Objective:

To identify HK2-associated tumour processes that could serve as therapeutic co-targets by profiling the transcriptomic consequences of HK2 knockdown in glioblastoma cell lines and patient-derived cultures.

Approach:

Key Findings:

• HK2KD was associated with reduced glycolytic activity in high-HK2-expressing models.
• Extensive transcriptional remodelling was observed, linking metabolic activity to inflammatory and angiogenic gene programmes.
• Inflammatory pathway responses diverged markedly between independent glioblastoma models.

Interpretation:

HK2KD is associated with transcriptional changes that extend beyond glycolytic pathways, linking metabolic activity to immunological and angiogenic transcriptional networks in a model-dependent manner.

Limitations:

• Functional effects on the tumour microenvironment were not directly assessed.

Conclusion:

The study provides a transcriptomic framework for understanding how HK2 targeting may be associated with changes in tumour-associated signalling pathways.

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