Ra-223 induces clustered DNA damage and inhibits cell survival in several prostate cancer cell lines
Andris Abramenkovs, Mehran Hariri, Diana Spiegelberg, Sten Nilsson, Bo Stenerlöw
Abstract
M) and almost no dissociation was detected within 24 h. Importantly, there was no significant uptake of Ra-223 in cells. The Ra-223 alpha-particle decay produced track-like distributions of the DNA damage response proteins 53BP1 and ɣH2AX induced high amounts of clustered DSBs in prostate cancer cells and activated DSB repair through non-homologous end-joining (NHEJ). Ra-223 inhibited growth of prostate cancer cells, independent of cell type, and induced high levels of apoptosis. In summary, we suggest the high cell killing efficacy of the Ra-223 was attributed to the clustered DNA damaged sites induced by α-particles.
Topics & Concepts
Prostate cancerCancer researchDNA damageApoptosisProgrammed cell deathCellCancer cellChemistryDNADNA repairCancerMedicineMolecular biologyBiologyInternal medicineBiochemistryRadiopharmaceutical Chemistry and ApplicationsProstate Cancer Treatment and ResearchDNA Repair Mechanisms