AC099850.3/NCAPG Axis Predicts Poor Prognosis and is Associated with Resistance to EGFR Tyrosine-Kinase Inhibitors in Lung Adenocarcinoma
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Updated: Aug 29, 2025
Establishment and Characterization of Three Afatinib-resistant Lung Adenocarcinoma PC-9 Cell Lines Developed with Increasing Doses of Afatinib
Published on: June 26, 2019
Jiaqi Bao1, Yanlong Wu2, Kun Zhang3
1Department of Thoracic Surgery, Affiliated Hospital of Chifeng University, Chifeng, People's Republic of China.
Background:
TKI-acquired resistance markedly interferes with treatment of lung cancer patients with EGFR mutant features. Long non-coding RNAs (lncRNAs) modify EGFR-TKI resistance during tumor progression. Non-structural maintenance of chromosomes condensin I complex subunit G (NCAPG) is a mitosis-related protein that is involved in tumorigenesis. We investigated the potential regulatory lncRNAs of NCAPG in lung adenocarcinoma (LUAD) and assessed their roles in EGFR-TKI resistance.
Methods:
Data for 1678 lung cancer patients were retrieved from TCGA and GEO databases and used to evaluate NCAPG and lncRNAs expressions, as well as their prognostic significance in LUAD. Protein levels of NCAPG in LUAD were validated by immuno-histochemistry. To assess the relationship between NCAPG levels and EGFR-TKIs sensitivity, a cohort of 57 LUAD patients administered with EGFR-TKIs was used.
Results:
Both NCAPG and lncRNA AC099850.3 were over-expressed in LUAD tissues, and correlated with tumor progression and poor prognosis in LUAD. LncRNA AC099850.3 was identified as a potential regulator of NCAPG expressions. The AC099850.3/NCAGP axis was markedly correlated with EGFR mutations and IC50 of EGFR-TKIs. Besides, elevated NCAPG levels were associated with EGFR-TKIs resistance in 57 LUAD patients undergoing TKIs treatment. Gene set enrichment analysis revealed that both AC099850.3 and NCAGP were abundant in the cell cycle and the p53 signaling pathway.
Conclusion:
The AC099850.3/NCAPG axis is a potential prognostic predictor and therapeutic biomarker for EGFR-TKIs in LUAD.
Insights
The AC099850.3/NCAPG axis is a potential prognostic predictor and therapeutic biomarker for EGFR-TKIs in lung adenocarcinoma (LUAD). This axis correlates with tumor progression, poor prognosis, and EGFR-TKI resistance in LUAD patients.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Acquired resistance to tyrosine kinase inhibitors (TKIs) poses a significant challenge in treating EGFR-mutant lung adenocarcinoma (LUAD).
- Long non-coding RNAs (lncRNAs) play a role in modulating TKI resistance during LUAD progression.
- Non-structural maintenance of chromosomes condensin I complex subunit G (NCAPG), a mitosis-related protein, is implicated in tumorigenesis.
Purpose of the Study:
- To investigate potential regulatory lncRNAs of NCAPG in LUAD.
- To assess the role of the NCAPG regulatory network in EGFR-TKI resistance.
Main Methods:
- Utilized TCGA and GEO databases for expression analysis of NCAPG and lncRNAs in 1678 LUAD patients.
- Validated NCAPG protein levels via immunohistochemistry.
- Assessed the correlation between NCAPG levels and EGFR-TKI sensitivity in a cohort of 57 LUAD patients.
Main Results:
- NCAPG and lncRNA AC099850.3 were overexpressed in LUAD, correlating with tumor progression and poor prognosis.
- LncRNA AC099850.3 was identified as a regulator of NCAPG, forming the AC099850.3/NCAPG axis.
- This axis showed a strong correlation with EGFR mutations, EGFR-TKI IC50, and elevated NCAPG levels were linked to EGFR-TKI resistance.
Conclusions:
- The AC099850.3/NCAPG axis serves as a potential prognostic predictor in LUAD.
- This axis represents a promising therapeutic biomarker for EGFR-TKI treatment in LUAD.
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