Open Access

Silencing of NACC1 inhibits the proliferation, migration and invasion of nasopharyngeal carcinoma cells via regulating the AKT/mTOR signaling pathway

  • Authors:
    • Zhengyong Cao
    • Hong Chen
    • Xiaoli Mei
    • Xiaobo Li
  • View Affiliations

  • Published online on: October 12, 2021
  • Article Number: 828
  • Copyright: © Cao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Nucleus accumbens‑associated protein 1 (NACC1) has been reported to serve as an oncogenic role in several types of cancer; however, its role in nasopharyngeal carcinoma (NPC) remains to be determined. The present study aimed to investigate the role of NACC1 in NPC and elucidate the underlying mechanisms. Therefore, NACC1 expression in the normal nasopharyngeal epithelial cell line, NP69, and various NPC cell lines was determined by reverse transcription‑­quantitative PCR and western blot analyses. NACC1 expression was silenced in the NPC SUNE‑1 cell line by transfection with a short hairpin RNA. Cell viability, proliferation, migration, invasion and epithelial‑mesenchymal transition (EMT) were then evaluated using MTT, colony formation, wound healing, Transwell and western blot assays, respectively. SC79 was employed to activate AKT expression in NACC1‑silenced SUNE‑1 cells, and the aforementioned cellular processes were observed. The results revealed that NACC1 expression was upregulated in NPC cell lines. NACC1‑knocdown inhibited SUNE‑1 cell proliferation, migration, invasion and EMT. Moreover, the levels of phosphorylated AKT and mTOR were decreased upon NACC1 silencing. Mechanistically, the presence of SC79 significantly blocked all the effects of NACC1‑knockdown on SUNE‑1 cells. The findings of the present study demonstrated that NACC1‑knockdown effectively suppressed NPC cell proliferation, migration and invasion by inhibiting the activation of the AKT/mTOR signaling pathway. NACC1 may thus serve as a potential target for the diagnosis and therapy of NPC.
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