MYCN Antibodies

N-myc proto-oncogene protein (MYCN)

Positively regulates the transcription of MYCNOS in neuroblastoma cells. .

Gene Information

Human
Gene Name:	MYCN
Uniprot:	P04198
Entrez:	4613

Family

Belongs to:
No superfamily

Alternative Names

BHLHE37; bHLHe37N-myc proto-oncogene protein; Class E basic helix-loop-helix protein 37; MODED; neuroblastoma-derived v-myc avian myelocytomatosis viral related oncogene; N-myc; NMYCneuroblastoma MYC oncogene; ODED; oncogene NMYC; pp65/67; v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived; v-myc myelocytomatosis viral related oncogene, neuroblastoma derived (avian)

Molecular Weight

Mass (kDA):
49.561 kDA

Genomic Context

Human
Location:	2p24.3
Sequence:	2; NC_000002.12 (15940550..15947004)

Tissue Specificity

Expressed in the neuronal cells of the cerebrum, neuroblastomas and thyroid tumors (at protein level).

Subcellular Localizations

Nucleus.

Diseases

• Neuroblastoma
• Neoplasms
• Malignant Neoplasms
• Neoplasm Metastasis
• Malignant Paraganglionic Neoplasm
• Cell Transformation, Neoplastic
• Nervousness
• Cytogenetic Abnormality
• Stage 4s Neuroblastoma
• Tumor Progression
• Nmyc Gene Amplification Dysfunction
• Brain Neoplasms

• Pediatric Neoplasm
• Medulloblastoma
• Solid Tumor
• Ganglioneuroma
• Crest Syndrome
• Primary Neoplasm
• Retinoblastoma

Interacting Proteins

• AURKA
• Aurka
• CDKN2A
• MAX
• NMI

• SIRT1
• ZBTB17

Pathways

• Cell Cycle
• Pathogenesis
• Cell Proliferation
• Cell Death
• Methylation
• Cell Growth
• Angiogenesis
• Interphase
• Cell Differentiation
• Localization
• Drug Resistance
• Metaphase
• Translation

• Oncogenesis
• Rna Interference
• Cell Cycle Arrest
• Reverse Transcription
• Dna Methylation
• Programmed Cell Death
• Induction Of Apoptosis

PTMs

• Methylation
• Phosphorylation
• Cleavage
• Acetylation
• Demethylation

• Deacetylation
• Dephosphorylation
• Ubiquitination
• Carboxylation
• Reduction

• Prenylation

Research Areas

• Cancer
• Cell Cycle and Replication
• Transcription Factors and Regulators
• Tumor Suppressors

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/MYCN

Best Uses Of The MYCN Marker

Steven Boster is the founder of PicoKine and the creator of the MYCN ELISA. He founded the company in 1993. Then, he received the nicknamed "he who changed science in the lavatory". Since then, the company has become one of the largest catalogs of antibodies in China. One of the products Boster has created is the exclusive ELISA platform PicoKine(tm). This platform makes use of proprietary trade secrets to create high-sensitivity ELISA kits.

MYCN amplification

MTAP and MYCN are two enzymes found in the transsulfuration pathway. They are responsible for increasing the production of cysteine. Furthermore, MYCN directly upregulates MTAP, which shunts methionine to the transsulfuration pathway , and thus contributes to cysteine. This pathway could be targeted as an exciting option for treating MYCN-amplified NB.

The reporter constructs were transfected into BE(2)C cells using Lipofectamine(r), using RNAiMAX to boost MYCN amplifying. The reporter constructs used for amplifying the gene were TFAP4 and MYCN siRNAs from Dharmacon. After transfection, the results were analyzed by employing the DDCT method. The control was used to determine the amount of transcripts present in each of the samples.

The odds ratios obtained from the univariate logistic regression include all pathology and clinical factors associated with MYCN amplification. The highest OR for MNA was found in patients with primary tumors in the thoracic and adrenal regions. The patients with the most frequent INPC tumors had MNA that was low and MKI that was low, were diploid, and MYCN-amplified in 85.9 percent of cases.

MYCN is an immediate transcriptional target for TFAP4 or PRPS2 proteins. TFAP4-depleted BE(2)-C cells showed a decrease in migration, and transiently overexpression of MYCN significantly improved the ability to form colonies in MYCN-overexpressing SH-EP/S1 cells. Furthermore siRNAs of TFAP4 prevented MYCN from affecting cells.

EZH2 inhibitors are currently in clinical trials for a variety of malignancies. Numerous studies have proven that EZH2 inhibits MYCN-amplified neuroblastoma cell growth. This study supports the need for a comprehensive CRISPR Cas9 screening effort to develop of effective therapeutics for neuroblastomas. It could be a step towards the development of a precise cancer dependency map.

The amplification of MYCN is also associated with higher levels of TFAP4 protein expression as well as TFAP4 protein. Boster Bio is an option for a therapeutic approach for this disease , by increasing the MYCN level. However, a greater level of MYCN could lead to better survival and treatment outcomes for neuroblastoma. However, it is important to determine the appropriate threshold for MYCN expression in each cell.

Predictive value of MYCN amplification in neuroblastoma

MYCN Amplification is a unique diagnostic marker that can determine the outcome of patients diagnosed with cancer. In an article published in journal Neuroblastoma Research, researchers discovered patients with an amplification of the MYCN gene as having a lower risk of relapse and a less favorable three-year survival rate than those who had normal MYCN amplification.

The study found that MYCN amplifying was linked to low overall survival in children with NB metastatic to the BM. The study's results revealed that the amplification of MYCN was linked to age and the highest incidence was found in children who are more than two years old. MYCN Amplification was not observed in patients younger than 18 months of age.

The researchers also discovered that the increase in MYCN is a significant predictor of prognosis in infants with NB. This was true in both metastatic and nonmetastatic tumors. This could be crucial in clinical decision-making. The importance of cMYC inhibitors in neuroblastoma was also highlighted by the study.

Other studies have found that patients with intermediate-risk neuroblastoma were more likely to have poor outcomes due to the amplifying effects of MYCN. However, this correlation was not true for patients with high-risk neuroblastoma. Further research is needed to confirm this conclusion in the high-risk category. However these studies aren't sufficient due to the size of the samples that were used to construct the associations aren't uniform and include only a small proportion of patients suffering from high-risk neuroblastoma.

This study revealed that MYCN amplifying is associated with an increase in EZH2 protein expression than non-amplified cells. Two primary tumor data sets confirmed this relationship. MYCN amplification also was linked to higher expression of apoptosis gene genes such as NGFR. These results suggest that EZH2 inhibition is an effective therapy for neuroblastoma.

Additionally, MYCN amplification is associated with a low risk of progression in patients with pediatric neuroblastoma. However the presence of other factors that can predict outcome such as age at diagnosis as well as stage of disease is necessary for the use of MYCN amplification as a clinical indicator of the outcome. This could be an important factor in determining a more precise risk assessment for neuroblastoma.

EZH2 is the primary target of MYCN methyltransferase activity within human neuroblastoma cells. This gene is a major target of MYCN which is a tumor-causing protein, during cell differentiation. This enzyme plays a vital role in the survival of human neuroblastoma cells (SK-N-BE(2)).

The MYCN/NAGK proportion of NB can be used to measure the effectiveness of therapy. It is a early biomarker of the growth of tumors and their progression. A lower ratio of MYCN/NAGK is an improvement in response to treatment, whereas higher levels indicate worse outcomes. This indicator is especially useful for patients with recurrence.