ArticleActa neuropathologica communications2026
LncRNA-HLX-2-7/HLX axis-dependent metabolic reprogramming drives cancer progression in group 3 medulloblastoma.
Article in Acta neuropathologica communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Group 3 medulloblastoma (G3 MB) is an aggressive pediatric brain tumor with limited treatment options, necessitating the development of novel therapeutic strategies. The long noncoding RNA (lncRNA) lnc-HLX-2-7 and its host-coding transcription factor, HLX, are highly expressed in G3 MB and act as oncogenic drivers. However, their role in regulating metabolism in G3 MB remains poorly understood. In this study, we investigate the metabolic functions of lnc-HLX-2-7 in D425-Med and MED211 cells and uncover its role in regulating oxidative phosphorylation (OXPHOS) and ATP production through the TCA cycle. Our findings reveal that lnc-HLX-2-7 is an upstream regulator of HLX, which, in turn, directly controls the expression of OXPHOS-related genes. Specifically, inhibition of lnc-HLX-2-7 and HLX significantly reduces the expression of OXPHOS complexes I (NDUFB8), II (SDHB), and IV (MTCO1) by disrupting direct binding to and activating the promoters of these genes. Targeting oxidative phosphorylation with the small-molecule inhibitor IACS-010759 substantially inhibits G3 MB tumor progression in xenograft models, further supporting the critical role of OXPHOS in tumor progression. Rescue experiments demonstrate that overexpression of HLX in lnc-HLX-2-7-depleted cells restored OXPHOS gene expression and ATP production, confirming HLX as a downstream effector of lnc-HLX-2-7. These results highlight a coordinated lnc-HLX-2-7/HLX axis that regulates metabolism and oncogenesis in G3 MB. In conclusion, our findings establish lnc-HLX-2-7 and its host-coding gene, HLX, as critical regulators of OXPHOS reprogramming and propose these molecules as promising therapeutic targets for this high-risk MB subtype.
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