Bcl7a, a subunit of the SWI/SNF chromatin remodeling complexes, plays crucial roles in various biological processes. It is involved in regulating gene expression, and its function is associated with pathways such as Notch/Wnt signaling. Bcl7a is essential for neural progenitor cell (NPC) differentiation, mitochondrial bioenergetics, and also has implications in tumorigenesis [1].

In NPCs, conditional Bcl7a knockout mice revealed that Bcl7a expression in NPCs and postmitotic neurons is required for neuronal plasticity and supports behavioral and cognitive performance. Bcl7a-containing SWI/SNF/BAF complexes modulate mitochondrial respiration during NPC differentiation. Pharmacological stimulation of Wnt signaling or treatment with pioglitazone can restore mitochondrial respiration in Bcl7a-deficient NPCs [1].

In acute myeloid leukemia (AML), Bcl7a expression is silenced by promoter hypermethylation. Restoration of Bcl7a expression exerts tumor suppressor activity in AML cell lines and xenograft models [2]. Also, upregulation of Bcl7a in AML impedes cell growth, induces apoptosis, promotes differentiation, and decreases drug-resistance through the IRF7/HMGCS1 pathway [3].

In glioma, Bcl7a expression is lower in tumor tissues compared to non-tumor brain tissues, and it is an independent prognostic biomarker. High Bcl7a expression is associated with longer survival in glioblastoma patients receiving chemotherapy combined with radiotherapy [4].

In ovarian cancer, low Bcl7a expression is an independent risk factor for poor prognosis [5].

In summary, Bcl7a is essential for regulating mitochondrial bioenergetics during neural progenitor differentiation and acts as a tumor suppressor in multiple cancers including AML, glioma, and ovarian cancer. The use of Bcl7a knockout or conditional knockout mouse models has provided valuable insights into its role in neuronal plasticity, cognitive performance, and tumorigenesis, offering potential therapeutic targets for related diseases.