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

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.

Keywords: PFK1; RNA interference; carcinogenesis; nasopharyngeal carcinoma.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / genetics
  • Cell Line, Tumor
  • Cell Proliferation / genetics
  • Gene Expression Regulation, Neoplastic / genetics
  • Humans
  • Nasopharyngeal Carcinoma / genetics*
  • Nasopharyngeal Carcinoma / pathology
  • Nasopharyngeal Neoplasms / genetics
  • Nasopharyngeal Neoplasms / pathology*
  • Neoplasm Metastasis / pathology*
  • Neoplasm Recurrence, Local / genetics*
  • Neoplasm Recurrence, Local / pathology
  • Phosphofructokinase-1 / genetics*
  • RNA Interference / physiology

Substances

  • Phosphofructokinase-1

Grants and funding

This work was supported by grants from the Shenzhen Foundation of Science and Technology (JCYJ20180302144624391); Science and Technology Foundation of Guangdong Province of China (No. 2017A020215180) and Natural Science Foundation of Guangdong Province, China (No. 2018A030313399) and National Natural Science Foundation of China (No. 82071018).