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AMRI-59 functions as a radiosensitizer via peroxiredoxin I-targeted ROS accumulation and apoptotic cell death

Wan Gi Hong1, Ju Yeon Kim1, Jeong Hyun Cho1

  • 1Division of Applied Radiation Bioscience, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.

Oncotarget
|January 27, 2018
PubMed

Insights

AMRI-59 enhances cancer treatment by acting as a radiosensitizer for non-small cell lung cancer. This drug boosts radiation therapy effectiveness by targeting peroxiredoxin I, increasing cell death via the ROS/γH2AX/caspase pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Radiotherapy

Background:

  • Peroxiredoxin (PRX) I is an enzyme involved in cellular redox regulation.
  • AMRI-59 is a known specific pharmaceutical inhibitor of PRX I enzyme activity.
  • Radiosensitizers can enhance the efficacy of radiation therapy in cancer treatment.

Purpose of the Study:

  • To investigate the radiosensitizing potential of AMRI-59 in non-small cell lung cancer (NSCLC) cells.
  • To elucidate the intracellular mechanisms underlying AMRI-59-induced radiosensitization.
  • To evaluate the in vivo efficacy of AMRI-59 in combination with radiation therapy for NSCLC.

Main Methods:

  • Clonogenic assays were used to assess radiosensitization in NSCLC cells.
  • Immunoblotting, ROS generation, mitochondrial potential, and cell death assays were performed to determine intracellular mechanisms.
  • In vivo studies involved co-treatment of nude mice bearing NSCLC xenografts with AMRI-59 and gamma-ionizing radiation (IR).
  • Tumor volumes and apoptosis were measured in vivo.

Main Results:

  • AMRI-59 demonstrated dose enhancement ratios of 1.51 and 2.12 in NCI-H460 and NCI-H1299 cells, respectively.
  • Combination treatment augmented ROS production and mitochondrial disruption, leading to increased DNA damage (γH2AX) and apoptosis via caspase-3 activation.
  • AMRI-59 suppressed ERK phosphorylation, a pathway that, when blocked, enhanced apoptosis.
  • In vivo, combined AMRI-59 and IR delayed tumor growth significantly in xenograft models.

Conclusions:

  • AMRI-59 acts as a PRX I-targeted radiosensitizer in non-small cell lung cancer.
  • The radiosensitization mechanism involves the ROS/γH2AX/caspase pathway activation and ERK suppression.
  • AMRI-59 holds potential for improving radiation therapy outcomes in NSCLC treatment.
Keywords:
AMRI-59ROSnon-small cell lung cancerperoxiredoxinradiosensitizer

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