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Article Navigation >  Journal of Pharmaceutical Practice and Service  > 2016  >  34(3): 219-222,274

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

doi: 10.3969/j.issn.1006-0111.2016.03.007

  • Department of Biochemistry and Molecular Biology, Faculty of Basic Medicine, Second Military Medical University, Shanghai 200433, China

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

doi: 10.3969/j.issn.1006-0111.2016.03.007
  • Department of Biochemistry and Molecular Biology, Faculty of Basic Medicine, Second Military Medical University, Shanghai 200433, China
  • Received Date: 2016-01-27
  • Rev Recd Date: 2016-03-31

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
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