AIM2 overexpression

These results reveal the Ednrb-Aim2-AKT axis in regulating melanocyte development and suggest that Ednrb signaling functions as a negative regulator of Aim2, which inhibits the proliferation of melanoblasts in early development. These findings uncover a previously unreported role for Aim2 outside the inflammasome, showing that it is a significant regulator controlling NC stem cell-derived lineage development.

Overall, our study suggests that AIM2 is a reliable anti-inflammatory therapeutic target for AS. Inhibiting AIM2 expression may reduce foam cell formation and, consequently, inhibit the progression of AS plaques.

Altogether, our achievements distinctly underscored AIM2's antitumor role in CRC. AIM2 overexpression inhibited proliferation and migration and induced apoptosis of CRC cells via activating P38MAPK signaling pathway, indicating AIM2 as a prospective and novel therapeutic target for CRC.

Additionally, our study found that the suppression of AIM2 could significantly enhance the proliferation, invasion, and migration capabilities of colon cancer cells. In this research, we identified a novel prognostic signature suggesting that patients with higher AIM2 expression levels are more likely to respond favorably to immunotherapy.