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August 15, 2025Open Access

Figure S4 from MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non–Small Cell Lung Cancer

Tianyu Qu Lei Song Jiali Xu Xiyi Lu Dandan Yin Jiali Dai Chen Zhang Renhua Guo Erbao Zhang

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Key Points

MYLK-AS1 enhances glutamine metabolism to promote resistance to EGFR inhibitors in NSCLC, revealing a potential therapeutic target.
Key evidence shows that transcriptional activation of MYLK-AS1 is mediated by C-Myc in TKI-resistant models of NSCLC.
Analysis indicates MYLK-AS1's role in resistance mechanisms through metabolism, which could inform future treatment strategies.
Highlights the need for alternative approaches to overcome TKI resistance, particularly in non-small cell lung cancer patients.

Implication

Observational analysis showed MYLK-AS1 enhances glutamine metabolism in non-small cell lung cancer, suggesting a role in TKI resistance.

Abstract

C-Myc mediated transcriptional activation contributes to the activation of MYLK-AS1 in TKI resistance of NSCLC.

Discussion

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Cite This Study

Qu et al. (2025) studied this question.

synapsesocial.com/papers/68af59d2ad7bf08b1eade1e1 https://doi.org/10.1158/0008-5472.29919048

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Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

1Figure S6 from MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non–Small Cell Lung Cancer2025
2Figure S5 from MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non–Small Cell Lung Cancer2025
3Figure S2 from MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non–Small Cell Lung Cancer2025
4Figure S10 from MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non–Small Cell Lung Cancer2025
5Figure S7 from MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non–Small Cell Lung Cancer2025