A key tactic in cancer treatment is the suppression of oncogene expression, which aims to interfere with the molecular causes of carcinogenesis. Degrading oncogenic messenger RNAs (mRNAs) is one novel strategy for stopping the synthesis of proteins essential for tumor development and progression. Two promising medications that best represent this therapy paradigm are dovitinib, a multi-kinase inhibitor, and MRG-106, an antisense oligonucleotide. MRG-106 primarily targets miR-155, a microRNA linked to solid tumors and hematological malignancies’ deregulation of oncogenic pathways. By inhibiting miR-155, MRG-106 causes tumor cells to undergo apoptosis, decrease proliferation, and restore normal cellular signaling. A multi-kinase inhibitor called dovitinib provides a supplementary strategy by modifying fibroblast growth factor receptor (FGFR) and vascular endothelial growth factor receptor (VEGFR)-related pathways, which are essential for tumor angiogenesis and survival. Because dovitinib changes transcriptional activity, inhibits angiogenesis, and increases tumor cell susceptibility to death, it indirectly promotes the destruction of oncogenic mRNA. These two modes of action demonstrate how well dovitinib targets a variety of cancer types. This chapter offers a thorough analysis of MRG-106 and dovitinib’s molecular mechanisms of action, preclinical and clinical results, and therapeutic uses. Additionally, it talks about how they might be included into combination regimens to get around drawbacks like resistance, off-target effects, and delivery difficulties. To fully utilize these drugs’ therapeutic potential, these obstacles must be removed. In the age of precision medicine, these cutting-edge methods could transform cancer treatment and enhance patient outcomes by deepening our understanding of mRNA degradation technology.