Curcumin Nanoparticle Induces Apoptosis in Colon Cancer Cells via ROS-Mediated AMPK/mTOR/ULK1 Autophagy Pathway

Area of Science:

• Biochemistry
• Nanotechnology
• Oncology

Background:

• Curcumin exhibits anticancer properties but suffers from poor bioavailability.
• Nanoparticle formulations can improve drug delivery and therapeutic efficacy.
• Autophagy plays a critical role in cancer cell survival and death.

Purpose of the Study:

• To investigate the anti-colon cancer effects of Curcumin-loaded Pluronic F-127 nanoparticles.
• To explore the role of autophagy modulation in the nanoparticles' anti-cancer mechanism.
• To elucidate the specific signaling pathways involved in nanoparticle-induced cancer cell death.

Main Methods:

• Cell proliferation, migration, and apoptosis assays (CCK-8, wound healing, flow cytometry) were performed on CT26 cells.
• In vitro assessment of reactive oxygen species (ROS) and ATP levels.
• Western blotting was used to analyze autophagy- and apoptosis-related protein expression.

Main Results:

• Curcumin nanoparticles inhibited CT26 cell proliferation and colon tumor growth by promoting autophagy.
• Nanoparticles increased ROS levels, reduced mitochondrial membrane potential, and disrupted ATP biosynthesis.
• The decreased ATP/AMP ratio activated the AMPK/mTOR/ULK1 pathway, inducing autophagy-dependent apoptosis.

Conclusions:

• Curcumin-loaded Pluronic F-127 nanoparticles induce autophagy-dependent apoptosis in colon cancer cells.
• The mechanism involves ROS generation, disruption of ATP synthesis, and activation of the AMPK/mTOR/ULK1 signaling pathway.
• These findings offer new therapeutic strategies for colon cancer treatment.