Zn2+ is present at high concentrations in normal prostate where it elicits its tumour-suppressive function. SLC22A18 is possibly an organic cation transporter, but the identity of its physiological substrates is unknown. As such, there is no information on molecular pathways responsible for the tumour-suppressive function of this transporter. It is likely that additional SLC transporters will be discovered as tumour suppressors in the future.

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Section: Slc22a18mentioning

confidence: 99%

SLC transporters as a novel class of tumour suppressors: identity, function and molecular mechanisms

Bhutia

Babu

Ramachandran

et al. 2016

Biochemical Journal

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“…The SLC22A1 gene became suppressed, while the SOX2 gene was reactivated and overexpressed in malignant glioma cells [10, 9]. Similarly, low expression of another transporter gene, SLC22A18, was found to correlate with poor prognosis in patients with glioma [11]. There is a positive correlation between SOX2 expression and malignancy grade in gliomas, and hypercellular and hyperproliferative areas of glioblastomas are the areas with the highest SOX2 expression [12,13].…”

Section: Introductionmentioning

confidence: 99%

Glioblastoma Development in Mouse Brain: General Reduction of OCTs and Mislocalization of OCT3 Transporter and Subsequent Uptake of ASP<SUP>+</SUP> Substrate to the Nuclei

Kucheryavykh¹,

Rolón-Reyes²,

Kucheryavykh³

et al. 2014

J Neurosci Neuroengng

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Organic cation transporters (OCTs) were first found and then isolated from cultured glioma cells. When glioma cells are implanted into brain the fate of OCTs varies with time after implantation and transporter type. Here we report that OCT1, OCT2 and OCT3 immunofluorescence is significantly reduced over time in implanted GL261 glioma cells, during tumor development in the brain. By day 21 after glioma implantation, OCT1, OCT2 and OCT3 immunofluorescence was reduced more than 10-fold in the cytoplasm of glioma cells, while OCT3 immunofluorescence became concentrated in the nucleus. The well-known fluorescent substrate for OCT transporters, NIH-PA Author Manuscript, previously shown to accumulate in glioma-cell cytoplasm in in vivo slices, began to accumulate in the nucleus of these cells, but not in cytoplasm, after 21 days post-implantation. Considering this mislocalization phenomenon, and other literature on similar nuclear mislocalization of different transporters, receptors and channels in glioma cells, we suggest that it is one of the "omens" preceding the motility and aggressivity changes in glioma behavior.

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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.…”

mentioning

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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Correlation of low SLC22A18 expression with poor prognosis in patients with glioma

Cited by 37 publications

References 7 publications

SLC transporters as a novel class of tumour suppressors: identity, function and molecular mechanisms

SLC transporters as a novel class of tumour suppressors: identity, function and molecular mechanisms

Glioblastoma Development in Mouse Brain: General Reduction of OCTs and Mislocalization of OCT3 Transporter and Subsequent Uptake of ASP<SUP>+</SUP> Substrate to the Nuclei

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

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