Figure S1 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:10.1158/0008-5472.29919069

August 15, 2025Open Access

Figure S1 from MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non–Small Cell Lung Cancer

View Full Paper

Ask AI

Bookmark

Share

Key Points

Resistance to gefitinib is influenced by MYLK-AS1 and glutamine metabolism, enhancing survival rates for cancer cells.
Key evidence indicates cell lines exhibit increased resistance due to MYLK-AS1 with genomic alterations identified in resistant patients.
Assessment using gefitinib-resistant cell lines highlights the interaction between MYLK-AS1 and drug resistance pathways.
This work may enable new cancer treatment strategies by targeting MYLK-AS1 and metabolic pathways in therapy-resistant tumors.

Implication

Research shows glutamine metabolism boosts EGFR inhibitor resistance in non-small cell lung cancer, suggesting new avenues for treatment.

Abstract

The establishment of gefitinib-resistant cell lines, genomic alterations information of resistant patients, and the effect of MYLK-AS1 on the drug resistance of sensitive cells.

Discussion

No takes yet. Share an insight, caveat, or question.

Cite This Study

Qu et al. (2025) studied this question.

synapsesocial.com/papers/68af59d2ad7bf08b1eade1e7 https://doi.org/10.1158/0008-5472.29919069

View Full Paper

Ask AI

Bookmark

Share

Figure S1 from MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non–Small Cell Lung Cancer

Key Points

Implication

Abstract

Discussion

Cite This Study

Figure S1 from MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non–Small Cell Lung Cancer

Key Points

Implication

Abstract

Discussion

Cite This Study

Keep reading

Keep reading