Targeting CARM1 impairs DNA damage repair and attenuates B-cell acute lymphoblastic leukemia progression.

Authors

Peiyun Liao, Yingqi Qiu, Meifang Li, Rong Hu, Hao Wang, Honghao Zhang, Suwan Wu, Zhao Liang, Yuhua Li

Published in

Biochimica et biophysica acta. Molecular basis of disease. Pages 168444. Aug 30, 2026. Epub Aug 30, 2026.

Abstract

B-cell acute lymphoblastic leukemia (B-ALL) is a prevalent hematological malignancy, posing difficulties in identifying efficacious treatment strategies for refractory and recurrent patients. Our research revealed that coactivator-associated arginine methyltransferase 1 (CARM1) was highly expressed in B-ALL and associated with unfavorable prognostic outcomes. Down-regulation and inhibition of CARM1 effectively suppressed proliferation and colony formation of B-ALL, while also inducing apoptosis and cell cycle arrest. Mechanistically, inhibition or down-regulation of CARM1 reduced PARP1 level and contributed to double-strand breaks (DSBs) accumulation. Inhibition of CARM1 and PARP1 synergistically supressed B-ALL development. Significantly, the inhibition of CARM1 was found to promote memory differentiation and reduce the exhaustion of CD19-CAR-T cells. Taken together, CARM1 inhibition not only suppressed B-ALL but also enhanced the durability of CAR-T cells against B-ALL, which provides novel insights into the tumor suppression and immune regulation of CARM1 inhibition on cancer therapy.

PMID:
42669369
Bibliographic data and abstract were imported from PubMed on 31 Aug 2026.

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