Association of genetic variants in the CART gene with glioma susceptibility in a Chinese population

Wang, Liang; Li, Gang; Liu, Nan; Wang, Zhen; Xu, Xiaoshan; Qi, Jing; Ren, Dongni; Zhang, Pengxing; Zhang, Yongsheng; Tu, Yanyang

doi:10.18632/oncotarget.11763

Cited by 5 publications

(4 citation statements)

References 43 publications

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“…Gliomas account for approximately 80% of all malignant primary central nervous system tumors [ 1 , 2 ]. Stage I and II gliomas are lower-risk tumors and have a better prognosis, whereas stage III and IV gliomas, including anaplastic astrocytomas and glioblastomas, are high-grade malignant tumors [ 3 , 4 ].…”

Section: Introductionmentioning

confidence: 99%

TLR4 interaction with LPS in glioma CD133+ cancer stem cells induces cell proliferation, resistance to chemotherapy and evasion from cytotoxic T lymphocyte-induced cytolysis

et al. 2017

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Despite advances in treatment modalities, 5-year survival among glioma patients remains poor. Glioma cancer stem cells (CSCs) exhibit high tumorigenic activity and are associated with resistance to treatment and tumor recurrence. Because overexpression of toll-like receptor 4 (TLR4) correlated with cancer development, we investigated LPS-induced TLR4 signaling in glioma CD133-positive (CD133+) CSCs. The proliferation of CD133+ CSCs isolated from CSCs derived from the U251 and SF295 glioma cell lines and from human glioma samples was upregulated on a time- and concentration-dependent basis by LPS stimulation, with increases in CD133, NANOG, and NESTIN mRNA and protein levels. Also elevated was cytokine expression, which was coupled to phosphorylation of mitogen-activated protein kinase, and activation of cyclins and cyclin-dependent kinase complexes. TLR4 knockdown reduced LPS-induced CD133+ CSC proliferation, whereas Adriamycin-induced CD133+ CSC apoptosis was moderately inhibited by treatment with LPS, implying a protective effect of LPS. The capacity of glioma CD133+ CSC-reactive cytotoxic T lymphocyte to selectively kill CD133+ CSCs was reduced by LPS, and this effect was not apparent after TLR4 knockdown in CD133+ CSCs. These data suggest TLR4 signaling is a factor in CD133+ CSC immune evasion, and thus disruption of TLR4 signaling is a potential therapeutic strategy in glioma.

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Section: Introductionmentioning

confidence: 99%

TLR4 interaction with LPS in glioma CD133+ cancer stem cells induces cell proliferation, resistance to chemotherapy and evasion from cytotoxic T lymphocyte-induced cytolysis

et al. 2017

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“…These results were further validated based on 800 glioma cases and 800 healthy controls. Finally, a statistically significant association between rs2239670 (OR = 1.27; 95% CI = 1.10–1.46; p = 0.001) and rs11575893 (OR = 1.25; 95% CI = 1.09–1.45; p = 0.002) with a higher glioma risk was confirmed in the pooled patient and control groups [ 57 ].…”

Section: Resultsmentioning

confidence: 99%

“…In the publication by Wang et al [ 57 ] the correlation between variations of the CARTPT gene and susceptibility to glioma in the Chinese population was evaluated. The stage I study included 400 patients with a glioma and 400 healthy controls.…”

Section: Resultsmentioning

confidence: 99%

The Role of Cocaine- and Amphetamine-Regulated Transcript (CART) in Cancer: A Systematic Review

Owe-Larsson,

Pawłasek,

Piecha

et al. 2023

IJMS

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The functions of cocaine- and amphetamine-regulated transcript (CART) neuropeptide encoded by the CARTPT gene vary from modifying behavior and pain sensitivity to being an antioxidant. Putative CART peptide receptor GPR160 was implicated recently in the pathogenesis of cancer. However, the exact role of CART protein in the development of neoplasms remains unclear. This systematic review includes articles retrieved from the Scopus, PubMed, Web of Science and Medline Complete databases. Nineteen publications that met the inclusion criteria and describe the association of CART and cancer were analyzed. CART is expressed in various types of cancer, e.g., in breast cancer and neuroendocrine tumors (NETs). The role of CART as a potential biomarker in breast cancer, stomach adenocarcinoma, glioma and some types of NETs was suggested. In various cancer cell lines, CARTPT acts an oncogene, enhancing cellular survival by the activation of the ERK pathway, the stimulation of other pro-survival molecules, the inhibition of apoptosis or the increase in cyclin D1 levels. In breast cancer, CART was reported to protect tumor cells from tamoxifen-mediated death. Taken together, these data support the role of CART activity in the pathogenesis of cancer, thus opening new diagnostic and therapeutic approaches in neoplastic disorders.

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“…The etiology of glioma involves various aspects, among which the role of genetic factors including genetic polymorphisms in the susceptibility and prognosis of glioma has aroused great concern. Single nucleotide polymorphisms of some genes have been shown to be associated with the risk or prognosis of glioma, such as IL-4R, EFEMP1, RTEL1, CART and IDH1 [5][6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

Impact of AKAP6 Polymorphisms on Glioma Susceptibility and Prognosis

Zhang

Zhao

Huang

et al. 2019

Preprint

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Purpose Glioma is the most common primary malignant brain tumor with high mortality and poor prognosis. Our aim was to clarify the correlation between AKAP6 gene polymorphisms and glioma susceptibility and prognosis in Chinese Han population. Methods Five single-nucleotide polymorphisms (SNPs) of AKAP6 were genotyped by Agena MassARRAY in 575 glioma patients and 500 healthy controls. Logistic regression model was utilized to calculate odds ratios (OR) and 95% confidence intervals (CI). The associations between polymorphisms and survival were assessed using the log-rank test, Kaplan-Meier analysis and Cox regression model. Results We found that rs2239647 polymorphism was strongly associated with an increased risk of glioma (OR = 1.90, p = 0.007) and a worse prognosis for glioma, especially in high-grade glioma (HR = 1.67, p = 0.034). Stratified analysis showed that rs2239647 increased the risk of glioma in female (OR = 1.62, p = 0.016). Whereas, rs4261436 (HR = 0.70, p = 0.045) and rs17522122 (HR = 0.75, p = 0.016) were associated with better prognosis of astrocytoma. In addition, we also found that surgical methods and chemotherapy are critical factors for the prognosis of glioma patients. Conclusions This study firstly provided evidence for the impact of AKAP6 polymorphisms on susceptibility and prognosis of glioma, suggesting AKAP6 variants might have potential roles in the etiology of glioma.

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Association of genetic variants in the CART gene with glioma susceptibility in a Chinese population

Abstract: Glioma, which is a rare and highly fatal brain cancer, has been studied for many

Cited by 5 publications

References 43 publications

TLR4 interaction with LPS in glioma CD133+ cancer stem cells induces cell proliferation, resistance to chemotherapy and evasion from cytotoxic T lymphocyte-induced cytolysis

TLR4 interaction with LPS in glioma CD133+ cancer stem cells induces cell proliferation, resistance to chemotherapy and evasion from cytotoxic T lymphocyte-induced cytolysis

The Role of Cocaine- and Amphetamine-Regulated Transcript (CART) in Cancer: A Systematic Review

Impact of AKAP6 Polymorphisms on Glioma Susceptibility and Prognosis

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