miR-577 Regulates TGF-β Induced Cancer Progression through a SDPR-Modulated Positive-Feedback Loop with ERK-NF-κB in Gastric Cancer

Mol Ther. 2019 Jun 5;27(6):1166-1182. doi: 10.1016/j.ymthe.2019.02.002. Epub 2019 Feb 10.

Abstract

Transforming growth factor β (TGF-β) drives epithelial-mesenchymal transition (EMT), playing vital roles in cancer metastasis. The crosstalk between microRNAs (miRNAs) and TGF-β are frequently observed and involved in TGF-β-induced EMT. Here, we determine that miR-577 is significantly upregulated in gastric cancer (GC). miR-577 expression is positively correlated with GC metastasis status and poor patient prognosis. Functional assays demonstrate that miR-577 promotes metastasis and chemoresistance by inducing EMT and stemness-like properties. Moreover, TGF-β promotes the expression of miR-577, and miR-577 participates TGF-β-mediated cancer metastasis. Mechanistically, TGF-β activates miR-577 via NF-κB-mediated transcription, and miR-577 enhances TGF-β signaling by targeting the serum deprivation protein response (SDPR), which directly interacts with ERK to inactivate the ERK-NF-κB pathway, hence forming a feedback loop to drive tumor metastasis. A plausible mechanism of EMT induction by the TGF-β network is elucidated. Our findings suggest that the TGF-β-miR-577-SDPR axis may be a potential prognostic marker and therapeutic target against cancer metastasis in GC.

Keywords: TGF-β; feedback loop; gastric cancer; metastasis; miR-577-SDPR axis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line, Tumor
  • Disease Progression*
  • Epithelial-Mesenchymal Transition
  • Feedback, Physiological
  • HEK293 Cells
  • Heterografts
  • Humans
  • MAP Kinase Signaling System*
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • NF-kappa B / metabolism*
  • Phosphate-Binding Proteins / metabolism*
  • Plasmids / genetics
  • Prognosis
  • RNA, Small Interfering / genetics
  • Stomach Neoplasms / genetics
  • Stomach Neoplasms / metabolism*
  • Stomach Neoplasms / mortality
  • Stomach Neoplasms / pathology
  • Survival Rate
  • Transcriptional Activation / genetics
  • Transfection
  • Transforming Growth Factor beta / metabolism*
  • Tumor Burden / genetics
  • Up-Regulation

Substances

  • CAVIN2 protein, human
  • MIRN577 microRNA, human
  • MicroRNAs
  • NF-kappa B
  • Phosphate-Binding Proteins
  • RNA, Small Interfering
  • Transforming Growth Factor beta