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H3K27 activates USP53. 3 / 3
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"USP53 activated by H3K27 acetylation regulates cell viability, apoptosis, and metabolism in esophageal carcinoma via the AMPK signaling pathway."
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"This study finally revealed that USP53 was activated by H3K27 acetylation in a variety of ESCA cells, whereafter suppressing proliferation, promoting apoptosis, and inducing mitochondrial damage by inactivating the AMPK pathway.Radiotherapy is one of the main treatments for ESCA, but some patients are susceptible to radiotherapy resistance."
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"Cheng et al. [60] reported that USP53 inhibited the proliferation and growth of esophageal carcinoma cells in vitro and in vivo, and that USP53 activation by H3K27 acetylation modulates cell viability via the AMPK signaling pathway."
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