食管鳞状细胞癌（ESCC）是人类消化道癌症的常见类型，生存率较差。含三联基序的蛋白 11 (TRIM11) 是某些癌症中的癌基因，可以调节糖酵解和信号转导以及转录因子 3 (STAT3) 信号传导的激活。本研究旨在探讨TRIM11在ESCC中的作用和机制。首先，利用生物信息学工具分析TRIM11在ESCC组织中的表达以及TRIM11表达与预后的相关性。 Western blot检测ESCC细胞中TRIM11的表达后，沉默TRIM11以评价其对ESCC细胞恶性表型的影响。分别通过细胞计数试剂盒8测定、乙炔基-2'-脱氧尿苷染色和流式细胞术评估细胞增殖和凋亡。检测葡萄糖摄取和乳酸分泌以检查糖酵解。此外，还采用Western blot检测与凋亡、糖酵解和STAT3/c-Myc信号传导相关的蛋白的表达。然后，用STAT3激活剂处理ESCC细胞，进一步阐明TRIM11对STAT3/c-Myc信号传导的调节作用。 TRIM11在ESCC组织和细胞中表达上调，TRIM11的高表达与不良预后相关。 TRIM11 敲低抑制增殖和糖酵解，同时促进 ESCC 细胞凋亡。此外，TRIM11 沉默显着下调 p-STAT3 和 c-Myc 的表达。值得注意的是，STAT3 激活剂部分逆转了 TRIM11 缺失对 ESCC 细胞增殖、凋亡和糖酵解的影响。总的来说，TRIM11 功能丧失通过灭活 STAT3/c-Myc 信号传导来影响 ESCC 细胞的增殖、凋亡和糖酵解。版权所有 © 2024 版权所有：© 2024 Journal of Physiological Investigation。

Esophageal squamous cell carcinoma (ESCC) is a common type of human digestive tract cancer with poor survival. Tripartite motif-containing protein 11 (TRIM11) is an oncogene in certain cancers that can regulate glycolysis and signal transduction and activation of transcription factor 3 (STAT3) signaling. This study was designed to investigate the role and the mechanism of TRIM11 in ESCC. First, TRIM11 expression in ESCC tissues and the correlation between TRIM11 expression and prognosis were analyzed using bioinformatics tools. After TRIM11 expression was detected by Western blot in ESCC cells, TRIM11 was silenced to evaluate its effect on the malignant phenotypes of ESCC cells. Cell proliferation and apoptosis were assessed by cell counting kit-8 assay, ethynyl-2'- deoxyuridine staining, and flow cytometry, respectively. The glucose uptake and lactate secretion were detected to examine glycolysis. In addition, Western blot was employed to detect the expression of proteins related to apoptosis, glycolysis, and STAT3/c-Myc signaling. Then, ESCC cells were treated with STAT3 activator further to clarify the regulatory effect of TRIM11 on STAT3/c-Myc signaling. TRIM11 was upregulated in ESCC tissues and cells, and high expression of TRIM11 was associated with a poor prognosis. TRIM11 knockdown inhibited the proliferation and glycolysis while facilitating apoptosis of ESCC cells. Besides, the expression of p-STAT3 and c-Myc was significantly downregulated by TRIM11 silencing. Of note, the STAT3 activator partially reversed the effects of TRIM11 depletion on the proliferation, apoptosis, and glycolysis in ESCC cells. Collectively, TRIM11 loss-of-function affects the proliferation, apoptosis, and glycolysis in ESCC cells by inactivating STAT3/c-Myc signaling.Copyright © 2024 Copyright: © 2024 Journal of Physiological Investigation.