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Roles of AKR1C1 in Non-small Cell Lung Cancer.
Xinran Zhang1, Qi Zhang1, Yuting Chang1
1Department of Oncology, The Affiliated Taizhou People's Hospital of Nanjing Medical University, 225300 Taizhou, Jiangsu, China.
Frontiers in Bioscience (Landmark Edition)
|April 29, 2026
Summary
Aberrant aldo-keto reductase 1C1 (AKR1C1) expression is linked to lung squamous cell carcinoma (LUSC) progression. Targeting AKR1C1 may offer a new therapeutic strategy for LUSC by modulating ferroptosis.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Therapeutics
Background:
- Non-small cell lung cancer (NSCLC), particularly lung squamous cell carcinoma (LUSC), has high global incidence and mortality.
- Current targeted therapies and immunotherapies are ineffective for a majority of LUSC patients lacking actionable mutations.
- Chemotherapy remains a primary treatment for LUSC but has limited efficacy and significant toxicity.
Purpose of the Study:
- To investigate the role of aldo-keto reductase family 1 member C1 (AKR1C1) in LUSC.
- To explore the potential of targeting AKR1C1 as a therapeutic strategy for LUSC by modulating ferroptosis.
Main Methods:
- Analysis of aberrant AKR1C1 expression in LUSC.
- Investigating the association between AKR1C1 and tumor progression, invasiveness, and prognosis.
- Exploring the implication of AKR1C1 in ferroptosis pathways.
Main Results:
- Aberrant AKR1C1 expression is strongly associated with tumor progression, invasiveness, and poor prognosis in several cancers, including potentially LUSC.
- AKR1C1 is implicated in ferroptosis, a regulated cell death pathway.
Conclusions:
- Targeting AKR1C1 may represent a novel therapeutic approach for LUSC.
- Modulating ferroptosis pathways via AKR1C1 inhibition could impact LUSC cell proliferation.
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