Fig. 9: CYLD induces high oxidative stress and DNA damage through class I HDACs to promote radiosensitivity in nasopharyngeal carcinoma. | Cell Death & Disease

Fig. 9: CYLD induces high oxidative stress and DNA damage through class I HDACs to promote radiosensitivity in nasopharyngeal carcinoma.

From: CYLD induces high oxidative stress and DNA damage through class I HDACs to promote radiosensitivity in nasopharyngeal carcinoma

Fig. 9

We discovered a mechanism which CYLD binds to and inhibits class I HDACs enzyme functions by inducing HDAC1 acetylation. While class I HDACs mediate redox abnormalities and DNA damage repair, which leading to radiotherapy resistance in CYLD low-expressing tumors. Blocking HDACs by class I HDACs inhibitor Chidamide could effectively decrease radioresistance in vitro and in vivo. HDACi Chidamide could be a promising therapeutic strategy in CYLD low-expressing tumors to increase tumor radiotherapy sensitivity. (Ac acetylation, HDAC1(blue background: inactive; red background: active)).

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