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Life sciences · Journal article
Pharmacological Research · October 24, 2026
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Differentiation-based cancer therapy is a potentially low-toxicity approach with demonstrated clinical benefits. However, the therapeutic efficacy of differentiation therapy remains limited in tumor types other than acute promyelocytic leukemia (APL). Our previous studies reported that diptoindonesin G (Dip G), a natural compound, can induce differentiation in both acute myeloid leukemia (AML) cells and basal-like breast cancer cells. In this study, we report a crucial role of GABAA receptor-associated protein-like 1 (GABARAPL1) in driving cancer cell differentiation. By utilizing myeloid cell differentiation models and primary leukemic cells, we demonstrate that upregulation of GABARAPL1 expression was crucial for Dip G-induced differentiation and that Dip G upregulated GABARAPL1 expression by targeting nucleolin (NCL). Also, GABARAPL1 promoted differentiation independent of its autophagic function. Both pharmacological and genetic upregulation of GABARAPL1 expression effectively overcame the differentiation blockade in various tumor models, including AML cells. Mechanistically, GABARAPL1 interacted with splicing factor proline and glutamine rich (SFPQ) and recruited MDM2 to promote the degradation of SFPQ by the proteasome. Upon SFPQ depletion, the transcription of linker histone H1.2 gene was repressed, which in turn rescued the transcription of the differentiation-related pathway. Our study not only highlights the contribution of GABARAPL1 to differentiation but also provides a potential therapeutic strategy aimed at expanding the scope of application of differentiation-based cancer therapy.