Message Board

Respected readers, authors and reviewers, you can add comments to this page on any questions about the contribution, review,        editing and publication of this journal. We will give you an answer as soon as possible. Thank you for your support!

Name
E-mail
Phone
Title
Content
Verification Code

JIANG Wenli, HUANG Caiguo. Wentilactone A inhibition of migration of small cell lung carcinoma NCI-H1688 cell line[J]. Journal of Pharmaceutical Practice and Service, 2016, 34(3): 219-222,274. doi: 10.3969/j.issn.1006-0111.2016.03.007
Citation: JIANG Wenli, HUANG Caiguo. Wentilactone A inhibition of migration of small cell lung carcinoma NCI-H1688 cell line[J]. Journal of Pharmaceutical Practice and Service, 2016, 34(3): 219-222,274. doi: 10.3969/j.issn.1006-0111.2016.03.007

Wentilactone A inhibition of migration of small cell lung carcinoma NCI-H1688 cell line

doi: 10.3969/j.issn.1006-0111.2016.03.007
  • Received Date: 2016-01-27
  • Rev Recd Date: 2016-03-31
  • Objective To investigate mechanism of Wentilactone A (WA) inhibition of small cell lung cancer(SCLC) cell line NCI-H1688 migration. Methods The migration and proliferation were analyzed by wounding-healing assay and MTT assay[3- (4, 5-Dimethylthiazol-2-yl) -2, 5-diphenyltetrazolium bromide, MTT]. Immunofluorescence was used to confirm the expression of ATF3 protein after WA treatment. Western blot was used to examine the expression of key proteins in ATF3/Nrf2/AKR1C1 signal pathway. Results WA inhibits the proliferation and migration of SCLC. MTT analysis showed WA inhibits the proliferation of NCI-H1688 cell line in a time-dependent manner. The number of migrated cells in WA treatment group was (8.73±1.06) mm, which was lower than that of control group (15.63±3.11) mm, The number of migrated cells in AKR1C1 expression group was (24.37±0.90) mm, the number of migrated cells in AKR1C1 expression and WA treatment group was (14.17±1.31) mm, with significant difference (P<0.05). WA enhances the nuclear expression of ATF3, and then reduces the expression of p-Nrf2 and AKR1C1. Conclusion WA inhibits the proliferation and migration of SCLC through ATF3/Nrf2/AKR1C1 signal pathway.
  • [1] Chen W, Zheng R, Baade PD, et al. Cancer statistics in China, 2015[J]. CA Cancer J Clin, 2016, 66(2):115-132.
    [2] Chen W, Zheng R, Zhang S, et al. Report of cancer incidence and mortality in China, 2010[J]. Ann Transl Med, 2014, 2(7):61.
    [3] Ulahannan SV, Brahmer JR. Antiangiogenic agents in combination with chemotherapy in patients with advanced non-small cell lung cancer[J]. Cancer Invest, 2011,29(4):325-337.
    [4] Modesto JL, Hull A, Angstadt AY, et al. NNK reduction pathway gene polymorphisms and risk of lung cancer[J]. Mol Carcinog, 2015, 54(Suppl 1):E94-E102.
    [5] Siegel RL, Miller KD, Jemal A. Cancer statistics, 2016[J]. CA Cancer J Clin, 2016,66(1):7-30.
    [6] Stinchcombe TE,Gore EM, Limited-stage small cell lung cancer:current chemoradiotherapy treatment paradigms[J]. Oncologist, 2010,15(2):187-195.
    [7] Johnson BE. Management of small cell lung cancer[J]. Clin Chest Med, 2002,23(1):225-239.
    [8] Traven K, Sinreih M, Stojan J, et al. Ruthenium complexes as inhibitors of the aldo-keto reductases AKR1C1-1C3[J]. Chem Biol Interact, 2015, 234:349-359.
    [9] Stefane B, Brozic P, Vehovc M, et al. New cyclopentane derivatives as inhibitors of steroid metabolizing enzymes AKR1C1 and AKR1C3[J]. Eur J Med Chem, 2009,44(6):2563-2571.
    [10] Penning TM. The aldo-keto reductases (AKRs):Overview[J]. Chem Biol Interact, 2015,234:236-246.
    [11] Rizner TL, Penning TM. Role of aldo-keto reductase family 1(AKR1) enzymes in human steroid metabolism[J]. Steroids, 2014,79:49-63.
    [12] Haddad SA, Lunetta KL, Ruiz-Narváez EA, et al. Hormone-related pathways and risk of breast cancer subtypes in African American women[J]. Breast Cancer Res Treat, 2015,154(1):145-154.
    [13] Naumann JM, Messinger J, Bureik M. Human 20alpha-hydroxysteroid dehydrogenase (AKR1C1)-dependent biotransformation with recombinant fission yeast Schizosaccharomyces pombe[J]. J Biotechnol, 2010,150(1):161-170.
    [14] Byrns MC, Jin Y, Penning TM. Inhibitors of type 517beta-hydroxysteroid dehydrogenase (AKR1C3):overview and structural insights[J]. J Steroid Biochem Mol Biol, 2011,125(1-2):95-104.
    [15] Matsunaga T, Hojo A, Yamane Y, et al. Pathophysiological roles of aldo-keto reductases (AKR1C1 and AKR1C3) in development of cisplatin resistance in human colon cancers[J]. Chem Biol Interact, 2013,202(1-3):234-242.
    [16] Jaiswal AK. Nrf2 signaling in coordinated activation of antioxidant gene expression[J]. Free Radic Biol Med, 2004,36(10):1199-1207.
    [17] Nishinaka T, Miura T, Okumura M, et al. Regulation of aldo-keto reductase AKR1B10 gene expression:involvement of transcription factor Nrf2[J]. Chem Biol Interact, 2011,191(1-3):185-191.
    [18] Kaspar JW, Niture SK, Jaiswal AK. Nrf2:INrf2(Keap1) signaling in oxidative stress[J]. Free Radic Biol Med, 2009,47(9):1304-1309.
    [19] Cheng X, Ku CH, Siow RC. Regulation of the Nrf2 antioxidant pathway by microRNAs:New players in micromanaging redox homeostasis[J]. Free Radic Biol Med, 2013,64:4-11.
    [20] Brown SL, Sekhar KR, Rachakonda G, et al. Activating transcription factor 3 is a novel repressor of the nuclear factor erythroid-derived 2-related factor 2(Nrf2)-regulated stress pathway[J]. Cancer Res, 2008,68(2):364-368.
    [21] 田鹤,姜文丽,楼国良,等.AKR1C1在非小细胞肺癌的表达及功能分析[J].临床肿瘤学杂志,2015,20(6):487-491.
  • 加载中
通讯作者: 陈斌, bchen63@163.com
  • 1. 

