LEPR Contributes to Lung Squamous Cell Carcinoma: Insights From Mendelian Randomization and Experimental Studies
Wenhua Hu1, Guowei Wu2, Yanming Lin2
1Pathological Diagnosis Center, The Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Cancer Informatics
|June 9, 2026
Summary
Leptin receptor (LEPR) is linked to lung squamous cell carcinoma (LUSC) risk and progression. Targeting LEPR may offer new therapeutic strategies for LUSC patients.
Area of Science:
- Oncology
- Genetics
- Molecular Biology
Background:
- Adipokines are implicated in carcinogenesis, but their specific roles in lung cancer subtypes are unclear.
- Understanding adipokine involvement is crucial for advancing lung cancer research and treatment.
Purpose of the Study:
- To investigate the causal relationship between adipokines and lung cancer, including its histological subtypes.
- To explore the potential of adipokines as therapeutic targets in lung cancer.
Main Methods:
- Utilized two-sample Mendelian randomization (MR) with summary-level data from large consortia (OpenGWAS, ILCCO).
- Employed single nucleotide polymorphisms (SNPs) as instrumental variables to assess causality.
- Validated adipokine expression using human tissue microarrays and immunohistochemistry (IHC).
- Performed in vitro functional assays (siRNA-mediated knockdown) to assess Leptin Receptor (LEPR) effects in LUSC cell lines.
Main Results:
- Leptin receptor (LEPR) showed a significant association with an increased risk of lung squamous cell carcinoma (LUSC).
- High LEPR expression in LUSC tumors correlated with poorer survival outcomes.
- In vitro studies demonstrated that LEPR knockdown inhibited LUSC cell proliferation and invasion while promoting apoptosis.
Conclusions:
- LEPR plays a critical role in the development and progression of LUSC.
- LEPR represents a potential therapeutic target for LUSC intervention.
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