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.

糖酵解是包括肺腺癌（LUAD）在内的多种癌症的共同特征。睾丸表达 19 (TEX19) 与癌症进展相关。但它对 LUAD 的影响仍然是一个悬而未决的问题。我们研究的重点主要是研究 TEX19 在 LUAD 中的确切工作原理。我们首先从TCGA-LUAD下载mRNA数据并进行差异表达分析。然后，我们进行了 Kaplan-Meier 分析来分析 mRNA 表达与患者预后之间的关系。 hTFtarget数据库用于预测mRNA上游转录因子。接下来，采用 qRT-PCR 检测 TEX19 和 Forkhead box A1 (FOXA1) 的表达。采用Western blot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活力、增殖和凋亡。引进Seahorse XF细胞外通量分析仪来分析细胞外酸化率（ECAR）和耗氧率（OCR）。使用检测试剂盒检测丙酮酸、乳酸、柠檬酸和苹果酸。 TEX19 在 LUAD 组织中高表达。实时定量PCR（qRT-PCR）检测显示，与正常支气管上皮细胞BEAS-2B相比，TEX19在LUAD细胞系中显着过表达。敲低TEX19可显着抑制细胞活性和增殖，促进细胞凋亡，TEX19在糖酵解途径中富集。同时，TEX19的敲低显着降低了丙酮酸、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沉淀（ChIP）分析表明FOXA1与TEX19结合。 FOXA1 在 LUAD 中高表达。 救援实验表明，FOXA1 通过激活 TEX19 表达，增强 LUAD 细胞的糖酵解和增殖并抑制凋亡。综上所述，FOXA1通过激活TEX19促进LUAD细胞的糖酵解和增殖。该结果可为未来LUAD的研究提供理论基础。