What question did this study set out to answer?

This research aims to uncover the role of NUPR1 in colorectal cancer progression and its mechanisms through LCN2 interaction.

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

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

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.

Luo et al. (2026) studied this question.

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