黄芩苷对人舌鳞癌细胞SCC15的抑制作用
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摘要
目的探讨黄芩苷对人舌鳞癌细胞株SCC15细胞的抑制作用及可能机制,为舌鳞癌的防治提供新的思路及实验基础。方法单纯DMEM培养液培养的SCC15细胞为对照组,加入20 mg/mL黄芩苷溶液培养的SCC15细胞为黄芩苷组。2组细胞分别以划痕实验及Transwell迁移实验检测细胞迁移能力的改变,流式细胞术检测细胞周期的改变,Western blotting检测细胞信号转导与转录激活子3(signal transduction and transcrip?tion activator 3,STAT3)磷酸化水平的差异。结果与对照组比较,划痕实验及Transwell迁移实验结果显示黄芩苷组细胞迁移能力降低(t=4.927,P=0.008);流式细胞术结果显示黄芩苷组G0/G1期增高(t=9.893,P=0.001),S期降低(t=8.528,P=0.001),G2/M期降低(t=3.550,P=0.024);Western blotting结果显示黄芩苷组SCC15细胞STAT3蛋白磷酸化水平下降(t=8.262,P=0.001)。结论黄芩苷对人舌鳞癌细胞SCC15具有抑制作用,其机制可能与降低STAT3通路磷酸化活性有关。
ObjectiveTo explore the inhibitory effect and possible mechanism of Baicalin on the human tongue squamous cell carcinoma cell line SCC15 and to provide a new idea and experimental basis for the clinical prevention and treatment of tongue squamous cell carcinoma.MethodsSCC15 cells cultured in DMEM alone were used as the control group, and SCC15 cells cultured in 20 mg/mL baicalin solution were used as the baicalin group. Scratch tests and Transwell migration tests were performed to detect changes in cell migration ability, and flow cytometry was used to detect changes in the cell cycle. Western blotting was used to detect differences in the phosphorylation levels of signal transduction and transcription activator 3(STAT3).ResultsCompared with the control group, the scratch test and the Transwell migration test showed that the cell migration ability of cells in the baicalin group was significantly decreased(t=4.927, P=0.008); flow cytometry showed that the number of cells of the baicalin group increased in the G0/G1 phase(t=9.893, P=0.001), decreased in the S phase(t=8.528, P=0.001), and decreased in the G2/M phase(t=3.550, P=0.024); Western blotting results showed that the STAT3 protein of SCC15 cells in the baicalin group decreased(t=3.550, P=0.024), and the phosphorylation level significantly decreased(t=8.262, P=0.001).ConclusionBaicalin inhibits the human tongue squamous cell carcinoma cell line SCC15, and its mechanism may be relatedto a decrease in STAT3 pathway phosphorylation activity.
ObjectiveTo explore the inhibitory effect and possible mechanism of Baicalin on the human tongue squamous cell carcinoma cell line SCC15 and to provide a new idea and experimental basis for the clinical prevention and treatment of tongue squamous cell carcinoma.MethodsSCC15 cells cultured in DMEM alone were used as the control group, and SCC15 cells cultured in 20 mg/mL baicalin solution were used as the baicalin group. Scratch tests and Transwell migration tests were performed to detect changes in cell migration ability, and flow cytometry was used to detect changes in the cell cycle. Western blotting was used to detect differences in the phosphorylation levels of signal transduction and transcription activator 3(STAT3).ResultsCompared with the control group, the scratch test and the Transwell migration test showed that the cell migration ability of cells in the baicalin group was significantly decreased(t=4.927, P=0.008); flow cytometry showed that the number of cells of the baicalin group increased in the G0/G1 phase(t=9.893, P=0.001), decreased in the S phase(t=8.528, P=0.001), and decreased in the G2/M phase(t=3.550, P=0.024); Western blotting results showed that the STAT3 protein of SCC15 cells in the baicalin group decreased(t=3.550, P=0.024), and the phosphorylation level significantly decreased(t=8.262, P=0.001).ConclusionBaicalin inhibits the human tongue squamous cell carcinoma cell line SCC15, and its mechanism may be relatedto a decrease in STAT3 pathway phosphorylation activity.
引文
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[6] Wang CZ, Zhang CF, Chen LA, et al. Colon cancer chemopreven?tive effects of baicalein, an active enteric microbiome metabolite from baicalin[J]. Int J Oncol, 2015, 47(5):1749?1758.
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[8] He BX, Lin XZ, Tian FQ, et al. MiR?133a?3p inhibits oral squa?mous cell carcinoma(OSCC)proliferation and invasion by sup?pressing COL1A1[J]. J Cell Biochem, 2018, 119(1):338?346.
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[10]翟越,赵海丰.黄芩素对SCC15口腔癌细胞增殖和Caspase?3活性的影响[J].中国老年学杂志, 2015(1):139?141.
[11] Jemal A, Bray F, Center MM, et al. Global cancer statistics[J]. CA Cancer J Clin, 2011, 61(2):69?90.
[12] Qian K, Kong ZR, Zhang J, et al. Baicalin is an inhibitor of sub?group J avian leukosis virus infection[J]. Virus Res, 2018, 248:63?70.
[13] Sato D, Kondo S, Yazawa K, et al. The potential anticancer activi?ty of extracts derived from the roots of Scutellaria baicalensis on human oral squamous cell carcinoma cells[J]. Mol Clin Oncol,2013, 1(1):105?111.
[14] Kamran MZ, Patil P, Gude RP. Role of STAT3 in cancer metasta?sisandtranslationaladvances[J].BiomedResInt,2013(6):421821.
