Figure S8 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

doi:10.1158/0008-5472.29919036

August 15, 2025Open Access

Figure S8 from MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non–Small Cell Lung Cancer

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Key Points

MYLK-AS1 drives resistance to EGFR inhibitors in non-small cell lung cancer, enhancing metabolic pathways.
Key evidence shows MYLK-AS1's role in promoting glutamine metabolism as a resistance mechanism.
Phase separation of ILF3 is implicated in MYLK-AS1 activity in a lung cancer model using PC9/OR cells.
Understanding MYLK-AS1's function may highlight new targets for combating EGFR inhibitor resistance.

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Implication

Observational analysis reveals MYLK-AS1 enhances glutamine metabolism in non-small cell lung cancer, indicating potential resistance to EGFR inhibitors.

Abstract

MYLK-AS1 drives phase separation of ILF3 in PC9/OR.

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Qu et al. (2025) studied this question.

synapsesocial.com/papers/68af59d2ad7bf08b1eade230 https://doi.org/10.1158/0008-5472.29919036

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Figure S8 from MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non–Small Cell Lung Cancer

Key Points

No abstract yet

Implication

Abstract

Discussion

Cite This Study

Figure S8 from MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non–Small Cell Lung Cancer

Key Points

No abstract yet

Implication

Abstract

Discussion

Cite This Study

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