Colon Cancer

P1/2, N=83, Recruiting, Virginia Commonwealth University | Trial completion date: May 2027 --> Jan 2031 | Trial primary completion date: May 2026 --> Dec 2029

P2, N=128, Enrolling by invitation, Blokhin's Russian Cancer Research Center

P3, N=190, Recruiting, Taizhou Hanzhong biomedical co. LTD | Not yet recruiting --> Recruiting | Trial primary completion date: Jan 2026 --> Jun 2026

MIc promoted apoptosis in CT26 and HCT116 cells and inhibited CAC progression. MIc effectively suppresses CAC development by regulating macrophage mitochondrial function via the SENP1/MTCH2 pathway, reducing M1 polarization and promoting apoptosis in colorectal cancer cells.

RMSD and RMSF analyses revealed that naringin, the major compound of I. aschersoniana, exhibited dynamically stable binding within the active sites of AKT1, EGFR, and PPARG proteins, with AKT1@Naringin and PPARG@Naringin complexes displaying a more stable dynamic profile. In this network pharmacology study, forty-five common targets between the major compounds of I. aschersoniana with breast and colon cancers were identified.

Our findings establish engineered STING-activating bacteria as a transformative approach for cancer immunotherapy, offering: 1) targeted delivery of STING agonists to tumors, 2) reversal of immunosuppressive microenvironments, and 3) synergy with existing checkpoint blockade therapies. This platform addresses critical challenges in the field and presents new opportunities for treating immunotherapy-resistant cancers.

RT-PCR confirmed the downregulation of METTL3, aligning with tumor suppression. These results demonstrated that hypoxia-sensitive mPEG-Azo-PEI@siRNA2 nanoparticles effectively delivered siRNA2 and inhibited HCT116 cell proliferation, offering a promising hypoxia-activated targeting strategy for colon cancer therapy.

Targeting fatty acid metabolism-related genes represents a promising therapeutic strategy for colon cancer (CC) that could pave the way for personalized treatment and enhanced patient survival.

This study suggests that CCL3 could serve as a potential prognostic marker for COAD and other cancers. Because CCL3 expression was strongly associated with immune modulation within the tumor microenvironment, this pointed out that CCL3 could serve as a promising therapeutic target with significant implications for immunotherapy and chemotherapy response.

In the validation set, the combined model maintained an AUC of 0.92 (95% CI: 0.86-0.99), outperforming the clinical model (AUC=0.71, P=0.004), and showed good calibration (Hosmer-Lemeshow P=0.364) and positive net benefits in DCA. The combined model integrating clinical features and CT radiomics exhibits excellent performance in preoperative prediction of LVSI in colon cancer, providing a reliable tool for individualized treatment decision-making.

In conclusion, Scd1 knockout in macrophages accelerates colon cancer by promoting M2 polarization via inhibition of the Hippo-YAP pathway, impairing CD8+ T cell function. Targeting the Scd1-Hippo-YAP signaling axis may offer a promising new approach for immunotherapy in colon cancer.

These findings suggest that increased RUVBL1 expression is associated with poor prognosis and altered immune infiltration in COAD patients. RUVBL1 may serve as a potential therapeutic target for COAD.