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. 2011 Dec;137(12):1739-47.
doi: 10.1007/s00432-011-1050-9. Epub 2011 Sep 10.

Solute carrier protein family may involve in radiation-induced radioresistance of non-small cell lung cancer

Li Xie  1 , Xianrang Song, Jinming Yu, Wei Guo, Ling Wei, Yanli Liu, Xingwu Wang
Affiliations

V体育2025版 - Solute carrier protein family may involve in radiation-induced radioresistance of non-small cell lung cancer

"VSports" Li Xie et al. J Cancer Res Clin Oncol. 2011 Dec.

Abstract

Purpose: To find new signaling pathways that may be involved in the cellular response to ionizing radiation VSports手机版. .

Methods: Two radioresistant subclones (A549/R and SPCA1/R) derived from lung adenocarcinoma cell lines A549 and SPCA1 were established after eight rounds of sublethal irradiation. The new subclones were tested for radioresistant features using clonogenic assay and apoptosis analysis. The genes expressed differentially were screened with cDNA microarray analysis consisting of 48,000 transcript probes and confirmed by quantitative real-time PCR V体育安卓版. .

Results: Stable and significant radioresistance was observed in the screened subclones V体育ios版. The microarray analysis showed 65 genes were up-regulated and 141 genes down-regulated in SPCA1/R cells. The up-regulated and down-regulated genes were 708 and 230 in A549/R cells, respectively. Twenty-seven altered genes were consistent in both subclones. Interestingly, members the of human solute carrier (SLC) gene superfamily were among in 27 genes. .

Conclusions: The differentially expressed genes in both cell lines may contribute to their radioresistant phenotype VSports最新版本. This extensive list of genes identified in the experiment provides a large body of potentially valuable information for studying the molecular mechanism(s) of radiosensitivity and identification of candidate molecular markers of radiation sensitivity. Thus, to our knowledge, the SLC gene superfamily is the first being reported to involve in acquired radioresistance. .

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Conflict of interest statement

We declare that we have no conflict of interest.

Figures

Fig. 1
Fig. 1
Survival curves for parent and radioresistant cells 1 month (a) and 3 months (b) after cessation of fractionated irradiation. The clonogenic assay was described in “Materials and methods”. There was a significant difference in survival fraction between parent and radioresistant cells (P < 0.05)
Fig. 2
Fig. 2
Irradiation-induced apoptosis in parent and radioresistant cells. Cells (1 × 106 each) were seeded in 60-mm dishes and incubated for 48 h after treatment with 10-Gy irradiation. Annexin V-FITC and PI (propidium iodide) staining was performed, followed by FACS analysis. The percentage of early apoptotic cells (Annexin V positive, PI negative) was counted. Similar results were obtained in three independent experiments
Fig. 3
Fig. 3
Cell proliferation assays of SPCA1 and SPCA1/R cells. Cells were cultured in 96-well plates for 0, 48, 96, and 144 h. Cell proliferation was determined by the MTT assay. Each point represents the mean ± SD of triplicate experiments. Statistically significant differences were obtained (P < 0.05; n = 6)
Fig. 4
Fig. 4
Radiosensitivity of SPCA1 and SPCA1/R xenografts to irradiation. Tumors were permitted to grow to a mean volume of 250 mm3 and then subjected to 0, 8, or 16 Gy irradiation as described in “Materials and methods”. Measurements of relative tumor volumes were performed over 28 days. Errors bar represent the standard error of the mean (P < 0.05)
Fig. 5
Fig. 5
Quantitative real-time PCR verification of genes that have not been classified as mediators of radiotherapy. For each gene, the left side bar (gray) indicates the expression ratio of cancer cells by microarray while the right side bar (black) indicates the expression ratio by quantitative real-time PCR. All quantitative real-time PCR data were consistent with microarray data
See this image and copyright information in PMC

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