c-Myc (Myc) is an oncoprotein, considered one of the most attractive cancer targets given that it is upregulated in most tumors (hematopoietic, central nervous system, GI tract, breast, prostate, lung and more). The inhibition of Myc has been shown to reduce tumor growth and/or survival but after decades of failures to directly drug this protein, C-Myc remains a nearly “undruggable” target. c-Myc overexpression in tumor cells results from direct alterations in its expression or from the constitutive activation of signaling pathways.
As shown in the image above, c-Myc coordinates global cellular protein synthesis through ribosome biogenesis: by the transcriptional control of RNA and protein components of ribosomes, and of gene products required for the processing of ribosomal RNA, the nuclear export of ribosomal subunits and the initiation of mRNA translation. c-Myc regulation of ribosome biogenesis is essential to its physiological functions as well as its pathological role in tumorigenesis (Nat Rev Cancer. 2010 Apr; van Riggelen J.)
Our platform can monitor C-Myc protein translation in tumor cells and identify novel regulators of its translation.
The following images show Anima’s technology being used to detect the down-regulation of total protein translation in Non-Small Cell Lung Cancer (NSCLC) cells in response to C-Myc inhibition. In cells expressing high C-Myc protein (lower left panel, green), high PSM signal is detected (upper left panel, yellow spots), indicating high cellular translation. When C-Myc levels are reduced by siRNA (lower right panel), a marked reduction in total cellular translation is observed (upper right panel, yellow dots).
Status: High content screening assays under validation