Lung cancer continues to pose a serious global public health challenge. Timely evidence on the global epidemiological profile of the disease is crucial to facilitate the implementation to lung cancer control efforts. This study provides updated global estimates for lung cancer incidence and mortality in 2022, along with projections for new cases and deaths up to 2050. In the population-based study, we extracted data about lung cancer new cases and deaths from GLOBOCAN 2022 database across 185 countries or territories. We analyzed age-standardized rates by sex, country, region, and human development index (HDI). Projected new cases and deaths for 2050 were estimated using global demographic projections. In 2022, lung cancer stood as the most frequently diagnosed cancer and the primary cause of cancer-related deaths on a global scale with approximately 2.48 million new cases and 1.8 million deaths, respectively. The incidence and mortality rates of lung cancer exhibited disparities in sex and world regions. Furthermore, incidence and mortality rates increasing as HDI increased. If the incidence and mortality rates remain stable as in 2022, the burden of lung cancer is projected to increase to 4·62 million new cases and 3·55 million deaths by 2050. Lung cancer is the predominant form of cancer and the foremost contributor to cancer-related mortality in 2022 with notable geographical, sex, and socioeconomic disparities.

Background: Metabolic reprogramming is a core hallmark of cancer, enabling tumor progression, immune evasion, and therapy resistance. Solute carrier (SLC) transporters, which govern the cellular flux of all nutrients and metabolites, are increasingly recognized as critical drivers of this pathological reprogramming. The altered expression and activity of SLCs in both tumor cells and immune cells profoundly shape the tumor microenvironment (TME) and are directly implicated in clinical outcomes. Main Body: This review critically examines the roles of key SLC families, particularly those transporting glucose, amino acids, and lipids. We elucidate their dual function in fueling oncogenic proliferation while simultaneously dictating the metabolic competition that leads to the functional suppression of immune cells, including T cells, dendritic cells, and macrophages. We further explore the emerging therapeutic landscape, evaluating strategies that either inhibit SLCs to starve tumors or leverage them to enhance drug delivery and mitigate treatment-related toxicities. Conclusion: Targeting SLC-mediated metabolic pathways represents a novel and highly promising therapeutic axis in oncology. We conclude by outlining the key translational challenges and future opportunities for SLC-targeted strategies. These approaches hold the potential to overcome immunotherapy resistance, reprogram the immunosuppressive TME, and exploit fundamental metabolic dependencies to improve patient outcomes.