MYC

Official Full Name

lysozyme

Organism

Homo sapiens

GeneID

4069

Background

This gene encodes human lysozyme, whose natural substrate is the bacterial cell wall peptidoglycan (cleaving the beta[1-4]glycosidic linkages between N-acetylmuramic acid and N-acetylglucosamine). Lysozyme is one of the antimicrobial agents found in human milk, and is also present in spleen, lung, kidney, white blood cells, plasma, saliva, and tears. The protein has antibacterial activity against a number of bacterial species. Missense mutations in this gene have been identified in heritable renal amyloidosis. [provided by RefSeq, Oct 2014]

Synonyms

LZM; LYZF1; AMYLD5;

Bio Chemical Class

Glycosylase

Protein Sequence

MKALIVLGLVLLSVTVQGKVFERCELARTLKRLGMDGYRGISLANWMCLAKWESGYNTRATNYNAGDRSTDYGIFQINSRYWCNDGKTPGAVNACHLSCSALLQDNIADAVACAKRVVRDPQGIRAWVAWRNRCQNRDVRQYVQGCGV

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Detailed Information

MYC is a potent proto-oncogene originally found in the Burkitt's lymphoma t(8; 14) (q24; q32) chromosome. MYC is a member of the nuclear transcription factor helical leucine zipper family. Like its family members C-MYC, N-MYC, and L-MYC, MYC is a transcription factor. MYC plays its functional role based on nuclear localization sequences, DNA binding regions, helix-loop-helix dimerization regions and transcriptional regulatory regions.

The Role of MYC

Most of the MYC-regulated genes are activated genes, but a few are inhibitory gene expressions. The most common suppressor genes are cell cycle checkpoints such as cell growth arrest and death, and cell communication. It can be seen that when the activation function and the inhibitory function of the MYC gene are combined to stimulate cell growth and cell cycle inhibition, unrestricted replication of the cells is caused, thereby causing cell transformation. In addition to the role of MYC in transcriptional regulation, MYC may also have a direct regulatory effect on DNA replication. Studies have confirmed that MYC stimulates DNA replication by promoting replication initiation activity in the resting state of gene transcription. At the cost of increased DNA damage associated with replication, cell cycle checkpoints are activated and channel replication is inhibited.

In addition to its role at the level of DNA replication and transcription, MYC also plays a direct and indirect (independent of transcription) role in regulatory protein translation. For example, the MYC transactivation gene encoding RNA, ribosome constituent proteins, nutrient carriers, and nucleotide synthetases provide support for ribosome transfer. In addition, MYC promotes cap-dependent translation through direct stimulation of cap methylation, translation initiation factors, and transcriptional activation of mRNA capping genes. The production of tRNA is also stimulated by the action of the MYC gene under the action of transcribed RNA polymerase III.

Figure 1. MYC regulation in noncancerous and cancerous cells. (Stine, Z. E., et al. 2015)

MYC and Cancer

Small cell lung cancer (SCLC) is an aggressive malignant tumor. Several recurrent genetic aberrations have been identified in SCLC, including the MYC gene, including C-MYC, L-MYC, and N-MYC. MYC family members were observed to expand and overexpress in a mutually exclusive manner in 20% to 40% of SCLC cell lines and patient tumors. Studies have shown that C-MYC gene amplification in 2% to 7% of SCLC is more common in patients with SCLC. C-MYC amplification can lead to morphological changes in SCLC and rapid growth in vitro, resulting in radiation tolerance and shortened survival in patients.

N-MYC was found to be highly expressed in epithelial cells of embryonic rat lungs, and conditional deletion of N-MYC leads to inhibition of cell proliferation and extensive cell death, so N-MYC is essential for the normal development of early cells. However, N-MYC expansion or overexpression further leads to the development of lung cancer and may occur early in metastasis. It has been demonstrated in patients with SCLC that N-MYC overexpression has a major impact on the treatment and prognosis of patients with SCLC. Patients with N-MYC overexpression had a short survival period and a positive correlation with the adverse reactions of chemoradiotherapy in these patients.

References:

Huijbers, I. J. , Bin Ali, R. , Pritchard, C. , Cozijnsen, M. , Kwon, M. C. , & Proost, N. , et al. (2014). Rapid target gene validation in complex cancer mouse models using re-derived embryonic stem cells. EMBO Molecular Medicine, 6(2), n/a-n/a.
Mollaoglu, G. , Guthrie, M. R. , B?Hm, S. , Br?Gelmann, J. , Can, I. , & Ballieu, P. M. , et al. (2017). Myc drives progression of small cell lung cancer to a variant neuroendocrine subtype with vulnerability to aurora kinase inhibition. Cancer Cell, 31(2), 270-285.
Stine, Z. E. , Walton, Z. E. , Altman, B. J. , Hsieh, A. L. , & Dang, C. V. . (2015). Myc, metabolism, and cancer. Cancer Discovery,5(10), 1024.

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