How does Myc contribute to cancer?
MYC activation leads to tumorigenesis through suppression of critical safeguards such as apoptosis, proliferative arrest, differentiation, and senescence. Activation of MYC also facilitates engagement of hallmarks of tumor growth, as well as cell-extrinsic phenomena such as host immunity.
Why is Myc hard Targeting?
Yet, drug development aimed at directly targeting Myc has proved challenging. First, as a transcription factor, Myc lacks a specific active site for small molecules, making it difficult to functionally inhibit its activities using strategies similar to those used for kinases.
Does overexpression of Myc cause cancer?
MYC is documented to be involved broadly in many cancers, in which its expression is estimated to be elevated or deregulated in up to 70% of human cancers. High levels of MYC expression have been linked to aggressive human prostate cancer and triple negative breast cancer (Gurel et al., 2008; Palaskas et al., 2011).
What is Myc driven cancer?
As expected, the MYC oncogene is a central driver in multiple cancers, such as breast cancer,6 liver tumor,7 colorectal carcinoma,8 and prostatic neoplasia. 9. High and/or aberrant Myc expression occurs in >70% human cancers and is related to poor prognosis and aggressive conditions.
Is Myc an oncogene or tumor suppressor?
Although the Myc gene was originally identified as an oncogene, it is involved in various cellular processes, including cell growth, proliferation, loss of differentiation, and apoptosis (Adhikary and Eilers, 2005; Pelengaris et al., 2002; Thompson, 1998).
How is Myc mutated?
In addition to MYC rearrangement, MYC mutation is another form of genetic abnormality found in Burkitt lymphoma. Multiple nonsynonymous mutations in the coding sequence (CDS) of the MYC gene have been found in approximately 40–70% of Burkitt lymphoma leading to a mutated Myc protein with amino acid changes (6–9).
How does myc become an oncogene?
In B cells, Myc acts as a classical oncogene by regulating a number of pro-proliferative and anti-apoptotic pathways, this also includes tunning of BCR signaling and CD40 signaling is regulation of microRNAs (miR-29, miR-150, miR-17-92).
Is Myc a tumor suppressor gene?
The tumor suppressor p53 negatively regulates a number of genes, including the proto-oncogene c-Myc, in addition to activating many other genes. One mechanism of the p53-mediated c-Myc repression may involve transcriptional regulation.
How is myc regulated?
Because of its oncogenic potential, the MYC proto-oncogene is tightly regulated in normal cells at the transcriptional and posttranscriptional levels (Fig. 1A; ref. 10). Posttranscriptionally, it is regulated by miRNAs and by translation of its mRNA (11–13).
Why myc is a proto-oncogene?
The proto-oncogene Myc is a transcription factor that promotes cell growth and proliferation, and regulates cell metabolism. Its overexpression also causes chromosomal instability. Overexpression of myc directed by the albumin promoter leads to development of HCC in more than 80% of male mice at 16 months.
What is the difference between myc and c-myc?
In cancer, c-myc is often constitutively (persistently) expressed. This leads to the increased expression of many genes, some of which are involved in cell proliferation, contributing to the formation of cancer….Myc.
|MYC proto-oncogene, bHLH transcription factor|
|Alt. symbols||c-Myc, v-myc|
Is there a therapeutic inhibition of Myc in cancer?
Therapeutic Inhibition of Myc in Cancer. Structural Bases and Computer-Aided Drug Discovery Approaches Therapeutic Inhibition of Myc in Cancer.
What is Myc and why is it so important?
MYC certainly seems to be at the crossroads of many important biological pathways and processes involved in neoplastic cell growth and proliferation. MYC is documented to be involved broadly in many cancers, in which its expression is estimated to be elevated or deregulated in up to 70% of human cancers.
What is the role of Myc in the pathophysiology of cancer?
In cancer, genetic deregulation of MYC expression and loss of checkpoint components, such as TP53, permit MYC to drive malignant transformation.
How can we stop Myc-induced MYC on the path to cancer?
Other approaches to halt Myc on the path to cancer involve targeting Myc-Max dimerization or Myc-induced microRNA expression. Here the richness of our understanding of MYC is reviewed, highlighting new biological insights and opportunities for cancer therapies.