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RNAi 介导的 PFK1 基因敲低降低鼻咽癌细胞系 CNE-2 的侵袭和转移能力。

RNAi-mediated knockdown of PFK1 decreases the invasive capability and metastasis of nasopharyngeal carcinoma cell line, CNE-2.

机构信息

Department of Otolaryngology, Shenzhen Nanshan People's Hospital and the 6th Affiliated Hospital of Shenzhen University Health Science Center , Shenzhen, China.

Department of Otolaryngology Head and Neck Surgery, The 5th Affiliated Hospital of Sun Yat-sen University , Zhuhai, China.

出版信息

Cell Cycle. 2021 Jan;20(2):154-165. doi: 10.1080/15384101.2020.1866279. Epub 2021 Jan 6.

Abstract

Nasopharyngeal carcinoma (NPC) is the most prevailing malignancy of the head and neck with unique geographic distribution. Southern China has one of the highest incidence rates of NPC in the world. Although radiotherapy and chemotherapy are the most important treatment modalities for NPC, recurrence, and metastasis severely interfere with the survival quality of patients. It is much-needed to find an effective method of NPC treatment with a good prognosis such as gene therapy. PFK1, a key regulatory enzyme of glycolysis, is frequently shown to be amplified and overexpressed in a variety of human cancers. However, the function of PFK1 and molecular mechanism in NPC is elusive. Here, we knockdown PFK1 expression by utilizing DNA vector-based RNA Interference. Western blotting and real-time PCR show that the expression of PFK1 is efficiently down-regulated in both protein and mRNA levels by stable transfection with PFK1 siRNA expression vector. In addition, stable knockdown of PFK1 expression inhibits cell growth, induces apoptosis, decreases the invasive capability and metastasis in the CNE2 human NPC cell line. This present study finds the importance of PFK1 which can be worked as a novel target in NPC treatment and holds great potential to be extended to other malignant cancers.

摘要

鼻咽癌(NPC)是头颈部最常见的恶性肿瘤,具有独特的地理分布。中国南方是世界上 NPC 发病率最高的地区之一。尽管放疗和化疗是 NPC 最重要的治疗方法,但复发和转移严重影响了患者的生存质量。因此,迫切需要寻找一种有效的 NPC 治疗方法,如基因治疗,以获得良好的预后。PFK1 是糖酵解的关键调节酶,在多种人类癌症中常被发现扩增和过表达。然而,PFK1 的功能及其在 NPC 中的分子机制尚不清楚。在这里,我们利用基于 DNA 载体的 RNA 干扰来敲低 PFK1 的表达。Western blot 和实时 PCR 显示,通过稳定转染 PFK1 siRNA 表达载体,PFK1 的表达在蛋白和 mRNA 水平上均被有效下调。此外,PFK1 表达的稳定敲低抑制细胞生长,诱导细胞凋亡,降低 CNE2 人 NPC 细胞系的侵袭能力和转移能力。本研究发现 PFK1 的重要性,它可以作为 NPC 治疗的一个新靶点,并有可能扩展到其他恶性肿瘤。

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