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Melittin treatment suppressed malignant NSCLC progression through enhancing CTSB-mediated hyperautophagy

Yuhan Wang1, Tailei Yuan2, Longyue He3

  • 1Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PR China; Shanghai Key Laboratory of Molecular Imaging, Shanghai University of Medicine and Health Sciences, Shanghai 201318, PR China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|October 19, 2024
PubMed

Insights

Melittin, a bee venom component, inhibits non-small cell lung cancer (NSCLC) by enhancing CTSB-mediated hyperautophagy. This study reveals Melittin

Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • Melittin shows preclinical anticancer potential, but its mechanism in non-small cell lung cancer (NSCLC) is unclear.
  • Understanding Melittin's regulatory role and mechanism in NSCLC is crucial for its therapeutic development.

Purpose of the Study:

  • To investigate the regulatory role and mechanism of Melittin in non-small cell lung cancer (NSCLC).
  • To identify proteins differentially expressed in NSCLC cells treated with Melittin.
  • To elucidate the direct interaction between Melittin and its target in NSCLC.

Main Methods:

  • Proteomic analysis to identify differentially expressed proteins in Melittin-treated NSCLC cells.
  • Lung cancer tissue chip experiments to validate CTSB expression in NSCLC tissues.
  • Molecular docking and LiP-SMap analysis to determine Melittin-CTSB binding.
  • In vitro and in vivo studies using NSCLC cell lines (A549, HCC1833) and animal models.
  • Treatment with CTSB-specific inhibitor (CA-074 Me) and autophagy inhibitor (3-MA) to assess Melittin's effects.

Main Results:

  • Proteomic analysis identified CTSB (Cathepsin B) as a key protein upregulated in lysosomes of Melittin-treated NSCLC cells.
  • CTSB expression was significantly higher in NSCLC tissues compared to adjacent normal tissues.
  • Melittin directly binds to CTSB, increasing its lysosomal levels and promoting hyperautophagy, thereby inhibiting NSCLC progression.
  • Melittin demonstrated significant inhibition of A549 and HCC1833 cell proliferation and tumor growth in vivo.
  • CTSB and autophagy inhibition reversed Melittin's anti-cancer effects in NSCLC.

Conclusions:

  • Melittin inhibits the malignant progression of non-small cell lung cancer (NSCLC) by directly targeting and upregulating CTSB.
  • Melittin-induced CTSB upregulation leads to hyperautophagy, a key mechanism for its anti-cancer activity in NSCLC.
  • These findings support Melittin as a potential therapeutic agent for NSCLC, acting through the CTSB-mediated hyperautophagy pathway.
Keywords:
AutophagyCTSBMalignant progressionMelittinNSCLC

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