Prognostic significance of MYCN gene amplification and protein expression in primary brain tumors: Astrocytoma and meningioma

Estiar, Mehrdad Asghari; Javan, Firouzeh; Zekri, Ali; Mehrazin, Masoud; Mehdipour, Parvin

doi:10.3233/cbm-160546

Cited by 11 publications

(7 citation statements)

References 58 publications

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“…As the receptor subtype of angiotensin II, AGTR2 is expressed in sensory neurons and could be a potential target for nociception and neuronal regeneration [17]. MYCN, a member of MYC proto-oncogenes, expression levels may have a positive relationship with disease-free survival in astrocytoma and meningioma [18]. Also, potassium voltage-gated channel subfamily J member 8 (KCNJ8) may help to regulate blood pressure with the help of ABCC9 [19].…”

Section: Discussionmentioning

confidence: 99%

Sirt2-associated transcriptome modifications in cisplatin-induced neuronal injury

Zhao

Zhang

et al. 2020

BMC Genomics

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Background: Chemotherapy-induced peripheral neuropathy is not only one of the most common causes of dose reduction or discontinuation of cancer treatment, but it can also permanently decrease the quality of life of cancer patients and survivors. Notably, Sirt2 protects many organs from various injuries, including diabetic peripheral neuropathy. As demonstrated previously by our laboratory and others, the overexpression of Sirt2 can improve cisplatin-induced neuropathy, although the mechanism is still unclear. Results: In this study, the underlying mechanism by which Sirt2 protects neurons from cisplatin-induced injury was explored using the RNAseq technique in cultured rodent neurons. Sirt2 status was modified by genetic knockout (Sirt2/KO) and was then reconstituted in Sirt2/KO cells (Sirt2/Res). We observed 323 upregulated genes and 277 downregulated genes in Sirt2-expressing cells (Sirt2/Res) compared to Sirt2-deficient cells (Sirt2/KO). Pathway analysis suggested that Sirt2 may affect several pathways, such as MAPK, TNF, and cytokine-cytokine interaction. Furthermore, cisplatin-induced changes to the transcriptome are strongly associated with Sirt2 status. Cisplatin induced distinctive transcriptome changes for 227 genes in Sirt2-expressing cells and for 783 genes in Sirt2-deficient cells, while changes in only 138 of these genes were independent of Sirt2 status. Interestingly, changes in the p53 pathway, ECM-receptor interactions, and cytokine-cytokine receptor interactions were induced by cisplatin only in Sirt2-deficient cells. Conclusions: This study demonstrated that Sirt2 regulates the transcriptome in cultured rodent neuronal cells. Furthermore, Sirt2-associated transcriptome regulation may be an important mechanism underlying the role of Sirt2 in organ protection, such as in cisplatin-induced neuronal injury. Sirt2 may be a potential target for the prevention and treatment of chemotherapy-induced neuropathy.

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Section: Discussionmentioning

confidence: 99%

Sirt2-associated transcriptome modifications in cisplatin-induced neuronal injury

Zhao

Zhang

et al. 2020

BMC Genomics

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“…Moreover, a study by Liu et al found that MYCN was involved in the malignant characteristics of erythroleukemia by inhibiting the activation of p21 . What's more, amplified MYCN gene was observed in rhabdomyosarcoma, pediatric T‐cell acute lymphoblastic leukemia, astrocytoma, and meningioma …”

Section: Discussionmentioning

confidence: 99%

MYCN gene polymorphisms and Wilms tumor susceptibility in Chinese children

Huang

Zhao

Zhu

et al. 2019

Clinical Laboratory Analysis

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Background Wilms tumor, derived from embryonic cells, accounts for a large proportion of pediatric renal tumors. MYCN encoded by MYCN proto‐oncogene, a member of the MYC family, is a BHLH transcription factor. It plays a critical role in tumorigenesis and predicts poor clinical outcomes in various types of cancer. However, the role of MYCN remained unclarified in Wilms tumor. In this study, we investigated the association between MYCN gene polymorphisms and Wilms tumor susceptibility. Methods Four MYCN gene polymorphisms (rs57961569 G > A, rs9653226 T > C, rs13034994 A > G, and rs60226897 G > A) were genotyped in 183 cases and 603 controls. Adjusted odds ratios (AORs) and 95% confidence intervals (CIs) were calculated to evaluate the association between MYCN gene polymorphisms and Wilms tumor susceptibility. Results Overall, no significant association was found for any of the four MYCN gene polymorphisms. Interestingly, in the stratification analysis, the rs57961569 was found to be associated with decreased Wilms tumor susceptibility in the children older than 18 months (AOR = 0.65, 95% CI = 0.42‐1.00, P = .050). Moreover, older children carrying 2‐4 risk genotypes were at increased risk of Wilms tumor (OR = 1.55, 95% CI = 1.001‐2.40, P = .0497). Haplotype GCAA was shown to significantly increased Wilms tumor risk (AOR = 2.40, 95% CI = 1.12‐5.14, P = .024). Conclusion Our study demonstrated that these MYCN gene polymorphisms might be low penetrant variants in Wilms tumor.

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“…As an example, correlation between gene amplification at global level by qualitative polymerase chain reaction (qPCR) and expression by IF is reported to be a challenging item, and we found it inconsistent in brain tumors. 17 This finding has a key impact on the therapeutic approach, so it’s worth to emphasize on an EGF/VEGF chimer characterized with an adequate amount of antibodies in contradiction of the EGF and VEGF function which aimed to prevent angiogenic and growth of breast tumor in mouse model. 18…”

Section: Discussionmentioning

confidence: 99%

Diversity in tumor territory of meningioma: Protein expression in vascular endothelial growth factor and epidermal growth factor

Mehdipour

Javan

Faghih-Jouibari

et al. 2019

CJN

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Background: Vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF) are involved in tumor development and progression. But, the classified-based data of protein expression (PE) in meningiomas is unavailable. Therefore, we aimed to explore the PE of VEGF and EGF in meningiomas by considering evolutionary strategy and the regional tumor-based assay. Methods: PE was assayed using immunofluorescence (IF) within the peripheral, central, and basal sections of four meningioma tumors, and a lung metastatic brain tumor as a positive control. Results: Diverse characteristics and harmonic cross-talk in the individual sections and between different tumor sections were traced. The mode of PE was puzzling and personalized issue. Co-expression had a key impact on tumor evolution and diverse PE profiles led to draw the heterogenic classification, as the personalized/complementary insight in the functional behavior of VEGF and EGF. D1853N polymorphism of ATM gene was mosaics in two patients with meningiomas. Conclusion: The classified heterogeneity, harmonic co-expression, and diverse functional information in different regions of tumors may lead to predict the aggressiveness mode of tumors as a translational insight to the clinical managements including therapy in brain tumors.

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Prognostic significance of MYCN gene amplification and protein expression in primary brain tumors: Astrocytoma and meningioma

Abstract: Our results challenge the concept of the neural specificity of MYCN by demonstrating contribution of MYCN in meningioma. Moreover, this study highlights the importance of research at both level of DNA and protein, to determine the biological functions and medical impacts of MYCN.

Cited by 11 publications

References 58 publications

Sirt2-associated transcriptome modifications in cisplatin-induced neuronal injury

Sirt2-associated transcriptome modifications in cisplatin-induced neuronal injury

MYCN gene polymorphisms and Wilms tumor susceptibility in Chinese children

Diversity in tumor territory of meningioma: Protein expression in vascular endothelial growth factor and epidermal growth factor

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