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MiR-19 enhances pancreatic cancer progression by targeting PTEN through PI3K/AKT signaling pathway

Eur Rev Med Pharmacol Sci. 2020 Feb;24(3):1098-1107. doi: 10.26355/eurrev_202002_20160.

Abstract

Objective: Abnormal expression of micro ribonucleic acids (miRNAs) has become an important marker of cancer. However, the exact molecular mechanisms of miRNAs were not very clear. Here, we decided to investigate the miR-19 effect and molecular mechanism on pancreatic cancer, which was blank until now.

Patients and methods: Quantitative real-time polymerase chain reaction (qRT-PCR) analysis was applied for testing miR-19 and gene of phosphate and tensin homolog deleted on chromosome ten (PTEN) expression. Western blot was used for detecting the protein expression. Methyl thiazolyl tetrazolium (MTT) assay and transwell assay were carried out to measure cell proliferation, invasion, and migration.

Results: We showed that miR-19 expression was increased in cancerous tissues and was associated with the survival of patients, tumor node metastasis (TNM) stage, tumor size, and lymph node metastasis. MiR-19 mimic enhanced cell proliferation, invasion, and migration, while suppressing miR-19 cell progression was suppressed. With the help of TargetScanHuman and luciferase reporter assay, we verified PTEN as a specific target of miR-19. Moreover, PTEN expression was reduced by miR-19 mimic and was increased by miR-19 inhibitor. We next found that PTEN was elevated in cancerous tissues and its expression was negatively correlated with miR-19 expression. Furthermore, miR-19 regulated cell progression via activating phosphatidylinositol 3-hydroxy kinase/protein kinase B (PI3K/AKT) signaling pathway.

Conclusions: We demonstrated that miR-19 facilitated cell progression through modulating PI3K/AKT signaling pathway by targeting PTEN, which provided a potential therapeutic target for pancreatic cancer patients.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Animals
  • Disease Progression*
  • Female
  • Humans
  • Male
  • Mice
  • Mice, Nude
  • MicroRNAs / biosynthesis*
  • MicroRNAs / genetics
  • Middle Aged
  • PTEN Phosphohydrolase / biosynthesis*
  • PTEN Phosphohydrolase / genetics
  • Pancreatic Neoplasms / genetics
  • Pancreatic Neoplasms / metabolism*
  • Pancreatic Neoplasms / pathology
  • Phosphatidylinositol 3-Kinase / genetics
  • Phosphatidylinositol 3-Kinase / metabolism*
  • Proto-Oncogene Proteins c-akt / genetics
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Signal Transduction / physiology
  • Survival Rate / trends
  • Xenograft Model Antitumor Assays / methods

Substances

  • MIRN19 microRNA, human
  • MicroRNAs
  • Phosphatidylinositol 3-Kinase
  • Proto-Oncogene Proteins c-akt
  • PTEN Phosphohydrolase
  • PTEN protein, human