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中华口腔医学研究杂志(电子版) ›› 2015, Vol. 09 ›› Issue (04) : 277 -282. doi: 10.3877/cma.j.issn.1674-1366.2015.04.004

所属专题: 文献

基础研究

白细胞介素1β对两种肿瘤细胞活性氧含量及侵袭迁移能力影响
吕倩书1, 贺媛1, 吴桐1,()   
  1. 1. 510055 广州,中山大学光华口腔医学院·附属口腔医院,广东省口腔医学重点实验室
  • 收稿日期:2015-06-04 出版日期:2015-08-01
  • 通信作者: 吴桐
  • 基金资助:
    国家自然科学基金(81272948)

Influence of IL-1β on the intracellular reactive oxygen species level together with invasion and migration behavior of two kinds of cancer cells

Qianshu Lyu1, Yuan He1, Tong Wu1,()   

  1. 1. Guanghua School of Stomatology, Hospital of Stomatology, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Stomatology, Guangzhou 510055, China
  • Received:2015-06-04 Published:2015-08-01
  • Corresponding author: Tong Wu
  • About author:
    Corresponding author: Wu Tong, Email:
引用本文:

吕倩书, 贺媛, 吴桐. 白细胞介素1β对两种肿瘤细胞活性氧含量及侵袭迁移能力影响[J]. 中华口腔医学研究杂志(电子版), 2015, 09(04): 277-282.

Qianshu Lyu, Yuan He, Tong Wu. Influence of IL-1β on the intracellular reactive oxygen species level together with invasion and migration behavior of two kinds of cancer cells[J]. Chinese Journal of Stomatological Research(Electronic Edition), 2015, 09(04): 277-282.

目的

探讨白细胞介素1β(IL-1β)对口腔鳞癌CAL-27细胞及非小细胞肺癌A549细胞增殖、活性氧(ROS)含量及侵袭迁移能力的影响。

方法

用外源性重组人IL-1β作用于口腔鳞癌CAL-27细胞及非小细胞肺癌A549细胞,CCK8法检测其增殖能力,活性氧含量检测试剂盒检测其细胞内ROS含量的变化,Transwell法观察IL-1β作用后细胞侵袭迁移能力的改变,使用方差分析方法对所得结果进行统计学分析。

结果

IL-1β对两组细胞增殖能力无影响,50及100 ng/mL浓度的IL-1β在8、12 h可上调CAL-27细胞ROS含量(F8 h=24.436,P8 h=0.001;F12 h=64.579,P12 h < 0.05),在4、8及12 h可上调A549细胞ROS含量(F4 h=19.888,P4 h=0.002;F8 h=30.249,P8 h < 0.05;F12 h=32.703,P12 h=0.001),促进两组细胞侵袭迁移(FCAL-27侵袭=159.783,PCAL-27侵袭 < 0.05;FCAL-27迁移=264.045,PCAL-27迁移 < 0.05;FA549侵袭=936.278,PA549侵袭 < 0.05;FA549迁移=1389.961,PA549迁移 < 0.05)。

结论

IL-1β可以上调口腔鳞癌CAL-27细胞及非小细胞肺癌A549细胞ROS含量,同时促进其侵袭迁移。

Objective

To investigate the effect of IL-1β on cell proliferation, intracellular reactive oxygen species(ROS)level, and the invasion and migration ability of oral squamous cell carcinoma CAL-27 cell line and the non-small cell lung cancer A549 cell line.

Methods

Oral squamous cell carcinoma CAL27 cell line and non-small cell lung cancer A549 cell line, were treated with 0 ng/ml, 50 ng/ml and 100 ng/ml recombinant human IL-1β. The proliferation ability of CAL-27 and A549 cells were detected using CCK8 assay, the intracellular reactive oxygen species(ROS)levels were measured with Reactive Oxygen Species Assay Kit, the invasion and migration ability were investigated using Transwell assay. Statistical analysis of the results was performed using one-way ANOVA.

