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ABSTRACT Background The role of solute carrier family 35 member F3 (SLC35F3) in lung adenocarcinoma (LUAD) remains unclear. To address this gap, we conducted a study employing bioinformatics analysis and experimental validation. Methods This study aimed to examine the expression patterns of SLC35F3 in various cancer types, particularly focusing on LUAD, by analyzing data from the Cancer Genome Atlas (TCGA) database to evaluate its clinical relevance. The research also explored potential regulatory mechanisms of SLC35F3, including its interactions with immune infiltration, tumor mutational burden (TMB), and drug sensitivity in LUAD. The investigation included analyzing SLC35F3 expression in single‐cell sequencing of LUAD cells, examining genetic variations of SLC35F3 in LUAD, and assessing SLC35F3 expression in cell lines using quantitative real‐time PCR (qRT‐PCR). Results The aberrant expression of SLC35F3 was observed in both pan‐cancer and LUAD. In LUAD patients, a statistically significant increase in SLC35F3 expression was correlated with gender (p