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NMT1 inhibition modulates breast cancer progression through stress-triggered JNK pathway

Lu Deng1,2, Xinlei Gao2, Bingjie Liu1,2

  • 1Fudan University Shanghai Cancer Center and Institutes of Biomedical Sciences; Shanghai Medical College; Key Laboratory of Breast Cancer in Shanghai; Innovation Center for Cell Signaling Network; Cancer Institutes, Fudan University, 200032, Shanghai, China.

Cell Death & Disease
|November 18, 2018
PubMed

Insights

Targeting N-myristoyltransferase 1 (NMT1) inhibits breast cancer progression by inducing oxidative and ER stress, activating pathways that promote autophagy. This offers a new strategy for treating breast cancer, particularly triple-negative breast cancer (TNBC).

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cellular Signaling

Background:

  • Myristoylation is a crucial post-translational modification implicated in cancer development.
  • Targeting myristoylation presents a potential therapeutic strategy for cancer, but mechanisms remain unclear.
  • N-myristoyltransferase 1 (NMT1) plays a role in myristoylation and cancer.

Purpose of the Study:

  • To investigate the role of NMT1 in breast cancer progression.
  • To elucidate the mechanisms by which NMT1 inhibition affects cancer cells.
  • To explore the potential of targeting NMT1 as a breast cancer therapy.

Main Methods:

  • Genetic inhibition of NMT1 in breast cancer cells (in vitro and in vivo).
  • Analysis of reactive oxygen species (ROS) and endoplasmic reticulum (ER) stress.
  • Investigation of protein degradation, mitochondrial function, and JNK/autophagy pathways.

Main Results:

  • NMT1 inhibition suppressed breast cancer initiation, proliferation, and invasion.
  • A feedback loop between NMT1, ROS, and oxidative stress was identified.
  • NMT1 inhibition induced protein degradation, ER stress, and ROS production, activating JNK and autophagy, which inhibited cancer progression, especially in triple-negative breast cancer (TNBC).

Conclusions:

  • NMT1 is a critical regulator of breast cancer cell behavior.
  • Targeting NMT1 induces a cascade of cellular stresses (oxidative, ER) leading to autophagy.
  • NMT1 inhibition represents a promising preclinical strategy for breast cancer treatment, particularly TNBC.

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