Journal: Oncology Reports

Article Title: STK31 regulates the proliferation and cell cycle of lung cancer cells via the Wnt/β-catenin pathway and feedback regulation by c-myc

doi: 10.3892/or.2019.7441

Figure Lengend Snippet: STK31 regulates proliferation and the cell cycle in lung cancer cells via the activation of the Wnt/β-catenin pathway. NCIH1299 cells were treated with vector + DMSO, vector + 10 µmol/l XAV939 (a Wnt/β-catenin inhibitor), STK31 + DMSO, or STK31 + 10 µmol/l XAV939. (A and B) Cell viability and proliferation were assessed by CCK-8 and BrdU-ELISA assays, respectively, at 0, 24, 48 and 72 h. (C) The proportion of cells in each phase of the cell cycle was evaluated by flow cytometry after 48 h of treatment. (D) Proteins related to β-catenin, c-myc and cyclin D1 protein levels were detected by western blotting. Data are presented as the mean ± SD, **P<0.01 and ***P<0.001 compared to vector, ### P<0.001 compared to STK31. STK31, serine-threonine kinase 31; DMSO, dimethyl sulfoxide; CCK-8, Cell Counting Kit-8; BrdU-ELISA, bromodeoxyuridine-enzyme-linked immunosorbent assay.

Article Snippet: In addition, NCIH1299 cells were treated with vector + dimethyl sulfoxide (DMSO), vector + 10 μmol/l XAV939 (a Wnt/β-catenin inhibitor; cat. no. S1180; Selleck Chemicals, Houston, TX, USA), or STK31 + DMSO, STK31 + 10 μmol/l XAV939, and NCIH358 cells were treated with vector + DMSO, vector + 100 μmol/l 10058-F4 (a c-myc inhibitor; cat. no. S7153; Selleck Chemicals), STK31 + DMSO, or STK31 + 100 μmol/l 10058-F4.

Techniques: Activation Assay, Plasmid Preparation, CCK-8 Assay, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Western Blot, Cell Counting

Journal: Oncology Reports

Article Title: STK31 regulates the proliferation and cell cycle of lung cancer cells via the Wnt/β-catenin pathway and feedback regulation by c-myc

doi: 10.3892/or.2019.7441

Figure Lengend Snippet: The STK31-mediated regulation of proliferation and the cell cycle in lung cancer cells may act through the positive feedback regulation by c-myc. NCIH358 cells were treated with vector + DMSO, vector + 100 µmol/l 10058-F4 (a c-myc inhibitor), STK31 + DMSO, or STK31 +100 µmol/l 10058-F4. (A and B) Cell viability and proliferation were assessed by CCK-8 and BrdU-ELISA assays, respectively, at 0, 24, 48 and 72 h. (C) The proportion of cells in each phase of the cell cycle was evaluated by flow cytometry after 48 h of treatment. (D) The levels of STK31 mRNA (left) and protein (right) were determined. (E) The expression levels of TRRAP and STK31 were detected by RT-PCR and western blotting. (F) The direct binding of c-myc to the STK31 promoter was confirmed by a ChIP assay. The data are expressed as the mean ± SD, *P<0.05, **P<0.01 and ***P<0.001, compared to vector or shNC, ## P<0.01, ### P<0.001 compared to STK31. STK31, serine-threonine kinase 31; DMSO, dimethyl sulfoxide; CCK-8, Cell Counting Kit-8; TRRAP, transformation/transcription domain-associated protein; ChIP, chromatin immunoprecipitation; BrdU-ELISA, bromodeoxyuridine-enzyme-linked immunosorbent assay.

Article Snippet: In addition, NCIH1299 cells were treated with vector + dimethyl sulfoxide (DMSO), vector + 10 μmol/l XAV939 (a Wnt/β-catenin inhibitor; cat. no. S1180; Selleck Chemicals, Houston, TX, USA), or STK31 + DMSO, STK31 + 10 μmol/l XAV939, and NCIH358 cells were treated with vector + DMSO, vector + 100 μmol/l 10058-F4 (a c-myc inhibitor; cat. no. S7153; Selleck Chemicals), STK31 + DMSO, or STK31 + 100 μmol/l 10058-F4.

