MYC and colonic neoplasm: Notably, these attributes were evident in the sustained intracellular mRNA cleavage activity for both exogenously transfected eGFP and endogenously over-expressed c-MYC oncogene with no or minimal activation of RNase H. The potent inhibition of oncogenic c-MYC mRNA by these ASO-like 10–23 variants within colon cancer cell line HCT116, effectively reduced the c-Myc protein expression, which subsequently caused G1 phase cell cycle arrest, decreased proliferation, and increased apoptosis of HCT116 cells.