Figure 1.

Schematic illustration of the AO-induced anticancer effect. (Upper): normal cell and tissue. (Middle): activation of oncogene leads to production of oncogenic proteins, and the aberrant splicing of normal gene results in splice variants that are translated into carcinogenic protein isoforms; these carcinogenic proteins collectively promote cancer cell proliferation. (Lower): AO-mediated splice switching can not only correct the aberrant splicing, thus reducing the production of carcinogenic protein isoforms (this is the focus of the present review), but can also induce premature stop codons in oncogenic mRNA that results in the synthesis of largely truncated, nonfunctional oncogenic proteins (this is a potential anticancer strategy). Collectively, AO intervention can inhibit cancer cell proliferation.