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Updated: Nov 30, 2025

Author Spotlight: Unveiling Transmembrane Protein Family-Related Markers in Gastric Cancer and Implications for Targeted Therapies
07:47

Author Spotlight: Unveiling Transmembrane Protein Family-Related Markers in Gastric Cancer and Implications for Targeted Therapies

Published on: September 15, 2023

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High expression of NEK2 promotes gastric cancer progression via activating AKT signaling

Hao Wan1, Lin Xu2, Huangbin Zhang1

  • 1Department of General Surgery, The First Affiliated Hospital of Nanchang University, No.17 Yongwaizheng Street, Donghu District, Nanchang, 330006, Jiangxi, China.

Journal of Physiology and Biochemistry
|November 17, 2020
PubMed

Insights

Never in mitosis gene A-related kinase 2 (NEK2) drives gastric cancer by activating AKT pathways. NEK2 overexpression promotes tumor growth and impairs treatment response, suggesting NEK2 as a therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Never in mitosis gene A-related kinase 2 (NEK2) is an identified oncogene in various cancers.
  • Gastric cancer, prevalent in Eastern Asia, has a poor prognosis, and NEK2's role remains unclear.
  • Understanding NEK2's function in gastric cancer is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the association between NEK2 and gastric cancer development and progression.
  • To elucidate the molecular mechanisms by which NEK2 influences gastric cancer.
  • To explore NEK2 as a potential therapeutic target for gastric cancer.

Main Methods:

  • Investigated NEK2 expression levels in gastric cancer patients.
  • Examined the interaction between NEK2 and protein phosphatase 1 (PP1).
  • Analyzed the activation of AKT signaling pathways and downstream targets (HIF1α, mTOR) upon NEK2 modulation.
  • Assessed the impact of NEK2 on glucose metabolism and autophagy.
  • Evaluated the effects of NEK2 silencing on gastric cancer cell growth and treatment response.

Main Results:

  • NEK2 is overexpressed in gastric cancer, correlating with larger tumor size and lymph node metastasis.
  • NEK2 overexpression inhibits PP1, leading to AKT activation and downstream oncogenic signaling.
  • The AKT/HIF1α axis promotes aerobic glycolysis for cancer cell energy.
  • The AKT/mTOR axis suppresses autophagy, enhancing cell survival and treatment resistance.
  • NEK2 silencing reduces aerobic glycolysis, induces autophagic cell death, and inhibits tumor growth.

Conclusions:

  • NEK2 promotes gastric cancer progression through AKT-mediated activation of oncogenic pathways.
  • NEK2 influences glucose metabolism and autophagy in gastric cancer cells.
  • Targeting NEK2 offers a potential therapeutic strategy for gastric cancer treatment.
Keywords:
AKT signaling pathwayAerobic glycolysisAutophagyGastric cancerNEK2

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