Tumor-intrinsic PD-L1 drives lung cancer progression in response to TLR stimulation by promoting autophagy through the TRAF6–BECN1 signaling axis
This study identifies PD-L1 as a previously unrecognized intrinsic driver of NSCLC progression through activation of the TLR-TRAF6-BECN1 autophagy axis and promotion of EMT. Beyond its canonical role in immune evasion, PD-L1 functions as a dual-regulator of tumorigenesis by coordinating autophagy-dependent oncogenic processes. These findings provide novel mechanistic insight and support the therapeutic rationale for targeting PD-L1 not only as an immune checkpoint but also as a key modulator of cancer cell-intrinsic signaling in NSCLC.
Authors
- Duk-Hwan Kim (ORCID: https://orcid.org/0000-0003-1684-3267)
- Ha-Jeong Lee (ORCID: https://orcid.org/0009-0006-1517-2907)
- Chaeeun Lee (ORCID: https://orcid.org/0000-0003-4161-3375)
- Ki-young Lee
- Yeeun Kang (ORCID: https://orcid.org/0000-0003-0624-5992)
- Tae Jin Kim
- Ji Hye Shin (ORCID: https://orcid.org/0000-0002-2207-7346)
- Eunyoung Chun
- Yoolim Sung
- Jae-Hyuck Shim
- Ji Young Kim
- Mi-Jeong Kim
Institutions
- University of Massachusetts Chan Medical School (US)
- Samsung Medical Center (KR)
- CHA Vaccine Institute (South Korea) (KR)
- Sungkyunkwan University (KR)
Publication Details
- Journal
- Experimental Hematology and Oncology
- Published
- 2026-02-16
- DOI
- https://doi.org/10.1186/s40164-026-00761-9
- Primary Topic
- Autophagy in Disease and Therapy
- Type
- article
- Field-Weighted Citation Impact
- 0.00