Results

The proliferation ability of CAL-27 and A549 cells did not change significantly under treatment with IL-1β. The intracellular ROS levels of CAL-27 cells were up-regulated under treatment with IL-1β (50 and 100 ng/ml)for 8 and 12 h(F8 h=24.436, P8 h=0.001; F12 h=64.579, P12 h < 0.05), the intracellular ROS levels of A549 cells were upregulated under treatment with IL-1β(50 and 100 ng/ml)for 4, 8 and 12 h(F4 h=19.888, P4 h=0.002; F8 h=30.249, P8 h < 0.05; F12 h=32.703, P12 h=0.001). The invasion and migration ability of CAL-27 and A549 cells were obviously increased by recombinant human IL-1β(FCAL-27 invasion=159.783, PCAL-27 invasion < 0.05; FCAL-27 migration=264.045, PCAL-27 migration < 0.05; FA549 invasion=936.278, PA549 invasion < 0.05; FA549 migration=1389.961, PA549 migration < 0.05).

Conclusion

IL-1β could increase the ROS level as well as the invasion and migration ability of oral squamous cell carcinoma CAL-27 cells and the non-small cell lung cancer A549 cells.

图1 IL-1β对口腔鳞癌CAL-27细胞增殖能力无影响
图2 IL-1β对非小细胞肺癌A549细胞增殖能力无影响
图3 IL-1β上调口腔鳞癌CAL-27细胞ROS含量(aP < 0.05)
图4 IL-1β上调非小细胞肺癌A549细胞ROS含量(aP < 0.05)
图5 IL-1β增强口腔鳞癌CAL-27细胞侵袭迁移能力
图6 IL-1β增强非小细胞肺癌A549细胞侵袭迁移能力
[1]
Ralhan R, Desouza LV, Matta A, et al. iTRAQ-multidimensional liquid chromatography and tandem mass spectrometry-based identification of potential biomarkers of oral epithelial dysplasia and novel networks between inflammation and premalignancy[J]. J Proteome Res, 2009, 8(1): 300-309.
[2]
Lee CH, Chang JS, Syu SH, et al. IL-1β promotes malignant transformation and tumor aggressiveness in oral cancer[J]. J Cell Physiol, 2015, 230(4): 875-884.
[3]
Voronov E, Reich E, Dotan S, et al. Effects of IL-1 mole-cules on growth patterns of 3-MCA-induced cell lines: an inter-play between immunogenicity and invasive potential[J]. J Immunotoxicol, 2010, 7(1): 27-38.
[4]
Kim GY, Lee JW, Ryu HC, et al. Proinflammatory cytokine IL-1beta stimulates IL-8 synthesis in mast cells via a leukotriene B4 receptor 2-linked pathway, contributing to angiogenesis[J]. J Immunol, 2010, 184(7): 3946-3954.
[5]
Merry HE, Phelan P, Doaks M, et al. Functional roles of tumor necrosis factor-alpha and interleukin 1-Beta in hypoxia and reoxygenation[J]. Ann Thorac Surg, 2015, 99(4): 1200-1205.
[6]
Lewis AM, Varghese S, Xu H, et al. Interleukin-1 and cancer progression: the emerging role of interleukin-1 receptor antagonist as a novel therapeutic agent in cancer treatment[J]. J Transl Med, 2006(4): 48.
[7]
Puig-Vilanova E, Rodriguez DA, Lioreta J, et al. Oxidative stress, redox signaling pathways, and autophagy in cachectic muscles of male patients with advanced COPD and lung cancer[J]. Free Radic Biol Med, 2015(79): 91-108.
[8]
Huang M, Wang J, Lee P, et al. Human non-small cell lung cancer cells express a type 2 cytokine pattern[J]. Cancer Res, 1995, 55(17): 3847-3853.
[9]
Watari K, Shibata T, Kawahara A, et al. Tumor-derived interleukin-1 promotes lymphangiogenesis and lymph node metastasis through M2-type macrophages[J]. PLoS One, 2014, 9(6): e99568.
[10]
