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Inhibition of the m6A reader IGF2BP2 as a strategy against T-cell acute lymphoblastic leukemia.

ABSTRACT: T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignant leukemia with extremely limited treatment for relapsed patients. N6-methyladenosine (m6A) reader insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) participates in the initiation and growth of cancers by communicating with various targets. Here, we found IGF2BP2 was highly expressed in T-ALL. Gain and loss of IGF2BP2 demonstrated IGF2BP2 was essential for T-ALL cell proliferation in vitro and loss of IGF2BP2 prolonged animal survival in a human T-ALL xenograft model. Mechanistically, IGF2BP2 directly bound to T-ALL oncogene NOTCH1 via an m6A dependent manner. Furthermore, we identified a small-molecule IGF2BP2 inhibitor JX5 and treatment of T-ALL with JX5 showed similar functions as knockdown of IGF2BP2. These findings not only shed light on the role of IGF2BP2 in T-ALL, but also provide an alternative γ‑Secretase inhibitors (GSI) therapy to treat T-ALL.

SUBMITTER: Feng P 

PROVIDER: S-EPMC9417996 | biostudies-literature | 2022 Sep

REPOSITORIES: biostudies-literature

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Inhibition of the m<sup>6</sup>A reader IGF2BP2 as a strategy against T-cell acute lymphoblastic leukemia.

Feng Panpan P   Chen Dawei D   Wang Xia X   Li Yanxia Y   Li Zhenyu Z   Li Boya B   Zhang Yupeng Y   Li Wei W   Zhang Jingru J   Ye Jingjing J   Zhao Baobing B   Li Jingxin J   Ji Chunyan C  

Leukemia 20220801 9

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignant leukemia with extremely limited treatment for relapsed patients. N6-methyladenosine (m<sup>6</sup>A) reader insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) participates in the initiation and growth of cancers by communicating with various targets. Here, we found IGF2BP2 was highly expressed in T-ALL. Gain and loss of IGF2BP2 demonstrated IGF2BP2 was essential for T-ALL cell proliferation in vitro and loss of IGF  ...[more]

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