Journal: Journal of Clinical Medicine

Article Title: KCP10043F Represses the Proliferation of Human Non-Small Cell Lung Cancer Cells by Caspase-Mediated Apoptosis via STAT3 Inactivation

doi: 10.3390/jcm9030704

Figure Lengend Snippet: Activation of the caspase-dependent pathway by KCP10043F in A549 and NCI-H358 cells. ( A ) Cells were treated with 20 µM KCP10043F for the indicated times (6, 12, or 24 h) and ( B ) treated with the indicated concentrations (5, 10, or 20 µM) of KCP10043F for 24 h. The cells were harvested, and total cell lysates were prepared. The expression levels of procaspase-8, cleaved caspase-8, procaspase-9, cleaved caspase-9, procaspase-3, cleaved caspase-3, and poly (ADP-ribose) polymerase (PARP) were examined by Western blot analysis. β-actin was used as an internal control. ( C , D ) A549 and NCI-H358 cells with pretreated with a broad-caspase inhibitor (z-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk)) for 1 h, followed by treatment with 20 μM KCP10043F for 24 h. The cells were co-stained with annexin V-FITC and PI, and apoptosis was detected by flow cytometry. Data represent the mean ± SD of the results from three independent experiments. ### p < 0.001 vs. untreated control group, *** p < 0.001 vs. KCP10043F-treated group.

Article Snippet: Lipofectamine™ Transfection Reagent was obtained from Thermofisher Scientific (Waltham, MA, USA). z-VAD-fmk (z-Val-Ala-Asp-fluoromethylketone) was obtained from MP Biomedicals (Santa Ana, CA, USA).

Techniques: Activation Assay, Expressing, Western Blot, Staining, Flow Cytometry

Journal: International Journal of Molecular Sciences

Article Title: Polymeric Polylactic Acid–Glycolic Acid-Based Nanoparticles Deliver Nintedanib Across the Blood–Brain Barrier to Inhibit Glioblastoma Growth

doi: 10.3390/ijms26020443

Figure Lengend Snippet: BIBF inhibits the growth of GBM cells. ( A ) Efficiency screening of small-molecule drug library on glioblastoma cells; ★ indicates nintedanib with >95% inhibition. The drugs that achieve 50% cell death are shown above the red dotted line. ( B , C ) U251 and U87 cells were treated with different concentrations of BIBF for 12 h, 24 h, and 48 h, respectively. Cell viability was determined by CCK-8 assay. ( D ) U251 and U87 cells were treated with different concentrations of BIBF for 24 h. Inhibition of cell proliferation was detected by flow cytometry. ( E , F ) Percentage of cells in different cycles after BIBF treatment of U251 and U87 cells. ( G , H ) Cell wound healing ability of U251 and U87 cells treated with different concentrations of BIBF for 24 h. ( J , K ) Percentage of U251 and U87 cells that were able to migrate. ( I ) U251 and U87 cells that were treated with the indicated concentrations of BIBF for 24 h. Cells were analyzed for their invasive ability, ( L , M ) Number of U251 and U87 cells that permeated through the vesicles, compared to the control * p < 0.05, compared to the control ** p < 0.01, compared to the control *** p < 0.001, and compared to the control **** p < 0.0001.

Article Snippet: In this study, we utilized several reagents and antibodies, including Nintedanib (Targetmol, MA, USA, 65624-17-5), Z-VAD-FMK (Targetmol, MA, USA, 187389-52-2), bafilomycin (Targetmol, MA, USA, 88899-56-3), Cell Counting Kit-8 (CCK-8) (Sangon Biotech, Suzhou, China, C6030), PE Annexin V (Yeasen, Shanghai, China, 40,302), and a lysosomal red fluorescent probe (Beyotime, Shanghai, China, C1047S).

Techniques: Inhibition, CCK-8 Assay, Flow Cytometry, Control