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Lung cancer is the leading cause of cancer-related mortality worldwide. In particular, non–small cell lung cancer (NSCLC) is often diagnosed at an advanced stage due to the lack of early symptoms. Although targeted therapies such as EGFR-TKIs have significantly improved clinical outcomes, the rapid emergence of therapeutic resistance remains a major barrier to long-term survival. Consequently, identifying novel biomarkers that determine tumor progression and treatment responsiveness, as well as discovering therapeutic targets capable of overcoming resistance, has become a crucial strategy for transforming the lung cancer treatment paradigm.

Cancer precision medicine is an approach that integrates genomic, transcriptomic, and proteomic information to design personalized therapeutic strategies tailored to each patient’s molecular profile. This research, grounded in precision-medicine–based analyses, identifies previously unrecognized signaling networks driving NSCLC progression and highlights actionable targets with strong potential for future therapeutic development.

1. PYCR1–EGFR–TLR Signaling Axis: A Newly Identified Mechanism Driving Lung Cancer Progression

In the study “PYCR1 drives lung cancer progression through functional interactions with EGFR and TLR signaling pathways” (Experimental & Molecular Medicine, 2025, IF 12.9), the researchers uncovered a novel molecular mechanism in which PYCR1, a key enzyme in proline metabolism, functionally interacts with EGFR and TLR signaling to promote lung cancer growth and metastasis. This research is the first to demonstrate that PYCR1—traditionally viewed only as a metabolic enzyme—acts as a central regulatory node within the lung cancer signaling network. The findings highlight PYCR1 as a promising strategic target for developing lung cancer–specific therapeutics. (See Fig. 1.).

2. USP21–EGFR–Lyn Signaling Axis: A Therapeutic Target for Overcoming Resistance

The second study, “USP21–EGFR–Lyn axis drives NSCLC progression and therapeutic potential of USP21 inhibition” (Biomarker Research, 2025, IF 11.5), elucidates a mechanism in which the deubiquitinase USP21 simultaneously activates EGFR and Lyn kinase signaling to drive NSCLC progression. This work establishes USP21 as a key regulator of lung cancer progression and demonstrates its value as a biomarker and therapeutic target capable of overcoming resistance to EGFR-targeted therapy. The clinical significance of USP21 inhibition is particularly notable in the context of combination treatment strategies designed to counteract EGFR inhibitor resistance. (See Fig. 2.)

These studies were led by Ha-Jeong Lee, an Integrated B.S.–M.S. program applicant, in collaboration with graduate researchers Ji-Young Kim, Ji-Hye Shin, and Ye-Eun Kang from the Laboratory of Molecular Immunology (PI: Professor Kiyoung Lee, School of Medicine). Ha-Jeong’s achievements exemplify the fact that “undergraduate researchers can also produce world-class scientific outcomes.” Her work represents an outstanding model of SKKU’s research-oriented education and demonstrates the impact of a supportive research environment combined with rigorous scientific training.

鈥� Article title: PYCR1 drives lung cancer progression through functional interactions with EGFR and TLR signaling pathways.

鈥� Journal name: Experimental & Molecular Medicine.

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鈥� Article title: USP21-EGFR-Lyn axis drives NSCLC progression and therapeutic potential of USP21 inhibition.

鈥� Journal name: Biomarker research.

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