Johnson NW, Jayasekara P, Amarasinghe AA. Squamous cell carcinoma and precursor lesions of the oral cavity: epidemiology and aetiology[J]. Periodontol 2000, 2011, 57(1): 19-37.
[11]
Kumar A, Pant MC, Singh HS, et al. Determinants of oxidative stress and DNA damage(8-OhdG)in squamous cell carcinoma of head and neck[J]. Indian J Cancer, 2012, 49(3): 309-315.
[12]
Czesnikiewicz-Guzik M, Lorkowska B, Zapala J, et al. NADPH oxidase and uncoupled nitric oxide synthase are major sources of reactive oxygen species in oral squamous cell carcinoma. Potential implications for immune regulation in high oxidative stress conditions[J]. J Physiol Pharmacol, 2008, 59(1): 139-152.
[13]
Dequanter D, Van de Velde M, Nuyens V, et al. Assessment of oxidative stress in tumors and histologically normal mucosa from patients with head and neck squamous cell carcinoma: a preliminary study[J]. Eur J Cancer Prev, 2013, 22(6): 558-560.
[14]
Miura Y, Kozuki Y, Yagasaki K. Potentiation of invasive activity of hepatoma cells by reactive oxygen species is mediated by autocrine/paracrine loop of hepatocyte growth factor[J]. Biochem Biophys Res Commun, 2003, 305(1): 160-165.
[15]
Apte RN, Krelin Y, Song X, et al. Effects of micro-environment - and malignant cell-derived interleukin-1 in carcinogenesis, tumour invasiveness and tumour-host interactions[J]. Eur J Cancer, 2006, 42(6): 751-759.
[16]
Muqbil I, Beck FW, Bao B, et al. Old wine in a new bottle: the Warburg effect and anticancer mechanisms of resveratrol[J]. Curr Pharm Des, 2012, 18(12): 1645-1654.
[17]
Sung HJ, Ma W, Starost MF, et al. Ambient oxygen promotes tumorigenesis[J]. PLoS One, 2011, 6(5): e19785.
[18]
Kuykendall A, Chiappori A. Advanced EGFR mutation-positive non-small-cell lung cancer: case report, literature review, and treatment recommendations[J]. Cancer Control, 2014, 21(1): 67-73.
[19]
Dorsey JF, Kao GD, MacArthur KM, et al. Tracking viable circulating tumor cells(CTCs)in the peripheral blood of non-small cell lung cancer(NSCLC)patients undergoing definitive radiation therapy: pilot study results[J]. Cancer, 2015, 121(1): 139-149.
[20]
Fleury C, Mignotte B, Vayssière JL. Mitchondrial reactive oxygen species in cell death signaling[J]. Biochimie, 2002, 84(2-3): 131-141.
[21]
Sohal RS, Arnold L, Orr WC. Effect of age on superoxide dismutase, catalase, glutathione reductase, inorganic peroxides, TBA-reactive material, GSH/GSSG, NADPH/NADP+ and NADH/NAD+ in Drosophila melanogaster[J]. Mech Ageing Dev, 1990, 56(3): 223-235.
[22]
Cheng CY, Kuo CT, Lin CC, et al. IL-1beta induces expression of matrix metalloproteinase-9 and cell migration via a c-Src-dependent, growth factor receptor transactivation in A549 cells[J]. Br J Pharmacol, 2010, 160(7): 1595-1610.
[23]
Petrella BL, Armstrong DA, Vincenti MP. Interleukin-1 beta and transforming growth factor-beta 3 cooperate to activate matrix metalloproteinase expression and invasiveness in A549 lung adenocarcinoma cells[J]. Cancer Lett, 2012, 325(2): 220-226.
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