# The Role of Low CD36 Expression in the Development of Non-Small Cell Lung Cancer and Its Potential for Therapy

## TL;DR

This review explores how low CD36 expression contributes to non-small cell lung cancer and its potential as a therapeutic target.

## Contribution

The paper systematically reviews CD36's role in NSCLC progression and its therapeutic potential.

## Key findings

- CD36 influences NSCLC proliferation, migration, and tumor microenvironment modulation.
- Regulating CD36 expression can intervene in NSCLC malignant behavior.
- CD36 is a promising therapeutic target and prognostic marker for NSCLC.

## Abstract

Lung cancer continues to be among the most prevalent and lethal malignancies globally, with non-small cell lung cancer (NSCLC) constituting the majority of cases and presenting significant challenges in effective treatment. CD36 is integral to lipid metabolism, immune responses, and various critical biological processes, and accumulating evidence suggests a strong association with cancer progression. This review provides a comprehensive analysis of the role of CD36 in influencing lung cancer cell proliferation, metastasis, and the regulation of the tumor microenvironment, while also examining potential therapeutic strategies targeting CD36. The insights gained from these findings aim to pave the way for advancements in precision diagnosis and treatment, with the potential to enhance diagnostic and therapeutic standards and improve outcomes for patients with lung cancer.

Lung cancer remains one of the most prevalent and lethal malignancies worldwide. NSCLC, which constitutes approximately 85% of cases, continues to exhibit a poor prognosis despite advancements in therapeutic interventions, underscoring the urgent necessity to elucidate its molecular mechanisms and identify novel therapeutic targets. CD36, a multifunctional transmembrane glycoprotein, is integral to lipid uptake, immune recognition, inflammatory regulation, molecular adhesion, and apoptosis. Increasing evidence implicates CD36 in the progression of various cancers. In the context of lung cancer, CD36 facilitates tumorigenesis through multiple pathways, including the remodeling of tumor cell lipid metabolism, reprogramming of tumor-associated macrophages, and modulation of immune cell functions such as those of Tregs and CD8+ T cells. Additionally, CD36 is intricately linked with the function of cancer-associated fibroblasts and the remodeling of the tumor stromal microvasculature. This systematic review synthesizes the mechanisms by which CD36 contributes to NSCLC proliferation, migration, epithelial–mesenchymal transition, and modulation of the tumor microenvironment. Furthermore, we explore emerging therapeutic strategies that target CD36. Regulating CD36 expression effectively intervenes in the malignant behavior of NSCLC, underscoring its potential as a promising therapeutic target and prognostic marker.