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Pristimerin inhibits the proliferation of HT1080 fibrosarcoma cells by inducing apoptosis

Daichi Hayashi1, Toshiharu Shirai1, Ryu Terauchi1

  • 1Department of Orthopedics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.

Oncology Letters
|March 29, 2020
PubMed

Insights

Pristimerin (PM) shows significant anti-tumor effects against human fibrosarcoma cells by reducing viability and inducing apoptosis. This natural compound effectively inhibited tumor growth in mice with minimal impact on normal cells and organs, suggesting its potential as a fibrosarcoma therapeutic.

Area of Science:

  • Oncology
  • Pharmacology
  • Biochemistry

Background:

  • Fibrosarcoma is a rare soft tissue sarcoma lacking established drug therapies.
  • Pristimerin (PM) has demonstrated anti-tumor activity in various cancers, but its effect on soft tissue sarcoma is unexamined.

Purpose of the Study:

  • To investigate the anti-tumor potential of pristimerin (PM) on human fibrosarcoma cells (HT1080).
  • To evaluate the effects of PM on cell viability, apoptosis, and key signaling pathways (AKT, MAPK) in fibrosarcoma.
  • To assess the in vivo efficacy and safety of PM in a mouse model of fibrosarcoma.

Main Methods:

  • Cell viability, IC50 values, and apoptosis induction assays were performed on HT1080 and normal human dermal fibroblast (aHDF) cells treated with PM.
  • Western blotting was used to analyze the impact of PM on phosphorylated AKT, mTOR, NF-κB, and ERK signaling pathways.
  • In vivo studies involved subcutaneous transplantation of fibrosarcoma cells in mice, followed by PM treatment to assess tumor growth inhibition, body weight changes, and liver/renal function.

Main Results:

  • PM significantly reduced HT1080 cell viability and induced apoptosis in a dose-dependent manner, with IC50 values of 0.16 µM at 24h and 0.13 µM at 48h.
  • PM treatment decreased the levels of phosphorylated AKT, mTOR, NF-κB, and ERK, indicating modulation of key cell proliferation pathways.
  • In vivo, PM significantly inhibited tumor growth without adverse effects on body weight or significant alterations in liver and renal function. PM showed minimal toxicity to normal dermal fibroblasts.

Conclusions:

  • Pristimerin (PM) exhibits potent anti-fibrosarcoma activity by inducing apoptosis and inhibiting critical signaling pathways.
  • PM demonstrates a favorable therapeutic window, effectively targeting fibrosarcoma cells while sparing normal cells.
  • These findings suggest that PM holds promise as a potential therapeutic agent for treating fibrosarcoma.
Keywords:
AKTapoptosiscaspasefibrosarcomamitogen-activated protein kinasepristimerinproliferation

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