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Matrine inhibits the growth of natural killer/T-cell lymphoma cells by modulating CaMKIIγ-c-Myc signaling pathway

Jianyou Gu1,2, Yu Zhang1, Xiao Wang1,2

  • 1The First Affiliated Hospital, Zhejiang Chinese Medical University, No. 54 Youdian Road, Zhejiang, 310006, Hangzhou, China.

BMC Complementary Medicine and Therapies
|July 10, 2020
PubMed
Abstract

Insights

Matrine inhibits natural killer/T-cell lymphoma (NKTCL) growth by decreasing c-Myc protein stability and downregulating the CaMKIIγ-c-Myc pathway. This study reveals matrine as a potential therapeutic agent for NKTCL by targeting key oncogenic pathways.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • C-Myc overexpression is linked to poor prognosis in natural killer/T-cell lymphoma (NKTCL).
  • Matrine, derived from Sophora flavescens Ait, exhibits anti-proliferative and pro-apoptotic effects on cancer cells.
  • Investigating matrine's mechanisms against NKTCL is crucial for therapeutic development.

Purpose of the Study:

  • To investigate the effects of matrine on natural killer/T-cell lymphoma (NKTCL) cell growth.
  • To elucidate the molecular mechanisms underlying matrine's anti-NKTCL activity.
  • To assess matrine's impact on key signaling pathways, including CaMKIIγ/c-Myc.

Main Methods:

  • Cultured NKTCL cell line (NK92) was treated with matrine.
  • Proliferation, apoptosis, and expression of apoptotic molecules were assessed.
  • Levels of STAT3, LMP1, RUNX3, EZH2, CaMKIIγ, and c-Myc were analyzed.

Main Results:

  • Matrine inhibited NK92 cell proliferation in a dose- and time-dependent manner (IC50 = 1.71 mM at 72h).
  • Matrine induced apoptosis, decreased Bcl-2 expression, and promoted proteasome-dependent degradation of c-Myc.
  • Matrine reduced c-Myc half-life, downregulated c-Myc phosphorylation at Ser62 by inhibiting CaMKIIγ, and suppressed c-Myc transcription via LMP1 inhibition.

Conclusions:

  • Matrine effectively inhibits natural killer/T-cell lymphoma cell growth.
  • Matrine's anti-cancer effects are mediated through the modulation of the LMP1-c-Myc and CaMKIIγ-c-Myc signaling pathways.
  • Matrine demonstrates potential as a therapeutic agent for NKTCL.
Keywords:
C-MycCaMKIIγLMP1MatrineNK/T-cell lymphomaNK92 cell

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