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Updated: Aug 2, 2025

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
GTSE1 promotes the growth of NSCLC by regulating microtubule-associated proteins through the ERK/MAPK pathway
Chuanlin Wang1,2, Meiyan Wen1,2, Jiali Xu1,2
1Department of Clinical Nutrition, Yunnan Cancer Hospital/The Third Affiliated Hospital of Kunming Medical University, Kunming, China.
Abstract:
The role of G2 and S phase-expressed-1 (GTSE1), a microtubule-localized protein, in non-small-cell lung cancer (NSCLC) remains unknown. We explored its role in NSCLC growth. GTSE1 was detected in NSCLC tissues and cell lines using quantitative real-time polymerase chain reaction. The clinical significance of GTSE1 levels was evaluated. Biological and apoptotic effects of GTSE1 were evaluated using transwell, cell-scratch, and MTT assays, and flow cytometry and western blotting, respectively. Its association with cellular microtubules was shown by western blotting and immunofluorescence. GTSE1 expression was upregulated in NSCLC tissues and cell lines. GTSE1 levels correlated with lymph node metastasis. Higher GTSE1 mRNA expression correlated with shorter progression-free survival. GTSE1-knockdown decreased proliferation, colony formation, invasion, and migration of NSCLC cells, and inhibited tau and stathmin-1 microtubule-associated protein expression, via the extracellular-regulated protein kinase/mitogen-activated protein kinase (ERK/MAPK) signaling pathway, and microtubule disruption. GTSE1 may promote NSCLC growth by regulating tau and stathmin-1 through the ERK/MAPK signaling pathway.
Insights
G2 and S phase-expressed-1 (GTSE1) promotes non-small-cell lung cancer (NSCLC) growth by affecting microtubules. Upregulated GTSE1 correlates with metastasis and shorter survival, suggesting it as a potential therapeutic target.
Area of Science:
- Oncology
- Cell Biology
- Molecular Biology
Background:
- The role of G2 and S phase-expressed-1 (GTSE1), a microtubule-associated protein, in non-small-cell lung cancer (NSCLC) pathogenesis is not well understood.
- GTSE1's function in cancer progression warrants investigation for potential therapeutic strategies.
Purpose of the Study:
- To investigate the role and clinical significance of GTSE1 in non-small-cell lung cancer (NSCLC) growth and progression.
- To elucidate the molecular mechanisms by which GTSE1 influences NSCLC cell behavior and microtubule dynamics.
Main Methods:
- Quantitative real-time polymerase chain reaction (qRT-PCR) to assess GTSE1 expression in NSCLC tissues and cell lines.
- Transwell, cell-scratch, MTT assays, flow cytometry, and western blotting to evaluate biological and apoptotic effects.
- Immunofluorescence and western blotting to confirm GTSE1's association with cellular microtubules.
Main Results:
- GTSE1 expression was significantly upregulated in NSCLC tissues and cell lines compared to normal controls.
- Higher GTSE1 mRNA levels correlated with lymph node metastasis and shorter progression-free survival in NSCLC patients.
- GTSE1 knockdown suppressed NSCLC cell proliferation, colony formation, invasion, and migration, and inhibited microtubule-associated proteins tau and stathmin-1 via the ERK/MAPK pathway.
Conclusions:
- GTSE1 is upregulated in NSCLC and associated with adverse clinical outcomes, indicating its oncogenic potential.
- GTSE1 promotes NSCLC growth by modulating tau and stathmin-1 expression through the extracellular-regulated protein kinase/mitogen-activated protein kinase (ERK/MAPK) signaling pathway, leading to microtubule disruption.
- GTSE1 represents a potential therapeutic target for managing non-small-cell lung cancer.
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