    沈阳化工大学材料科学与工程学院 沈阳 110142

  1. 本站搜索
  2. 百度学术搜索
  3. 万方数据库搜索
  4. CNKI搜索

Article Metrics

Article views(3562) PDF downloads(12) Cited by()

Related
Proportional views

Wentilactone A inhibition of migration of small cell lung carcinoma NCI-H1688 cell line

doi: 10.3969/j.issn.1006-0111.2016.03.007

Abstract: Objective To investigate mechanism of Wentilactone A (WA) inhibition of small cell lung cancer(SCLC) cell line NCI-H1688 migration. Methods The migration and proliferation were analyzed by wounding-healing assay and MTT assay[3- (4, 5-Dimethylthiazol-2-yl) -2, 5-diphenyltetrazolium bromide, MTT]. Immunofluorescence was used to confirm the expression of ATF3 protein after WA treatment. Western blot was used to examine the expression of key proteins in ATF3/Nrf2/AKR1C1 signal pathway. Results WA inhibits the proliferation and migration of SCLC. MTT analysis showed WA inhibits the proliferation of NCI-H1688 cell line in a time-dependent manner. The number of migrated cells in WA treatment group was (8.73±1.06) mm, which was lower than that of control group (15.63±3.11) mm, The number of migrated cells in AKR1C1 expression group was (24.37±0.90) mm, the number of migrated cells in AKR1C1 expression and WA treatment group was (14.17±1.31) mm, with significant difference (P<0.05). WA enhances the nuclear expression of ATF3, and then reduces the expression of p-Nrf2 and AKR1C1. Conclusion WA inhibits the proliferation and migration of SCLC through ATF3/Nrf2/AKR1C1 signal pathway.

JIANG Wenli, HUANG Caiguo. Wentilactone A inhibition of migration of small cell lung carcinoma NCI-H1688 cell line[J]. Journal of Pharmaceutical Practice and Service, 2016, 34(3): 219-222,274. doi: 10.3969/j.issn.1006-0111.2016.03.007
Citation: JIANG Wenli, HUANG Caiguo. Wentilactone A inhibition of migration of small cell lung carcinoma NCI-H1688 cell line[J]. Journal of Pharmaceutical Practice and Service, 2016, 34(3): 219-222,274. doi: 10.3969/j.issn.1006-0111.2016.03.007
Reference (21)

Catalog

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return