糖酵解是包括肺腺癌（LUAD）在内的各种癌症的共同特点。睪丸表达19（TEX19）与癌症进展有关。但其对LUAD的影响仍然是一个未解答的问题。我们研究的重点是主要探究TEX19在LUAD中的作用方式。首先，我们从TCGA-LUAD下载了mRNA数据，并进行了差异表达分析。然后，我们进行了Kaplan-Meier分析，以分析mRNA表达与患者预后之间的关系。我们利用hTFtarget数据库预测了mRNA的上游转录因子。接下来，我们利用qRT-PCR检测TEX19和Forkhead box A1（FOXA1）的表达情况。西方博LOT法用于检测糖酵解相关蛋白的表达。我们还使用CCK-8、集落形成和流式细胞术检测细胞的存活性、增殖性和凋亡性。引入Seahorse XF细胞外酸化率（ECAR）和氧消耗率（OCR）分析仪进行分析。检测试剂盒用于检测丙酮酸、乳酸、柠檬酸和苹果酸。TEX19在LUAD组织中高度表达。实时定量PCR（qRT-PCR）分析显示，在与正常支气管上皮细胞BEAS-2B相比，LUAD细胞系中TEX19明显过表达。TEX19的沉默显著抑制了细胞活性和增殖，并促进了细胞凋亡，TEX19在糖酵解途径中富集。与此同时，TEX19的沉默显著阻碍了丙酮酸、乳酸、柠檬酸和苹果酸的含量。生物信息学分析、双荧光素酶报告基因实验和染色质免疫共沉淀（ChIP）分析表明FOXA1与TEX19结合。FOXA1在LUAD中具有较高的表达水平。拯救实验证实，FOXA1通过激活TEX19的表达，增强了LUAD细胞的糖酵解和增殖，并抑制了细胞的凋亡。总之，FOXA1通过激活TEX19促进了LUAD细胞的糖酵解和增殖。这个结果可以为今后的LUAD研究提供理论基础。© 2023. 作者，由Springer Science+Business Media，LLC独家许可，属于Springer Nature的一部分。

Glycolysis is a shared feature in various cancers including lung adenocarcinoma (LUAD). Testis Expressed 19 (TEX19) is correlated with cancer progression. But its effect on LUAD remains an unanswered question. The focus of our study was primarily to investigate how TEX19 works exactly in LUAD. We first downloaded mRNA data from TCGA-LUAD and performed differential expression analysis. Then, we performed a Kaplan-Meier analysis to analyze the relationship between mRNA expression and patients' prognoses. hTFtarget database was utilized for the prediction of upstream transcription factors of mRNA. Next, qRT-PCR was employed for detecting TEX19 and Forkhead box A1 (FOXA1) expression. Western blot was adopted to detect the expression of glycolysis-related proteins. We also used CCK-8, colony formation, and flow cytometry assays to detect cell viability, proliferation, and apoptosis. Seahorse XF Extracellular Flux Analyzers were introduced to analyze extracellular acidification rate (ECAR) and oxygen consumption rate (OCR). Detection kits were used to detect pyruvate, lactate, citric acid, and malic acid. TEX19 was highly expressed in LUAD tissues. Real-time quantitative PCR (qRT-PCR) assay showed that TEX19 was significantly overexpressed in LUAD cell lines compared with normal bronchial epithelial cells BEAS-2B. Knockdown of TEX19 remarkably inhibited cell activity and proliferation, and promoted cell apoptosis, TEX19 was enriched in the glycolytic pathway. Meanwhile, the knockdown of TEX19 significantly hampered the contents of pyruvate, lactate, citric acid, and malic acid. The bioinformatics analysis, dual luciferase reporter experiment, and chromatin immunoprecipitation (ChIP) assay showed that FOXA1 was bound with TEX19. FOXA1 had a high expression level in LUAD. The rescue assay demonstrated that FOXA1, by activating TEX19 expression, enhanced glycolysis and proliferation and inhibited apoptosis of LUAD cells. In summary, FOXA1 promoted glycolysis and proliferation of LUAD cells by activating TEX19. This result can provide a theoretical basis for future research on LUAD.© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.