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MiR-155 regulates lymphoma cell proliferation and apoptosis through targeting SOCS3/JAK-STAT3 signaling pathway

X-D Li1, X-M Li, J-W Gu

  • 1Dental Department, Yan'an People's Hospital of Shaanxi Province, Yan'an, Shaanxi, China. xiaochensunr@126.com.

European Review for Medical and Pharmacological Sciences
|December 12, 2017
PubMed
Abstract

Insights

Down-regulating microRNA-155 (miR-155) inhibits diffuse large B cell lymphoma (DLBCL) cell proliferation and promotes apoptosis. This occurs by increasing Suppressors of Cytokine Signaling 3 (SOCS3) expression, which suppresses the Janus kinase (JAK)-STAT signaling pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • The Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway is implicated in lymphoma pathogenesis.
  • Suppressors of Cytokine Signaling 3 (SOCS3) negatively regulates the JAK-STAT pathway.
  • Reduced SOCS3 and elevated microRNA-155 (miR-155) are linked to lymphoma development.

Purpose of the Study:

  • To investigate miR-155's role in regulating the SOCS3/JAK-STAT pathway.
  • To determine miR-155's effect on diffuse large B cell lymphoma (DLBCL) cell proliferation and apoptosis.

Main Methods:

  • Analysis of miR-155 and SOCS3 expression in DLBCL tissues versus controls.
  • Dual luciferase assay to confirm the interaction between miR-155 and SOCS3.
  • In vitro studies using OCI-LY10 cells with miR-155 inhibitors and SOCS3 expression vectors to assess effects on cell proliferation and apoptosis.

Main Results:

  • DLBCL tissues showed significantly higher miR-155 and lower SOCS3 expression compared to controls.
  • miR-155 was confirmed to directly target and regulate SOCS3.
  • Inhibition of miR-155 or restoration of SOCS3 expression reduced JAK-STAT pathway activation (p-JAK1, p-JAK2, p-STAT3) and Survivin levels, decreased cell proliferation, and increased apoptosis in DLBCL cells.

Conclusions:

  • Down-regulation of miR-155 suppresses the JAK-STAT3 signaling pathway by up-regulating SOCS3.
  • This mechanism inhibits DLBCL cell proliferation and promotes apoptosis.
  • Targeting miR-155 represents a potential therapeutic strategy for DLBCL.

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