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A Combined 3D Tissue Engineered In Vitro/In Silico Lung Tumor Model for Predicting Drug Effectiveness in Specific Mutational Backgrounds
Published on: April 6, 2016
tRF-Leu-CAG promotes cell proliferation and cell cycle in non-small cell lung cancer
Yang Shao1,2,3, Qiangling Sun4, Xiaomin Liu1
1Lab for Noncoding RNA & Cancer, School of Life Sciences, Shanghai University, Shanghai, China.
Abstract:
tRNA-derived RNA fragments (tRFs), non-coding single-stranded RNAs with 14-35 nt in length, were found to play important roles in gene regulation, even in carcinogenesis. In this study, we investigated the expression of tRF-Leu-CAG in human non-small cell lung cancer (NSCLC) and its function in the cell proliferation and cell cycle of NSCLC. The expression level of tRF-Leu-CAG was detected in NSCLC tissues, cell lines, and sera. tRF-Leu-CAG RNA levels were higher in NSCLC tumor tissues than in normal tissues, and also upregulated in NSCLC cell lines. A significant relationship was observed between stage progression and tRF-Leu-CAG in NSCLC sera. We found that in H1299 cells, inhibition of tRF-Leu-CAG suppressed cell proliferation and impeded cell cycle. AURKA was also repressed with the knockdown of tRF-Leu-CAG. Thus, our study revealed that tRF-Leu-CAG may be involved in regulating AURKA and could be a new diagnostic marker and potential therapeutic target in NSCLC.
Insights
tRNA-derived RNA fragments (tRFs), specifically tRF-Leu-CAG, are upregulated in non-small cell lung cancer (NSCLC). Inhibiting tRF-Leu-CAG suppressed NSCLC cell growth and proliferation by affecting the cell cycle and AURKA expression.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- Non-coding RNAs, including tRNA-derived RNA fragments (tRFs), are increasingly recognized for their regulatory roles in cellular processes.
- tRFs are implicated in gene regulation and have been linked to carcinogenesis, highlighting their potential involvement in cancer development.
Purpose of the Study:
- To investigate the expression of a specific tRF, tRF-Leu-CAG, in human non-small cell lung cancer (NSCLC).
- To elucidate the functional role of tRF-Leu-CAG in NSCLC cell proliferation and cell cycle progression.
- To explore tRF-Leu-CAG as a potential diagnostic marker and therapeutic target for NSCLC.
Main Methods:
- Quantitative analysis of tRF-Leu-CAG expression in NSCLC tissues, cell lines, and patient sera.
- Functional assays involving the inhibition of tRF-Leu-CAG in NSCLC cell lines (H1299).
- Assessment of cell proliferation, cell cycle, and AURKA gene expression following tRF-Leu-CAG knockdown.
Main Results:
- tRF-Leu-CAG expression was significantly higher in NSCLC tumor tissues compared to normal tissues.
- Upregulation of tRF-Leu-CAG was also observed in NSCLC cell lines.
- tRF-Leu-CAG levels in NSCLC sera showed a significant correlation with disease stage progression.
- Inhibition of tRF-Leu-CAG in H1299 cells led to suppressed cell proliferation and cell cycle arrest.
- Knockdown of tRF-Leu-CAG resulted in the repression of AURKA expression.
Conclusions:
- tRF-Leu-CAG is upregulated in NSCLC and plays a role in promoting cell proliferation and regulating the cell cycle.
- tRF-Leu-CAG may exert its function by modulating AURKA expression.
- tRF-Leu-CAG represents a promising novel diagnostic biomarker and a potential therapeutic target for NSCLC.
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