Lactate and protein lactylation play a vital role in tumor pathogenesis. Solute carrier 4A7 (SLC4A7), a crucial transporter, plays a role in cellular acid homeostasis. However, its impact on lactate transport and protein lactylation in solid tumors, especially lung adenocarcinoma (LUAD), remains largely unexplored. In this study, we conducted lactylome analysis and in vitro/in vivo assays to validate the functional regulation mediated by SLC4A7 in LUAD. We observed that SLC4A7 inhibits tumor progression, including metastasis, invasion and proliferation. Mechanistically, SLC4A7 reduces both intracellular and extracellular lactate accumulation and inhibits overall protein lactylation, as confirmed by lactylome analysis. Our findings from analyzing the lactylome revealed that SLC4A7 suppresses lysine lactylation (Kla) of numerous oncogenes as well as glycolysis activity. Additionally, our previous proteomic data focused on CSCs in LUAD indicated low expression levels of SLC4A7 which was further validated using tumor tissue samples from LUAD patients. Moreover, we verified the inhibitory role played by SLC4A7 in regulating tumor stemness. Collectively, our results uncover the inhibitory effect exerted by SLC4A7 on tumor progression through its regulation of lactate transport, protein lcatylation and stemness properties. We propose that targeting SLC4A7 may hold promise as a novel therapeutic strategy for treating LUAD patients.