Unraveling novel transposable elements (TEs)-driven gene dysregulation in non-small cell lung cancer (NSCLC) by integrated transcriptomic and TEs analysis.
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OpenAlex 토픽 ·
Chromosomal and Genetic Variations
Genomic variations and chromosomal abnormalities
RNA Research and Splicing
Transposable Elements (TEs) represent a class of mobile genomic sequences, which may seriously disrupt gene regulation and can contribute to tumorigenesis.
APA
S Shrinidhi, R Sagaya Jansi, Ameer Khusro (2026). Unraveling novel transposable elements (TEs)-driven gene dysregulation in non-small cell lung cancer (NSCLC) by integrated transcriptomic and TEs analysis.. Computational biology and chemistry, 122, 108942. https://doi.org/10.1016/j.compbiolchem.2026.108942
MLA
S Shrinidhi, et al.. "Unraveling novel transposable elements (TEs)-driven gene dysregulation in non-small cell lung cancer (NSCLC) by integrated transcriptomic and TEs analysis.." Computational biology and chemistry, vol. 122, 2026, pp. 108942.
PMID
41690151 ↗
Abstract 한글 요약
Transposable Elements (TEs) represent a class of mobile genomic sequences, which may seriously disrupt gene regulation and can contribute to tumorigenesis. Yet, their role in NSCLC has remained unexplored to a great degree. Therefore, an integrated transcriptomic and Transposable Element (TE) analysis was performed to investigate TE-driven gene dysregulation in NSCLC. Hierarchical clustering of differentially expressed TE revealed significant over-representation of LTR1A1 and HERVL18-int in the cancer samples, with notably high expression of LINE and ERV members, especially HERVL-int, L1MC5, and L1M5. The intersection of TE expression with differentially expressed genes revealed several TE-associated genes involved in cell cycle regulation, genomic stability, and tumor progression. Fusion transcript analysis highlighted unique cancer-specific events, offering insights into TE-mediated transcriptomic alterations. Molecular docking of TE-associated proteins, HMMR, and PBK suggested potential interactions that may influence oncogenic pathways. Collectively, our findings uncover novel TE-driven mechanisms of gene dysregulation in NSCLC and highlight specific TEs and associated genes as potential diagnostic markers and therapeutic targets, offering a framework for future experimental studies to explore their mechanistic and clinical significance.
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