enhanced cell counting kit-8  (TargetMol)

Journal: Poultry Science

Article Title: Brefeldin A inhibits duck plague virus replication by impairing virion envelopment

doi: 10.1016/j.psj.2026.106509

Figure Lengend Snippet: Brefeldin A inhibits DPV infection in DEF cells . (A-C) DEF cells were infected with DPV-CHv-GFP at 1 MOI for 1 h, then treated with different concentrations of Brefeldin A, DMSO was added as control. The viral fluorescence spots were photographed under fluorescence microscope at 24 hours post infection (hpi). The scale bar is 100 µm (A). The infected cells were collected and the copy number of the DPV gene was detected by Q-PCR (B), and the cell supernatant was collected to determine the virus titer TCID 50 (C). (D) DEF cells were treated with different concentrations of Brefeldin A for 48 h, and then the cell viability was determined using the CCK-8 cell viability assay kit.

Article Snippet: DEF cells were treated with BFA of different concentrations for 36 h, and the cell viability was determined using the cell counting CCK-8 kit (TargetMOI, c0005) according to the manufacturer's instructions.

Techniques: Infection, Control, Fluorescence, Microscopy, Virus, CCK-8 Assay, Viability Assay

Journal: Non-coding RNA Research

Article Title: SNHG5 enhances colorectal cancer metastasis through RNA–protein interaction with GNB2 and activation of canonical Wnt signaling

doi: 10.1016/j.ncrna.2025.12.002

Figure Lengend Snippet: Highly metastatic MC38-derived CRC cells exhibit enhanced proliferative, migratory, and invasive properties with mesenchymal characteristics . (A) CCK-8 assay demonstrated significantly higher proliferative capacity in the highly metastatic MC38-F3 subline compared to the parental low-metastatic MC38-F0 cells over a 96-h time course. (B) Representative colony formation images and quantification revealed increased clonogenicity in the MC38-F3 subline. (C) Wound healing assays indicated enhanced migratory ability in MC38-F3 cells at 48 h post-scratch. (D) Transwell migration and Matrigel-coated invasion assays showed that MC38-F3 cells exhibited significantly increased motility and invasiveness. Scale bars = 100 μm. (E) Western blot analysis revealed downregulation of the epithelial marker E-cadherin and upregulation of mesenchymal markers N-cadherin, Vimentin, and Slug in MC38-F3 cells. (F) RT-qPCR analysis confirmed significant upregulation of EMT-associated transcription factors (Snail, Slug, Twist1, ZEB1, ZEB2) in MC38-F3 cells. (G) Immunofluorescence staining corroborated the EMT phenotype, showing reduced E-cadherin and increased Vimentin expression in MC38-F3 cells. Nuclei were counterstained with DAPI. Scale bars = 20 μm. Data are presented as mean ± SEM from at least three independent experiments. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 (Student's t -test).

Article Snippet: Cell proliferation was assessed using the Cell Counting Kit-8 (CCK-8; HY-K0301, MedChemExpress, China) following the manufacturer's instructions.

Techniques: Derivative Assay, CCK-8 Assay, Migration, Western Blot, Marker, Quantitative RT-PCR, Immunofluorescence, Staining, Expressing

Journal: Non-coding RNA Research

Article Title: SNHG5 enhances colorectal cancer metastasis through RNA–protein interaction with GNB2 and activation of canonical Wnt signaling

doi: 10.1016/j.ncrna.2025.12.002

Figure Lengend Snippet: Snhg5 promotes proliferation, inhibits apoptosis, and enhances motility in CRC cells . (A) CCK-8 assays revealed that Snhg5 overexpression significantly promoted cell proliferation in low-metastatic MC38-F0 cells, while knockdown of Snhg5 suppressed proliferation in highly metastatic MC38-F3 cells over 96 h. (B) Colony formation assays showed increased clonogenic potential in Snhg5-overexpressing MC38-F0 cells and reduced colony formation following Snhg5 silencing in MC38-F3 cells. (C) EdU incorporation assays demonstrated elevated DNA synthesis in Snhg5-overexpressing cells and markedly reduced EdU-positive cell fractions upon Snhg5 knockdown. Scale bars = 100 μm. (D) Annexin V–FITC/PI staining followed by flow cytometry showed that Snhg5 overexpression reduced apoptosis, whereas its knockdown significantly increased apoptotic cell populations. (E) Cell cycle analysis indicated that Snhg5 knockdown induced G1 phase arrest and reduced the S-phase fraction, whereas overexpression promoted G1/S transition. (F) Wound healing assays demonstrated enhanced migration in MC38-F0 cells upon Snhg5 overexpression, and impaired migratory capacity in MC38-F3 cells following knockdown. (G) Transwell migration and invasion assays confirmed that Snhg5 facilitated motility and invasiveness in CRC cells. Snhg5 silencing significantly reduced both migratory and invasive capacities. Scale bars = 100 μm. Data are presented as mean ± SEM from at least three independent experiments. Statistical significance was determined using Student's t -test or ANOVA as appropriate. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.

