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March 26, 2026Journal of Biochemical and Molecular Toxicology

NUPR1 and LCN2: Potential Therapeutic Targets for Colorectal Cancer Via Modulating Cell Viability, Migration, and Ferroptosis‐Related Pathways

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Authors

DLDanni LuoXLXiaopan LuoSQShaojie Qian

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Overview

Demonstrates the role of NUPR1 and LCN2 in modulating cell viability in colorectal cancer, suggesting therapeutic implications.

Key Points

  • This research aims to uncover the role of NUPR1 in colorectal cancer progression and its mechanisms through LCN2 interaction.
  • Assessed cell viability and migration using cell counting kit-8 and Transwell assays.
  • Measured iron content, malondialdehyde (MDA), glutathione (GSH), reactive oxygen species (ROS), and lipid peroxidation with assay kits.
  • Examined NUPR1 and LCN2 interaction using co-immunoprecipitation and dual-luciferase reporter assays.
  • Utilized BALB/c nude mice for xenograft models to track tumor weight and volume.
  • Quantified gene expression via quantitative real-time PCR (qRT-PCR) and Western blotting.
  • NUPR1 and LCN2 were significantly overexpressed in colorectal cancer cell lines.
  • Knockdown of NUPR1 and LCN2 reduced cell viability, migration, and invasion.
  • NUPR1 knockdown affected GSH, ROS, lipid peroxidation, iron, and MDA levels similarly to erastin treatment.
  • In vivo, NUPR1 and LCN2 knockdown suppressed tumor growth, while NUPR1 overexpression promoted it.
  • NUPR1 overexpression effects were partially reversed by LCN2 knockdown.

Cite This Study

Luo et al. (2026) studied this question.

synapsesocial.com/papers/69c4cda5fdc3bde44891a450https://doi.org/10.1002/jbt.70809
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