investigation of the cytotoxic and antiproliferative effects of liposomal daunorubicin on human colorectal cancer (hct116) cell line

Background: the incidence of colorectal cancer is increasing globally. daunorubicin (dnr), an anthracycline antibiotic, is effective against various cancers. the pi3k/akt/mtor signaling pathway is crucial in regulating cell growth and cancer growth. objectives: this study aims to evaluate the effects of liposomal daunorubicin (lip-dnr) on cell proliferation and cell death induction in hct116 cells compared to free daunorubicin. methods: lip-dnr was synthesized, and its shape and size were analyzed using fe-sem imaging. hct116 cells were treated with lip-dnr concentrations of 0 (control), 0.125, 0.25, 0.5, 1, and 2 μm for 48 hours to determine the ic50. the effects of free (0.5 μm) and liposomal dnr (ic50 of 0.43 μm) on pi3k mrna levels were assessed using real-time pcr. the cell cycle was analyzed by flow cytometry. results: fe-sem imaging showed that the liposomes are spherical and range from 50 - 100 nm in size. lip-dnr induced cell death in hct116 cells in a dose-dependent manner, with 0.5 μm lip-dnr causing more cell death than an equivalent concentration of free dnr. analysis of pi3k gene expression showed that dnr decreases pi3k gene transcription in hct116 cells, with lip-dnr having a more substantial effect than the free form. both forms reduced the proportion of g2/m phase cells, but lip-dnr was more effective at inhibiting cell proliferation in hct116 cells. conclusions: dnr inhibits the proliferation of hct116 cells by downregulating pi3k gene expression and enhancing cell death, with the liposomal form demonstrating stronger effects than the free form.