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Published on: March 14, 2016
miR-101-3p sensitizes non-small cell lung cancer cells to irradiation
Zhonghui Li1, Zhenjie Qu1, Ying Wang2
1Department of Oncology, the Third Affiliated Hospital of Inner Mongolia Medical University, Inner Mongolia, China.
Abstract:
Recent studies have revealed that microRNAs regulate radiosensitivity of non-small cell lung cancer (NSCLC). The aim of this study was to investigate whether miR-101-3p is correlated with radiosensitivity of NSCLC. According to our results, miR-101-3p was downregulated in NSCLC tissues and cell lines. Moreover, miR-101-3p was decreased in A549 cells' response to irradiation in a dose-dependent manner. Upregulation of miR-101-3p decreased survival fraction and colony formation rate and increased irradiation-induced apoptosis in irradiation-resistant cells, while miR-101-3p depletion had the opposite effects in irradiation-sensitive cells. Furthermore, mechanistic target of rapamycin (mTOR) is a target gene of miR-101-3p. The expressions of mTOR, p-mTOR, and p-S6 were curbed by overexpression of miR-101-3p in A549R cells, which was enhanced by repression of miR-101-3p in A549 cells. Intriguingly, elevation in mTOR abated miR-101-3p upregulation-induced increase in irradiation sensitivity in irradiation-resistant cell line. In contrast, rapamycin undermined miR-101-3p inhibitor-mediated reduction of irradiation sensitivity in irradiation-sensitive cell line. Besides, miR-101-3p overexpression enhanced the efficacy of radiation in an NSCLC xenograft mouse model. In conclusion, miR-101-3p sensitized A549 cells to irradiation via inhibition of mTOR-signaling pathway.
Insights
MicroRNA miR-101-3p is downregulated in non-small cell lung cancer (NSCLC) and sensitizes cells to radiation therapy. It enhances radiation efficacy by inhibiting the mTOR signaling pathway.
Area of Science:
- Oncology
- Molecular Biology
- Radiotherapy
Background:
- MicroRNAs (miRNAs) are increasingly recognized as key regulators of radiosensitivity in non-small cell lung cancer (NSCLC).
- Understanding the specific roles of individual miRNAs in NSCLC radiosensitivity is crucial for developing novel therapeutic strategies.
Purpose of the Study:
- To investigate the correlation between miR-101-3p expression and radiosensitivity in NSCLC.
- To elucidate the underlying molecular mechanisms by which miR-101-3p influences cellular response to irradiation.
Main Methods:
- Quantitative real-time PCR to assess miR-101-3p expression in NSCLC tissues and cell lines.
- Cell viability assays (survival fraction, colony formation) and apoptosis assays in response to irradiation.
- Western blotting to analyze the expression of mTOR signaling pathway components.
- In vivo studies using an NSCLC xenograft mouse model.
Main Results:
- miR-101-3p was found to be downregulated in NSCLC tissues and cell lines, and its expression decreased with increasing radiation dose.
- Overexpression of miR-101-3p reduced cell survival and colony formation while increasing apoptosis in irradiation-resistant NSCLC cells.
- miR-101-3p directly targets the mechanistic target of rapamycin (mTOR) pathway, inhibiting mTOR, p-mTOR, and p-S6 expression.
- Restoring mTOR signaling partially abrogated the radiosensitizing effect of miR-101-3p, while mTOR inhibition enhanced radiation sensitivity.
- miR-101-3p overexpression improved radiation efficacy in an NSCLC xenograft mouse model.
Conclusions:
- miR-101-3p acts as a tumor suppressor and sensitizes NSCLC cells to irradiation.
- The radiosensitizing effect of miR-101-3p is mediated through the inhibition of the mTOR signaling pathway.
- miR-101-3p represents a potential therapeutic target for enhancing the efficacy of radiotherapy in NSCLC treatment.
