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Targeting surface nucleolin induces autophagy-dependent cell death in pancreatic cancer via AMPK activation

Cheng Xu1,2, Yunfei Wang1,2, Qiu Tu1

  • 1Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences/Key Laboratory of Bioactive Peptides of Yunnan Province, Kunming Institute of Zoology, Kunming, 650223, Yunnan, China.

Oncogene
|October 26, 2018
PubMed

Insights

A novel peptide, LZ1, derived from snake venom, effectively inhibits pancreatic cancer growth by triggering autophagy-dependent cell death. This promising agent shows significant antitumor efficacy with minimal side effects in preclinical models.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Pancreatic cancer is a highly lethal malignancy with limited effective treatments.
  • Conventional therapies like surgery and chemotherapy offer modest survival benefits.

Purpose of the Study:

  • To investigate the therapeutic potential of LZ1, a snake venom-derived peptide, against pancreatic cancer.
  • To elucidate the mechanism of action of LZ1 in pancreatic cancer cells.

Main Methods:

  • In vitro and in vivo studies using pancreatic cancer cell lines and orthotopic mouse models.
  • Pharmacological and genetic inhibition of autophagy.
  • Analysis of nucleolin expression and its downstream signaling pathways (AMPK/mTORC1).

Main Results:

  • LZ1 significantly inhibited pancreatic cancer cell growth and induced autophagy-dependent cell death.
  • Systemic LZ1 administration demonstrated potent antitumor efficacy and prolonged survival in mice.
  • LZ1 targets surface nucleolin, activating AMPK and inducing autophagic flux, leading to cancer cell death.

Conclusions:

  • LZ1 represents a promising novel therapeutic lead for pancreatic cancer.
  • The LZ1-nucleolin-AMPK-autophagy axis offers a potential therapeutic strategy.

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