MYCN neuroblastoma and focal adhesion kinase FAK

Beierle, Elizabeth A.

doi:10.2741/e257

Cited by 5 publications

(3 citation statements)

References 52 publications

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“…Cloning and evaluation of the FAK promoter has shown that it has many binding sites for various oncogenes, such as TP53 (44). The tumor protein TP53 (TP53 or TTP53) was the first tumor suppressor gene, discovered in 1979, and is the guardian of the genome (45).…”

Section: A B Cmentioning

confidence: 99%

Copy Number Analysis Reveal Genetic Risks of Penile Cancer

Gao

Chen

et al. 2020

Front. Oncol.

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ObjectivesTo evaluate copy number alterations (CNAs) in genes associated with penile cancer (PeC) and determine their correlation and prognostic ability with PeC.MethodsWhole-exome sequencing was performed for tumor tissue and matched normal DNA of 35 patients diagnosed with penile squamous cell carcinoma from 2011 to 2016. Somatic CNAs were detected using the Genome Analysis Toolkit (GATK). Retrospective clinical data were collected and analyzed. All the data were statistically analyzed using SPSS 16.0 software. The cancer-specific survival rates were estimated by Kaplan-Meier curves and compared with the log-rank test.ResultsCNAs in the MYCN gene was detected in 19 (amplification: 54.29%) patients. Other CNAs gene targets were FAK (amplification: 45.72%, deletion: 8.57%), TP53 (amplification: 2.86%, deletion: 51.43%), TRKA (amplification: 34.29%, deletion: 2.86%), p75NTR (amplification: 5.71%, deletion: 42.86%), Miz-1 (amplification: 14.29%, deletion: 20.00%), Max (amplification: 17.14%, deletion: 2.86%), Bmi1 (amplification:14.29%, deletion: 48.57%), and MDM2 (amplification: 5.71%, deletion: 45.72%). The CNAs in MYCN and FAK correlated significantly with patient prognosis (P<0.05). The 3-year Recurrence-free survival rate was 87.10% among patients followed up. The 5-year survival rate of patients with MYCN amplification was 69.2%, compared to 94.4% in the non-amplification group. The 5-year survival rate of patients with FAK amplification was 65.6%, compared to 94.7% in the non-amplification group. The PPI network showed that TP53 and MYCN might play meaningful functional roles in PeC.ConclusionMYCN and FAK amplification and TP53 deletion were apparent in PeC. MYCN and TP53 were hub genes in PeC. MYCN and FAK amplification was also detected and analyzed, and the findings indicated that these two genes are predictors of poor prognosis in PeC.

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Section: A B Cmentioning

confidence: 99%

Copy Number Analysis Reveal Genetic Risks of Penile Cancer

Gao

Chen

et al. 2020

Front. Oncol.

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“…The current study examined the mechanism TRPM7 expression has been shown to promote cell proliferation and metastasis in various cancers [10,16,19,22,36,43,48]. Previous studies have shown that MycN promotes NB migration and invasion by regulating the expression of genes involved in cell migration, invasion and metastasis, including integrin proteins, focal adhesion kinase [3,15,31,51], ODC and TRPM7 [27,29]. The results from the current study showed that TRPM7 expression correlated with MycN expression, and Kaplan-Meier survival data showed that TRPM7 expression correlated with decreased patient survival.…”

Section: Discussionmentioning

confidence: 98%

MycN promotes TRPM7 expression and cell migration in neuroblastoma through a process that involves polyamines

Lange

Koomoa

2014

FEBS Open Bio

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“…Further, EZH2 has been shown to activate Src, a protein kinase upstream from focal adhesion kinase (FAK). FAK, a nonreceptor protein tyrosine kinase, has been shown to play an important role in neuroblastoma tumorigenesis [9][10][11]. We further hypothesized that EZH2 inhibition with GSK343 would affect FAK expression.…”

Section: Introductionmentioning

confidence: 98%

EZH2 inhibition decreases neuroblastoma proliferation and in vivo tumor growth

et al. 2021

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Investigation of the mechanisms responsible for aggressive neuroblastoma and its poor prognosis is critical to identify novel therapeutic targets and improve survival. Enhancer of Zeste Homolog 2 (EZH2) is known to play a key role in supporting the malignant phenotype in several cancer types and knockdown of EZH2 has been shown to decrease tumorigenesis in neuroblastoma cells. We hypothesized that the EZH2 inhibitor, GSK343, would affect cell proliferation and viability in human neuroblastoma. We utilized four long-term passage neuroblastoma cell lines and two patient-derived xenolines (PDX) to investigate the effects of the EZH2 inhibitor, GSK343, on viability, motility, stemness and in vivo tumor growth. Immunoblotting confirmed target knockdown. Treatment with GSK343 led to significantly decreased neuroblastoma cell viability, migration and invasion, and stemness. GSK343 treatment of mice bearing SK-N-BE(2) neuroblastoma tumors resulted in a significant decrease in tumor growth compared to vehicle-treated animals. GSK343 decreased viability, and motility in long-term passage neuroblastoma cell lines and decreased stemness in neuroblastoma PDX cells. These data demonstrate that further investigation into the mechanisms responsible for the anti-tumor effects seen with EZH2 inhibitors in neuroblastoma cells is warranted.

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MYCN neuroblastoma and focal adhesion kinase FAK

Cited by 5 publications

References 52 publications

Copy Number Analysis Reveal Genetic Risks of Penile Cancer

Copy Number Analysis Reveal Genetic Risks of Penile Cancer

MycN promotes TRPM7 expression and cell migration in neuroblastoma through a process that involves polyamines

EZH2 inhibition decreases neuroblastoma proliferation and in vivo tumor growth

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