<i>Gemella morbillorum</i> Promotes Colorectal Carcinogenesis: LPBDCP‐Mediated Invasion Activates Ras Signaling and Destabilizes p53

influx, downregulates RASA4, and activates the PI3K-AKT-NF-κB and RAF-MEK-ERK signaling pathways. Following invasion, Gemella morbillorum secretes NAD-dependent protein deacetylase (NDPD), which induces p53 deacetylation and degradation. Collectively, these events accelerate cell proliferation, shorten the cell cycle, and inhibit apoptosis, thereby promoting malignant transformation. Genetic knockout of LPBDCP or TMEM140 effectively inhibits bacterial invasion and abrogates the oncogenic effects of Gemella morbillorum. In tumor-bearing mice, knockout of LPBDCP or NDPD eliminates the tumor-promoting effects of Gemella morbillorum. These results underscore Gemella morbillorum's role in CRC and pinpoint potential intervention targets.