Department of Surgical Group, Medical College of Pingdingshan University, Pingdingshan, Henan 467000, P.R. China.
Department of Respiratory Medicine, First People's Hospital of Jinan, Jinan, Shandong 250000, P.R. China.
Mol Med Rep. 2021 Jan;23(1). doi: 10.3892/mmr.2020.11712. Epub 2020 Nov 25.
The platelet isoform of phosphofructokinase (PFKP) is a rate‑limiting enzyme involved in glycolysis that serves an important role in various types of cancer. The aim of the present study was to explore the specific regulatory relationship between PFKP and non‑small cell lung cancer (NSCLC) progression. PFKP expression in NSCLC tissues and corresponding adjacent tissues was detected using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and immunohistochemical analysis. PFKP expression in human bronchial epithelial cells (16HBE) and NSCLC cells (H1299, H23 and A549) was also detected using RT‑qPCR. Cell proliferation was detected by Cell Counting Kit‑8 and colony formation assays. Transwell invasion and wound healing assays, and flow cytometry were used to detect cell invasion, migration and apoptosis, respectively. The expression levels of glycolysis‑associated enzymes (hexokinase‑2, lactate dehydrogenase A and glucose transporter‑1), epithelial‑mesenchymal transition‑related proteins (N‑cadherin, vimentin and E‑cadherin) and apoptosis‑related proteins (caspase‑3 and B‑cell lymphoma‑2) were detected by western blotting. Glucose uptake, lactate production and the adenosine trisphosphate/adenosine diphosphate ratio were measured using the corresponding kits. The results of the present study demonstrated that PFKP expression was upregulated in NSCLC tissues and cells, and PFKP expression was related to lymph node metastasis and histological grade. In addition, overexpression of PFKP inhibited cell apoptosis, and promoted proliferation, migration, invasion and glycolysis of H1299 cells, whereas knockdown of PFKP had the opposite effects. In conclusion, PFKP inhibited cell apoptosis, and promoted proliferation, migration, invasion and glycolysis of NSCLC cells; these findings may lay the foundation for novel treatments of NSCLC.
血小板型磷酸果糖激酶（PFKP）是糖酵解途径中的限速酶，在各种类型的癌症中发挥着重要作用。本研究旨在探讨 PFKP 与非小细胞肺癌（NSCLC）进展之间的特定调控关系。通过逆转录-定量聚合酶链反应（RT-qPCR）和免疫组织化学分析检测 NSCLC 组织及相应的癌旁组织中 PFKP 的表达。通过 RT-qPCR 检测人支气管上皮细胞（16HBE）和 NSCLC 细胞（H1299、H23 和 A549）中 PFKP 的表达。通过细胞计数试剂盒-8 和集落形成实验检测细胞增殖。通过 Transwell 侵袭和划痕愈合实验以及流式细胞术分别检测细胞侵袭、迁移和凋亡。通过 Western blot 检测糖酵解相关酶（己糖激酶 2、乳酸脱氢酶 A 和葡萄糖转运蛋白 1）、上皮-间充质转化相关蛋白（N-钙黏蛋白、波形蛋白和 E-钙黏蛋白）和凋亡相关蛋白（半胱氨酸蛋白酶 3 和 B 细胞淋巴瘤-2）的表达水平。使用相应的试剂盒测量葡萄糖摄取、乳酸生成和三磷酸腺苷/二磷酸腺苷比值。本研究结果表明，PFKP 在 NSCLC 组织和细胞中表达上调，PFKP 的表达与淋巴结转移和组织学分级有关。此外，PFKP 的过表达抑制细胞凋亡，并促进 H1299 细胞的增殖、迁移、侵袭和糖酵解，而 PFKP 的敲低则产生相反的效果。综上所述，PFKP 抑制 NSCLC 细胞的凋亡，并促进其增殖、迁移、侵袭和糖酵解；这些发现可能为 NSCLC 的新型治疗方法奠定基础。
