Elucidating the mechanism of cellular uptake and
Here we review structural and functional features of c-Myc and highlight to discuss possible small molecule modulators of c-Myc as promising anti-cancer therapeutics. Some 20 years ago, c-Myc was discovered in human Burkitt's lymphoma, as a celluar homologue of the viral oncogene v-Myc which was isolated from an avian retrovirus [7, 8].
It is considered as a master regulatory factor of cell proliferation, metabolism, differentiation, and apoptosis.
On the basis of the study of v-Myc in chicken, the expression of human c-Myc was found to be altered in cancer.
c-Myc is deregulated in a wide range of malignancies, such as mammary carcinoma, colon carcinoma, cervical carcinoma, myeloid leukaemia, melanoma osteosarcoma, glioblastoma, and small-cell lung carcinoma . 1) is located on chromosome 8 q24.1 and consists of three exons and two introns . Apoptosis triggered by Myc-induced suppression of Bcl-X(L) or Bcl-2 is bypassed during lymphomagenesis.
Small Molecules Targeting c-Myc Oncogene: Promising Anti-Cancer Therapeutics. The c-Myc gene is activated by chromosomal translocation, rearrangement, and amplification. c-Myc suppression of mi R-23a/b enhances mitochondrial glutaminase expression and glutamine metabolism.
Its encoded protein transduces intracellular signals to the nucleus, resulting in the regulation of cell proliferation, differentiation, and apoptosis, and has the ability to transform cells and bind chromosomal DNA.
Aberrant expression of c-Myc is likely to ascribable to direct gene alteration, which associates with tumorigenesis and sustained tumor growth [2-4].