Techniques: Plasmid Preparation, CCK-8 Assay, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Expressing, Reverse Transcription Polymerase Chain Reaction, Western Blot, Binding Assay, Cell Counting, Transformation Assay, Chromatin Immunoprecipitation

Journal: BMC Complementary Medicine and Therapies

Article Title: Ginkgolide B inhibits lung cancer cells promotion via beclin-1-dependent autophagy

doi: 10.1186/s12906-020-02980-x

Figure Lengend Snippet: Ginkgolide B (GKB) inhibited the proliferation, invasion and colony formation of lung cancer cells in vitro and induced apoptosis . a GKB significantly inhibited the proliferation of lung cancer cells. b GKB significantly inhibited the invasion of lung cancer cell. c GKB significantly inhibited the colony formation of lung cancer cells. Scale bar, = 200 μm. d Cancer cells were incubated with GKB for 48 h, and then apoptotic cells (stained with annexin V and propidium iodide) were detected by flow cytometry. Results are presented as mean ± SEM of three independent experiments. * P < 0.05, ** P < 0.01, *** P < 0.001, compared to the dimethyl sulfoxide (DMSO) only group

Article Snippet: GKB (CAS No.15291–76-6, BN52022) was obtained from the Tauto Biotech Co., Ltd., Shanghai, China, and dissolved in dimethyl sulfoxide (DMSO), chloroquine (S4157, Selleck, Houston, USA), 3-Methyladenine (S2767, Selleck, Houston, USA), GFP-LC3B virus vector (Genomeditech, Shanghai, China).

Techniques: In Vitro, Incubation, Staining, Flow Cytometry

Journal: BMC Complementary Medicine and Therapies

Article Title: Ginkgolide B inhibits lung cancer cells promotion via beclin-1-dependent autophagy

doi: 10.1186/s12906-020-02980-x

Figure Lengend Snippet: Role of autophagy in GKB induced inhibition of invasion and colony formation of lung cancer cells. a Cell invasion analysis to assess the role of autophagy in GKB induced inhibition invasion of H1975 cells. b Colony formation analysis to assess the role of autophagy in GKB induced inhibition of the proliferation of H1975 cells. Data shown represent the mean ± SEM of three independent experiments. * P < 0.05, compared to the dimethyl sulfoxide (DMSO) only group

Article Snippet: GKB (CAS No.15291–76-6, BN52022) was obtained from the Tauto Biotech Co., Ltd., Shanghai, China, and dissolved in dimethyl sulfoxide (DMSO), chloroquine (S4157, Selleck, Houston, USA), 3-Methyladenine (S2767, Selleck, Houston, USA), GFP-LC3B virus vector (Genomeditech, Shanghai, China).

Techniques: Inhibition

Journal: BMC Complementary Medicine and Therapies

Article Title: Ginkgolide B inhibits lung cancer cells promotion via beclin-1-dependent autophagy

doi: 10.1186/s12906-020-02980-x

Figure Lengend Snippet: Autophagy-induced inhibition of the NLRP3 inflammasome contributes to the anti-tumor effect of Ginkgolide B (GKB). a Western blot analysis of the expression of NLRP3 protein in H1975 cells treated with GKB for 24 h. b ELISA analysis of the expression of IL-1β and IL-18 protein after LPS was used as an NLRP3 inflammasome activator in H1975 cells. c Western blot analysis of the expression of NLRP3 protein in beclin-1 knock-down H1975 cells. d ELISA analysis the expression of IL-1β and IL-18 protein in beclin-1-knockdown H1975 cells. Data shown represent the mean ± SEM of three independent experiments. *** P < 0.001, compared to the dimethyl sulfoxide (DMSO) only group

Article Snippet: GKB (CAS No.15291–76-6, BN52022) was obtained from the Tauto Biotech Co., Ltd., Shanghai, China, and dissolved in dimethyl sulfoxide (DMSO), chloroquine (S4157, Selleck, Houston, USA), 3-Methyladenine (S2767, Selleck, Houston, USA), GFP-LC3B virus vector (Genomeditech, Shanghai, China).

Techniques: Inhibition, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay, Knockdown