MYC is a transcription factor that increases the expression of genes that are im

Question

MYC is a transcription factor that increases the expression of genes that are important for cell proliferation and survival. Overexpression of MYC protein is a common feature of many types of cancer cells. When MYC is overexpressed in NORMAL cells the result is not excessive cell proliferation, but cell-cycle arrest and apoptosis.

(1) Why would MYC be considered an oncogene rather than a tumor suppressor?

a. Myc is an oncogene, because it regulates cell proliferation

b. Myc is an oncogene, because overactivation of Myc leads to cancer

c. Myc is a tumor suppressor, because it regulates apoptosis.

d. Myc is tumor suppressor, because mutation in Myc would alter the rate of apoptosis

(2) What might need to occur in normal cells in addition to overexpression of MYC to produce the excessive cell proliferation phenotype?

a. Mutation in a growth factor receptor

b. Mutation in Ras

c. Mutation in p53

Explanation / Answer

(1)     b. Myc is a proto-oncogene. Its expression is highly regulated, hence its level of expression is tightly control by a number of mechanisms involving many transcriptional regulatory motifs found within its proximal promoter region. When there is a loss of transcriptional control, it becomes deregulated, leading to protein over-expression and thus oncogenesis (cancer delopment).

(2)     b. Mutation in Ras gene occurs, in addition to overexpression of MYC to produce the excessive cell proliferation phenotype. MYC is a proto-oncogene, codes for a transcription factor. Mutations in MYC lead its conversion from proto-oncogene to oncogene which is associated with seventy percent of cancers. Apart from MYC, RAS is another oncogene that normally functions as an “on-off” switch in the signal cascade. Mutations in RAS cause the signaling pathway to remain “on,” leading to uncontrolled cell growth. In proliferating cells, Myc protein is expressed at low levels with an extremely short half-life of 30 minutes. Upon serum stimulation, Ras mediates the stabilization of c-Myc by promoting its phosphorylation by ERK on Ser 62. This triggers subsequent phosphorylation of Thr 58 by GSK3 resulting in the destabilization of c-Myc.

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