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August 15, 2025Open Access

Figure S5 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 promotes TKI resistance in non-small cell lung cancer by enhancing glutamine metabolism,
Key evidence shows increased expression of MYLK-AS1 correlates with EGFR inhibitor resistance outcomes,
Observational analysis highlights the role of METTL3 in regulating MYLK-AS1 expression,
Study suggests targeting MYLK-AS1 may offer potential therapeutic strategies against TKI resistance.

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Implication

Research demonstrates MYLK-AS1 enhances glutamine metabolism in non-small cell lung cancer, suggesting a role in TKI resistance.

Abstract

METTL3 induces the expression of MYLK-AS1 and promotes TKI resistance.

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Cite This Study

Qu et al. (2025) studied this question.

synapsesocial.com/papers/68af59d2ad7bf08b1eade1e2 https://doi.org/10.1158/0008-5472.29919045

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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 S10 from MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non–Small Cell Lung Cancer2025
3Figure S4 from MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non–Small Cell Lung Cancer2025
4Figure S7 from MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non–Small Cell Lung Cancer2025
5Figure S2 from MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non–Small Cell Lung Cancer2025