[15] Wang Y, Shen Y, Wang S, et al. The role of STAT3 in leading the crosstalk between human cancers and the immune system[J]. Can?cer Lett, 2018, 415(9):117?128.
[16] Qi Z, Yin F, Lu L, et al. Baicalein reduces lipopolysaccharide?in?duced inflammation via suppressing JAK/STATs activation and ROS production[J]. Inflammation Res, 2013, 62(9):845?855.
[17] Xiong J, Wang C, Chen H, et al. Aβ?induced microglial cell acti?vation is inhibited by baicalin through the JAK2/STAT3 signaling pathway[J]. Int J Neurosci, 2014, 124(8):609?620.
[18] Li Y, Zhuang P, Shen B, et al. Baicalin promotes neuronal differ?entiation of neural stem/progenitor cells through modulating p?stat3 and bHLH family protein expression[J]. Brain Res, 2012,1429:36?42.
[19] Wang Y, Guo W, Li Z, et al. Role of the EZH2/miR?200 axis in STAT3?mediated OSCC invasion[J]. Int J Oncol, 2018, 52(4):1149?1164.
[20] Khalili MB, Yazdanparast R, Nowrouzi A, et al. Induction of tran?sient cell cycle arrest by H2O2via modulation of ultradian oscilla?tions of hes1, Socs3, and p?Stat3 in fibroblast cells[J]. J Cell Bio?chem, 2018, 119(2):1453?1462.
[2] Hussain QA, Awan KH. Effect on quality of Life in oral cancer pa?tients after radiation and chemotherapy[J]. J Contemp Dent Pract,2016, 17(2):97?98.
[3] Noh K, Kang Y, Nepal MR, et al. Role of intestinal microbiota in baicalin?induced drug interaction and its pharmacokinetics[J].Molecules, 2016, 21(3):337.
[4] Wu Y, Wang F, Fan L, et al. Baicalin alleviates atherosclerosis by relieving oxidative stress and inflammatory responses via inactivat?ing the NF?kappa B and p38 MAPK signaling pathways[J].Biomed Pharmacother, 2018, 97:1673?1679.
[5] Wu XJ, Zhi FC, Lun WJ, et al. Baicalin inhibits PDGF?BB?in?duced hepatic stellate cell proliferation, apoptosis, invasion, migra?tion and activation via the miR?3595/ACSL4 axis[J]. Int J Mol Med, 2018, 41(4):1992?2002.
[6] Wang CZ, Zhang CF, Chen LA, et al. Colon cancer chemopreven?tive effects of baicalein, an active enteric microbiome metabolite from baicalin[J]. Int J Oncol, 2015, 47(5):1749?1758.
[7] Chen HJ, Gao Y, Wu JL, et al. Exploring therapeutic potentials of baicalin and its aglycone baicalein for hematological malignancies[J]. Cancer Lett, 2014, 354(1):5?11.
[8] He BX, Lin XZ, Tian FQ, et al. MiR?133a?3p inhibits oral squa?mous cell carcinoma(OSCC)proliferation and invasion by sup?pressing COL1A1[J]. J Cell Biochem, 2018, 119(1):338?346.
[9] Fu XJ, Li HX, Yang K, et al. The important tumor suppressor role of PER1 in regulating the cyclin?CDK?CKI network in SCC15 hu?man oral squamous cell carcinoma cells[J]. Onco Targets Ther,2016, 9(1):2237?2245.
[10]翟越,赵海丰.黄芩素对SCC15口腔癌细胞增殖和Caspase?3活性的影响[J].中国老年学杂志, 2015(1):139?141.
[11] Jemal A, Bray F, Center MM, et al. Global cancer statistics[J]. CA Cancer J Clin, 2011, 61(2):69?90.
[12] Qian K, Kong ZR, Zhang J, et al. Baicalin is an inhibitor of sub?group J avian leukosis virus infection[J]. Virus Res, 2018, 248:63?70.
[13] Sato D, Kondo S, Yazawa K, et al. The potential anticancer activi?ty of extracts derived from the roots of Scutellaria baicalensis on human oral squamous cell carcinoma cells[J]. Mol Clin Oncol,2013, 1(1):105?111.
[14] Kamran MZ, Patil P, Gude RP. Role of STAT3 in cancer metasta?sisandtranslationaladvances[J].BiomedResInt,2013(6):421821.
[15] Wang Y, Shen Y, Wang S, et al. The role of STAT3 in leading the crosstalk between human cancers and the immune system[J]. Can?cer Lett, 2018, 415(9):117?128.
[16] Qi Z, Yin F, Lu L, et al. Baicalein reduces lipopolysaccharide?in?duced inflammation via suppressing JAK/STATs activation and ROS production[J]. Inflammation Res, 2013, 62(9):845?855.
[17] Xiong J, Wang C, Chen H, et al. Aβ?induced microglial cell acti?vation is inhibited by baicalin through the JAK2/STAT3 signaling pathway[J]. Int J Neurosci, 2014, 124(8):609?620.
[18] Li Y, Zhuang P, Shen B, et al. Baicalin promotes neuronal differ?entiation of neural stem/progenitor cells through modulating p?stat3 and bHLH family protein expression[J]. Brain Res, 2012,1429:36?42.
[19] Wang Y, Guo W, Li Z, et al. Role of the EZH2/miR?200 axis in STAT3?mediated OSCC invasion[J]. Int J Oncol, 2018, 52(4):1149?1164.
[20] Khalili MB, Yazdanparast R, Nowrouzi A, et al. Induction of tran?sient cell cycle arrest by H2O2via modulation of ultradian oscilla?tions of hes1, Socs3, and p?Stat3 in fibroblast cells[J]. J Cell Bio?chem, 2018, 119(2):1453?1462.