Emodin Triggers Telomere Dysfunction in Hela Cells

Abstract: This study was aimed to investigate the effect of emodin， an anticancer drug and chmosensitizer， on telomere and telomerase activity in Hela cells. Telomere specific DNA damage level was detected by phosphated histone family 2A variant (H2AX)， referred as γ-H2AX immunofluorescence-telomere fluorescence in situ hybridization. Metaphase-telomere FISH was used to detect abnormal telomere signals， including multitelomeric signals (MTSs) and telomere signal free ends (SFEs). Quantitative real-time PCR and telomere repeat amplification protocol were used to detect relative telomere length and telomerase activity respectively. The results demonstrated that compared with the control group (0 μmol/L)， emodin (20 μmol/L) treatment for 48 h shortened the telomere length to 80% and increased the frequency of telomere dysfunction induced foci (TIFs) and abnormal telomere signals， including MTSs increasing from 1.65% to 3.98% (P<0.01) and SFEs increasing from 2.74% to 8.49% (P<0.01). To our surprise， telomerase up-regulation was detected following emodin treatment. The telomerase activities of Hela cells treated by 10 μmol/L and 20 μmol/L emodin for 48 hours were up-regulated to 1.42 times (P<0.05) and 1.92 times (P<0.01) respectively compared with the control group. Taken together， the results suggested that emodin acute treatment triggered telomere dysfunction and telomerase activity up-regulation. The elevated telomerase activity induced by emodin may be related to repairment after telomere dysfunction.

CSTR: 32200.14.cjcb.2018.02.0003