PSMC2 knockdown exerts an anti-tumor role in nasopharyngeal carcinoma through regulating AKT signaling pathway

ABSTRACT

Nasopharyngeal carcinoma is a major public health problem in several countries, particularly in Southeast Asia and North Africa. However, the mechanism underlying the malignant biological behaviors of nasopharyngeal carcinoma is not fully clear. Our study intended to investigate the functional importance and molecular mechanism of proteasome 26 S subunit ATPase 2 (PSMC2) in the progression of nasopharyngeal carcinoma. We examined the expression of PSMC2 in both nasopharyngeal carcinoma tissues and normal healthy tissues using immunohistochemistry (IHC). Additionally, we conducted a series of cell experiments to verify the functional roles of PSMC2 and to explore the underlying pathway involved. The results revealed that PSMC2 was significantly upregulated in nasopharyngeal carcinoma tissues compared to normal tissues. Moreover, high PSMC2 was shown to closely correlate with the pathological stage and tumor infiltrate in nasopharyngeal carcinoma patients. Functionally, we observed a suppression of nasopharyngeal carcinoma progression upon knocking down PSMC2. This was evidenced by inhibited cell proliferation and migration in vitro, as well as impaired cell growth in vivo, along with increased apoptosis. Mechanistically, the inhibitory effects of PSMC2 silence on nasopharyngeal carcinoma could be reversed by the addition of AKT activator. Overall, our study sheds light on a novel mechanism underlying the development and progression of nasopharyngeal carcinoma, with PSMC2 exerting a positive regulatory role through the modulation of the AKT signaling pathway. A deeper understanding of PSMC2 may contribute to the development of improved treatment strategies for nasopharyngeal carcinoma.

KEYWORDS:

• Nasopharyngeal carcinoma
• PSMC2
• AKT pathway

Disclosure statement

No potential conflict of interest was reported by the author(s).

Ethics statement

This animal experiment was approved by Scientific Research and Clinical Trial Ethics Office, The First Affiliated Hospital of Zhengzhou University.

Author contributions

Jin Su and Kun Feng designed this research. Jin Su, ShouSen Hu and ShiPing Ding operated the cell and animal experiments. Jin Su, ShouSen Hu and Kun Feng conducted the data processing and analysis. Jin Su and ShiPing Ding completed the manuscript which was reviewed by ShouSen Hu, ShiPing Ding, Jin Su and Kun Feng. All the authors have confirmed the submission of this manuscript.

Data availability statement

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

Additional information

Funding

The author(s) reported there is no funding associated with the work featured in this article.