Experimental study demonstrates SETD2-mediated tumor suppression via CXCL1 inhibition in lung adenocarcinoma, highlighting potential therapeutic avenues targeting H3K36me3.
suppressing CXCL1-mediated activation of cell cycle, indicating that the regulation of H3K36me3 level by targeting SETD2 and/or the administration of downstream CXCL1 might represent a potential therapeutic way for new treatment in LUAD.
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Zhou et al. (2020) studied this question.
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