MiR-590-5p regulates cell proliferation, apoptosis, migration and invasion in oral squamous cell carcinoma by targeting RECK

Histol Histopathol. 2021 Mar;36(3):355-365. doi: 10.14670/HH-18-306. Epub 2021 Jan 15.

Abstract

Objective: To discover the role of miR-590-5p in oral squamous cell carcinoma (OSCC) progression and the corresponding mechanism via the targeting RECK.

Methods: OSCC (n=85) and normal oral tissues (n=60) were collected to quantify the miR-590-5p expression by using qRT-PCR. Then SCC-15 and OEC-M1 cells were selected and divided into Mock, inhibitor NC, miR-590-5p inhibitor, si-RECK and miR-590-5p inhibitor + si-RECK groups. Dual-luciferase reporter gene assay was used to verify if miR-590-5p could target RECK. The biological behaviors of OSCC cells were evaluated by MTT, Wound-healing, Transwell and Flow cytometry. The expression of miR-590-5p and RECK was measured by qRT-PCR and Western blotting , respectively.

Results: Overexpression of miR-590-5p was found in OSCC tissues. The expression of miR-590-5p was significantly associated with the clinical TNM stage, differentiation degree, and lymph node metastasis of OSCC. RECK was identified as a direct target of miR-590-5p. Compared with the Mock group, cells in the miR-590-5p inhibitor group were decreased in terms of proliferation, invasion, and migration, and increased in cell apoptosis, accompanied by down-regulated miR-590-5p, Bcl-2/Bax and MMP-9, and up-regulated RECK. By contrast, si-RECK group presented completely opposite changes, and si-RECK reversed the inhibitory effect of miR-590-5p inhibitor on the OSCC cell growth.

Conclusion: MiR-590-5p expression was obviously increased in OSCC, and inhibiting miR-590-5p enhanced the expression of its target gene RECK, thereby suppressing proliferation, migration and invasion of OSCC cells and promoting apoptosis of OSCC cells.

MeSH terms

  • Adult
  • Aged
  • Apoptosis*
  • Case-Control Studies
  • Cell Line, Tumor
  • Cell Movement*
  • Cell Proliferation*
  • Disease Progression
  • Female
  • GPI-Linked Proteins / genetics
  • GPI-Linked Proteins / metabolism*
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Male
  • Matrix Metalloproteinase 9 / metabolism
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Middle Aged
  • Mouth Neoplasms / enzymology*
  • Mouth Neoplasms / genetics
  • Mouth Neoplasms / pathology
  • Neoplasm Invasiveness
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Signal Transduction
  • Squamous Cell Carcinoma of Head and Neck / enzymology*
  • Squamous Cell Carcinoma of Head and Neck / genetics
  • Squamous Cell Carcinoma of Head and Neck / pathology
  • bcl-2-Associated X Protein / metabolism

Substances

  • BAX protein, human
  • BCL2 protein, human
  • GPI-Linked Proteins
  • MIRN590 microRNA, human
  • MicroRNAs
  • Proto-Oncogene Proteins c-bcl-2
  • RECK protein, human
  • bcl-2-Associated X Protein
  • MMP9 protein, human
  • Matrix Metalloproteinase 9

Grants and funding