Evidence map›Paper›PMID 40153115›Full record

ArticleDiscover oncology2025

NEK2 promotes cancer cell progression and 5-fluorouracil resistance via the Wnt/β-catenin signaling pathway in colorectal cancer.

Facai Cui, Yu Chen, Xiaoyu Wu, Weifeng Zhao

Abstract read
In one paragraph

Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Facai CuiDepartment of Clinical Laboratory, Henan Provincial People's Hospital, Zhengzhou, China. cuifacai1985@zzu.edu.cn.
Yu ChenDepartment of Pathology, Affiliated Tumor Hospital of Zhengzhou University, Zhengzhou, China.
Xiaoyu WuDepartment of Clinical Laboratory, Henan Provincial People's Hospital, Zhengzhou, China.
Weifeng ZhaoDepartment of Oncology, Henan Provincial People's Hospital, Zhengzhou, China.

Funding

Henan Province medical science and technology research project 201702220Henan Province medical science and technology research project 201702246
6 · The paper itself

Abstract

backgroundNever-in-mitosis gene A-related-kinase-2 (NEK2) plays a pivotal role in malignant progression and chemotherapy sensitivity. This study aimed to elucidate the role of NEK2 in colorectal cancer (CRC) and its potential contribution to 5-fluorouracil (5‑FU) resistance mechanisms.

methodsQuantitative real-time PCR (qRT‑PCR), western blotting, and immunohistochemical (IHC) staining were used to assess the expression of NEK2 in CRC tissues and cells. The effects of NEK2 and 5‑FU on the proliferation, apoptosis, migration, and invasion of cancer cells were investigated via Cell Counting Kit-8 (CCK-8), colony formation, flow cytometry, wound healing, and transwell assays, respectively. Methyl 3-(4-methylphenylsulfonamido) benzoate (MSAB) was used as a Wnt/beta (β)-catenin pathway inhibitor in this study.

resultsNEK2 expression was significantly upregulated in CRC tissues and cells compared to normal controls. High NEK2 expression in CRC tissues was correlated with advanced tumor-node-metastasis (TNM) stage, lymph node metastasis, distant metastasis, and a poor tumor prognosis. NEK2 overexpression promoted the proliferation, migration, and invasion of CRC cells. NEK2 overexpression inhibited the cytotoxic effect of 5-FU on CRC cells. NEK2 overexpression promoted the nuclear accumulation of β-catenin and activated the Wnt/β-catenin signaling pathway. MSAB reversed the stimulatory effect of NEK2 upregulation on proliferation and resistance to 5-FU in CRC cells.

conclusionsIn summary, NEK2 promotes cell survival and decreases sensitivity to 5-FU in CRC by activating the Wnt/β-catenin signaling pathway. Consequently, NEK2 holds promise as a potential therapeutic target for CRC management.

Indexed as

5-Fluorouracil resistanceColorectal cancerMigrationNEK2ProliferationWnt/β-catenin signaling pathway

Identifiers

PMID40153115
PMCPMC11953509

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.