Article Snippet: Cell proliferation was assessed using the Cell Counting Kit-8 (CCK-8; HY-K0301, MedChemExpress, China) following the manufacturer's instructions.

Techniques: CCK-8 Assay, Over Expression, Knockdown, DNA Synthesis, Staining, Flow Cytometry, Cell Cycle Assay, Migration

Journal: Non-coding RNA Research

Article Title: SNHG5 enhances colorectal cancer metastasis through RNA–protein interaction with GNB2 and activation of canonical Wnt signaling

doi: 10.1016/j.ncrna.2025.12.002

Figure Lengend Snippet: GNB2 overexpression functionally rescues the tumor-suppressive effects of Snhg5 knockdown in highly metastatic CRC cells . (A) CCK-8 assay showed that Snhg5 knockdown significantly suppressed cell viability over a 96-h period in MC38-F3 cells, whereas GNB2 overexpression partially restored proliferation. (B) Colony formation assays demonstrated that the reduction in clonogenicity induced by Snhg5 knockdown was significantly reversed by GNB2 overexpression. (C) EdU incorporation assay revealed that DNA synthesis was markedly decreased following Snhg5 silencing and partially rescued upon GNB2 overexpression. Scale bars = 100 μm. (D) Annexin V–FITC/PI apoptosis assay showed that Snhg5 depletion significantly increased apoptotic cell populations, which were reduced by GNB2 overexpression. (E) Cell cycle analysis revealed that Snhg5 knockdown induced G1 phase arrest and decreased the S-phase fraction, whereas co-expression of GNB2 alleviated these changes. (F) Wound healing assays demonstrated that the impaired migration capacity caused by Snhg5 silencing was significantly restored by GNB2 overexpression at 48 h. (G) Transwell migration and Matrigel-coated invasion assays further confirmed that GNB2 overexpression rescued the reduction in migratory and invasive abilities induced by Snhg5 knockdown. Scale bars = 100 μm. Data are presented as mean ± SEM from at least three independent experiments. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 (one-way ANOVA with Tukey's post hoc test unless otherwise indicated).

Article Snippet: Cell proliferation was assessed using the Cell Counting Kit-8 (CCK-8; HY-K0301, MedChemExpress, China) following the manufacturer's instructions.

Techniques: Over Expression, Knockdown, CCK-8 Assay, DNA Synthesis, Apoptosis Assay, Cell Cycle Assay, Expressing, Migration

Journal: Translational Oncology

Article Title: Construction and validation of golgi apparatus-related genes as predictors of the immune microenvironment and prognosis in colorectal cancer

doi: 10.1016/j.tranon.2026.102714

Figure Lengend Snippet: In Vitro functional experiments of GDI1 . (A). Expression differences of GDI1 among the NCM460, HCT116, and HT29 cell lines; (B)Verification of siRNA efficiency in knocking down GDI1 ; (C) Wound healing assay following GDI1 knockdown; (D) CCK-8 assay after GDI1 knockdown; (E) Apoptosis assay in the HT29 cell line after GDI1 knockdown; (F) Apoptosis assay in the HCT116 cell line after GDI1 knockdown. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: A suspension of 5000 transfected cells in 100 μL was distributed into each well of a 96-well plate, accompanied by the addition of 10 μL of CCK-8 solution (MCE, HY-K0301).

Techniques: In Vitro, Functional Assay, Expressing, Wound Healing Assay, Knockdown, CCK-8 Assay, Apoptosis Assay