Vitamin C and Antioxidants Research
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Analysis of in vivo residual disease after venetoclax/azacitidine treatment identified downregulation of the vitamin C and uric acid transporter SLC23A1, which mediated resistance to multiple therapies, and nominated targeting KHSRP to enhance treatment efficacy and selectively eradicate residual AML.
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Acute myeloid leukemia (AML) is prone to relapse driven by therapy-persistent residual cells. To discover specific vulnerabilities in this population, we performed genome-wide CRISPR interference screens in leukemia cells treated with multiple agents. KHSRP was the top hit, whose depletion sensitized AML cells to therapy and substantially prolonged survival in treated AML-bearing mice. Analysis of in vivo residual disease after venetoclax/azacitidine treatment identified downregulation of the vitamin C and uric acid transporter SLC23A1, which mediated resistance to multiple therapies. KHSRP depletion restored SLC23A1 expression by preventing its ZC3H4-mediated nuclear mRNA degradation. KHSRP depletion therefore enhanced the synergistic cytotoxicity of vitamin C and uric acid, particularly in therapy-persistent leukemia cells. Re-expression of TET2 overrode the chemosensitizing effect of KHSRP depletion in TET2-mutant leukemia, suggesting that KHSRP-linked phenotypes were related to vitamin C and uric acid-mediated TET activation. These findings nominate targeting KHSRP to enhance treatment efficacy and selectively eradicate residual AML.
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@article{Luo2026Therapy,
title = {Therapy-persistent leukemia is selectively vulnerable to SLC23A1 restoration via targeting KHSRP},
author = {Qingyu Luo and Karley S. Whalen and Xiaowei Wu and Anne Fortune and Jacqueline S. Garcia and Kate Marinchev and Lin Zhang and Weiye Qian and Evangeline G. Raulston and Yabing Nan and Christopher A.G. Booth and Kezhi Yan and David E. Root and John G. Doench and Andrew A. Lane},
journal = {Blood Cancer Discovery},
year = {2026},
doi = {10.1158/2643-3230.bcd-26-0030},
url = {https://doi.org/10.1158/2643-3230.bcd-26-0030}
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