Investigating the Regulatory Role of Neuritin in TUBB3 Expression and Akt-mTOR Signaling Pathway in Gastric Cancer Cells.

Authors

Chen Zhong, Yinan Lu, Xueru Chen, Xiangying Dong, Tongtong Wang, Licui Zhang

Published in

Clinical laboratory. Volume 72. Issue 6. Jun 01, 2026.

Abstract

Gastric cancer (GC) is a leading cause of cancer-related mortality worldwide. Understanding the molecular mechanisms underlying gastric cancer progression is essential for developing novel diagnostic and therapeutic strategies. Neuritin, a neurotrophic factor, has been implicated in various cellular processes, but its role in gastric cancer remains poorly understood. This study investigated the expression and function of neuritin in gastric cancer cells, focusing on its regulation of type III β-tubulin (TUBB3) and the Akt/mTOR signaling pathway.
Four human gastric cancer cell lines (KATOⅢ, SNU-1, AGS, and NCI-N87) and normal gastric mucosal epithelial cells (GES-1) were cultured. Neuritin expression was evaluated using quantitative reverse transcription qRT-PCR and Western blot analysis. Gastric cancer cells with low endogenous neuritin expression were transfected with a pcDNA3.1-neuritin plasmid, while those with high neuritin expression were transfected with siRNA-neuritin. Transfection efficiency was verified by qRT-PCR and Western blot. TUBB3 expression and key components of the Akt/mTOR signaling pathway were examined following neuritin overexpression or knockdown. Cellular proliferation, migration, and invasion capabilities were assessed using CCK-8 assays and Transwell experiments in neuritin-knockdown cell lines.
Neuritin mRNA and protein expression levels were significantly higher in gastric cancer cell lines (KATOⅢ, SNU-1, AGS, and NCI-N87) compared to normal gastric mucosal epithelial cells (GES-1). Overexpression of neuritin led to upregulation of TUBB3, p-Akt, and p-mTOR expression, whereas neuritin knockdown resulted in decreased expression of these markers. Neuritin depletion significantly attenuated cellular proliferation, migration, and invasion capacities. These findings indicate that neuritin promotes gastric cancer progression by upregulating TUBB3 and activating the Akt/mTOR pathway.
Neuritin is overexpressed in human gastric cancer cell lines and plays a crucial role in promoting malignant behaviors by regulating TUBB3 expression and the Akt/mTOR signaling pathway. Downregulation of neuritin effectively suppresses the proliferation, migration, and invasion of gastric cancer cells. This study suggests that neuritin may serve as a promising molecular target for the diagnosis and prognosis evaluation of gastric cancer.

PMID:
42295303
Bibliographic data and abstract were imported from PubMed on 15 Jun 2026.

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