In:
Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 1326-1326
Abstract:
Lung cancer is the leading cause of cancer-related mortality in the world. Metastasis is the leading cause of death and an enormous therapeutic challenge for non-small cell lung cancer. Radiation therapy is a treatment of unresectable lung cancer and may palliate the symptoms, locally control tumor growth, and provide higher survival rate. Yet, the molecular mechanism of radio-sensitivity in lung cancer still remains unclear. Two lung adenocarcinoma cell lines (CL1-0 and CL1-5) with different metastatic potentials were irradiated with 10Gy γ-radiation. CL1-5 showed more radio-sensitive than CL1-0 since the surviving fractions in CL1-5 were ten times lower than CL1-0 by clonogenic assays. Gene expression profiles were also analyzed using microarray in order to better understand differential gene expression between these two cell lines after radiation. Total RNAs for whole genome gene expression analysis were extracted from these two cell lines at 0, 1, 4, 9 and 24 h after 10Gy irradiation. Gene Set Enrichment Analysis (GSEA) revealed the pathways of death, cytokine, cell adhesion, IL1R, NF-κB, and TNFR had differences between these two cell lines following 10Gy radiation exposure. Tumor necrosis factor (TNF) cytokine family and interleukin-1 (IL1) was up-regulated in CL1-5 after irradiation. The expression level of TNF-α validated by quantitative real time PCR was increased in CL1-5 and was not detected in CL1-0. Therefore, TNF-α released into the culture medium in CL1-5 after irradiation might be a death signal to activate the NF-κB pathway and cause more cell death. Moreover, the different responses of NF-κB-related pathways induced by radiation between the two cell lines might contribute the different survival. These cytokine modulations might provide promising targets for further investigation regarding radiation treatment in lung cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1326.
Type of Medium:
Online Resource
ISSN:
0008-5472
,
1538-7445
DOI:
10.1158/1538-7445.AM10-1326
Language:
English
Publisher:
American Association for Cancer Research (AACR)
Publication Date:
2010
detail.hit.zdb_id:
2036785-5
detail.hit.zdb_id:
1432-1
detail.hit.zdb_id:
410466-3
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