Department of Obstetrics and Gynecology, Affiliated Hospital of Hebei University, Baoding 071000, China.
Department of Obstetrics and Gynecology, Affiliated Hospital of Hebei University, Baoding 071000, China.
Life Sci. 2020 Oct 1;258:118190. doi: 10.1016/j.lfs.2020.118190. Epub 2020 Aug 7.
Glycolysis is an important process for cervical carcinoma development. Previous studies have indicated that stress-induced phosphoprotein 1 (STIP1) is associated with development of multiple tumors. Nevertheless, the role and mechanism of STIP1 in glycolysis of cervical carcinoma remain unclear.
The association between STIP1 and survival probability and the correlation between STIP1 expression and pyruvate kinase M2 (PKM2) as well as lactate dehydrogenase isoform A (LDHA) levels in cervical carcinoma were analyzed via The Cancer Genome Atlas (TCGA). The expression of STIP1, PKM2, LDHA, and cytochrome c (Cyt C) was measured via western blot or quantitative reverse transcription polymerase chain reaction. Cell viability and apoptosis were examined via cell counting kit 8 and flow cytometry, respectively. Glycolysis was assessed via detection of glucose consumption and lactate production. The protein involved in the Wnt/β-catenin pathway was measured via western blot.
STIP1 abundance was elevated in cervical carcinoma cells. High expression of STIP1 indicated poor survival probability. Knockdown of STIP1 inhibited cervical carcinoma cell viability and promoted apoptosis. STIP1 expression was positively correlated with PKM2 and LDHA levels in cervical carcinoma. Silence of STIP1 inhibited glycolysis and decreased PKM2 and LDHA expression. Down-regulation of STIP1 repressed the Wnt/β-catenin pathway. Overexpression of β-catenin reversed the effect of STIP1 silence on viability, apoptosis, glycolysis, and levels of PKM2 and LDHA.
STIP1 knockdown suppressed glycolysis in cervical carcinoma by inhibiting PKM2 and LDHA expression and activation of the Wnt/β-catenin pathway.
糖酵解是宫颈癌发展的一个重要过程。先前的研究表明，应激诱导磷蛋白 1（STIP1）与多种肿瘤的发生有关。然而，STIP1 在宫颈癌糖酵解中的作用和机制尚不清楚。
通过癌症基因组图谱（TCGA）分析 STIP1 与生存概率的相关性，以及 STIP1 表达与丙酮酸激酶 M2（PKM2）和乳酸脱氢酶同工酶 A（LDHA）在宫颈癌中的相关性。通过 Western blot 或定量逆转录聚合酶链反应测量 STIP1、PKM2、LDHA 和细胞色素 c（Cyt C）的表达。通过细胞计数试剂盒 8 和流式细胞术分别检测细胞活力和细胞凋亡。通过检测葡萄糖消耗和乳酸生成来评估糖酵解。通过 Western blot 测量 Wnt/β-catenin 通路中的蛋白。
STIP1 在宫颈癌细胞中表达上调。STIP1 高表达预示着生存概率差。STIP1 敲低抑制宫颈癌细胞活力并促进凋亡。STIP1 的表达与宫颈癌中 PKM2 和 LDHA 的水平呈正相关。STIP1 沉默抑制糖酵解并降低 PKM2 和 LDHA 的表达。下调 STIP1 抑制 Wnt/β-catenin 通路。β-catenin 的过表达逆转了 STIP1 沉默对活力、凋亡、糖酵解以及 PKM2 和 LDHA 水平的影响。
STIP1 敲低通过抑制 PKM2 和 LDHA 的表达以及 Wnt/β-catenin 通路的激活来抑制宫颈癌中的糖酵解。
