Overexpression of microRNA-107 suppressed proliferation, migration, invasion, and the PI3K/Akt signaling pathway and induced apoptosis by targeting Nin one binding (NOB1) protein in a hypopharyngeal squamous cell carcinoma cell line (FaDu)

Bioengineered. 2022 Mar;13(3):7881-7893. doi: 10.1080/21655979.2022.2051266.

Abstract

Hypopharyngeal squamous cell carcinoma (HSCC) is one of the most common head and neck cancers, with a worst prognosis owing to its aggressivity. MicroRNA-107 (miR-107) is reported to regulate the progression of various cancers. Nevertheless, its implied function in HSCC remains unclear. This study is aimed to exploring the roles and potential mechanisms of miR-107 in HSCC. We found that miR-107 expression was significantly decreased in HSCC tissues compared with the para-cancer tissues. Moreover, miR-107 overexpression by miR-107 mimics decreased FaDu cell viability, led to cell cycle arrest in G1/S phase, accelerated apoptosis, and reduced cell migration and invasion. MiR-107 possibly resulted in deactivation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway, evidenced by the decrease of phosphorylated (p-) PI3K and p-Akt. Besides, dual-luciferase reporter assay confirmed that miR-107 might bind to the 3'UTR of Nin one binding protein 1 (NOB1), and elevated NOB1 expression in HSCC tissues and a negative correlation between miR-107 and NOB1 were found. Rescue assays demonstrated the significant roles of miR-107 in FaDu cell behavior by modulating NOB1. In addition, the tumorigenic potential of miR-107 in vivo was conducted. It was found that miR-107 overexpression in FaDu cells significantly inhibited tumor growth and led to inactivation of the PI3K/Akt signaling. The above findings revealed that miR-107 could suppress FaDu cell proliferation, migration, invasion and induced apoptosis by targeting NOB1 through the PI3K/Akt pathway, suggesting that miR-107/NOB1 axis may exert a key role in FaDu HSCC development.

Keywords: Hypopharyngeal squamous cell carcinoma; NOB1; PI3K/Akt; cell behavior; miR-107.

MeSH terms

  • Apoptosis / genetics
  • Cell Line, Tumor
  • Cell Movement / genetics
  • Cell Proliferation / genetics
  • Head and Neck Neoplasms*
  • Humans
  • MicroRNAs* / genetics
  • MicroRNAs* / metabolism
  • Nuclear Proteins / metabolism
  • Phosphatidylinositol 3-Kinase / metabolism
  • Phosphatidylinositol 3-Kinases / genetics
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / genetics
  • Proto-Oncogene Proteins c-akt / metabolism
  • RNA-Binding Proteins / metabolism
  • Signal Transduction / genetics
  • Squamous Cell Carcinoma of Head and Neck

Substances

  • MIRN107 microRNA, human
  • MicroRNAs
  • NOB1 protein, human
  • Nuclear Proteins
  • RNA-Binding Proteins
  • Phosphatidylinositol 3-Kinase
  • Proto-Oncogene Proteins c-akt

Grants and funding

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