Li Lab Finds Intracellular Copper Disrupts Apoptosis

Copper levels increase in inflamed tissues and have been shown to promote colorectal cancer progression. Given that chronic inflammation is distinguished as a cancer risk factor, Xiaoxia Li, PhD, a researcher at Cleveland Clinic Lerner Research Institute and member of the Case CCC's Hematopoietic and Immune Cancer Biology Program, pursued better understanding of the elaborate relationship between inflammation and cancer and how, and why, copper becomes elevated in these conditions.

Her team's investigations revealed that with the presence of the pro-inflammatory cytokine interleukin 17 (IL-17), expression of the STEAP4 protein increased. Increased STEAP4 allowed more copper to enter cells, ultimately decreasing cell death, possibly attributed to intracellular interactions between copper and the XIAP protein which inhibits apoptosis.

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