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

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
• nasopharyngeal carcinoma
• carcinogenesis
• RNA interference

Data availability statement

The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

Disclosure statement

The authors declare no potential conflicts of interest.

Ethical approval

All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.

Informed consent

Informed consent was obtained from all individual participants included in the study.

Additional information

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).