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Journal: iScience
Article Title: SKA2 promotes gastric cancer progression by regulating glutathione metabolism
doi: 10.1016/j.isci.2026.115202
Figure Lengend Snippet: Knocking down SKA2 induces gastric cancer cell lines G2/M arrest (A and B) Cell cycle analysis of SKA2 knockdown in SNU638 and NUGC3 cell lines. Percentage of flow cytometric histogram images shows the effects of SKA2. (C) Western blotting analysis of the expression of Cyclin D1, Cyclin A2, Cyclin B1, and SKA2 in SNU638 and NUGC3 SKA2-knockdown cell lines. α-Tubulin was used as the internal control. (D and E) Cell cycle analysis of SKA2 overexpression in SNU638 and NUGC3 SKA2-knockdown cell lines. Percentage of flow cytometric histogram images shows the effects of SKA2. (F) Western blotting analysis of SKA2 overexpression in SNU638 and NUGC3 SKA2-knockdown cell lines using anti-Cyclin D1, anti-Cyclin A2, anti-Cyclin B1, and anti-SKA2 antibodies. α-Tubulin was used as the internal control. Representative flow cytometry histograms and blotting images are shown from 3 biologically independent experiments. Data in (A)–(B) and (D)–(E) are presented as mean ± SD, n = 3 biologically independent experiments. p values are based on a one-way ANOVA test. ns, no significance (∗∗ p < 0.01; ∗∗∗ p < 0.001).
Article Snippet:
Techniques: Cell Cycle Assay, Knockdown, Western Blot, Expressing, Control, Over Expression, Flow Cytometry
Journal: iScience
Article Title: SKA2 promotes gastric cancer progression by regulating glutathione metabolism
doi: 10.1016/j.isci.2026.115202
Figure Lengend Snippet: Knocking down SKA2-induced cell-cycle arrest and apoptosis through the SKA2/ROS/ATM axis in GC cell lines (A) Western blotting analysis of γ-H2AX (Ser139), ATM, p -ATM (Ser1981), p -Chk2 (Thr68), and SKA2 expression in SNU638 and NUGC3 SKA2-knockdown cell lines. (B) Western blotting analysis of SKA2 overexpression in SNU638 and NUGC3 SKA2-knockdown cell lines using antibodies against γ-H2AX (Ser139), ATM, p -ATM (Ser1981), p -Chk2 (Thr68), and SKA2. (C) Western blotting analysis of KU-55933 treatment in SNU638 and NUGC3 SKA2-knockdown cell lines using antibodies against cyclin D1, cyclin A2, cyclin B1, p -Chk2 (Thr68), PARP, Cleaved-Caspase3, JNK, p -JNK (Thr183/Tyr185), ATM, p -ATM (Ser1981), and SKA2. (D) Western blotting analysis of BML-277 treatment in SNU638 and NUGC3 SKA2-knockdown cell lines using antibodies against cyclin D1, cyclin A2, cyclin B1, p -Chk2 (Thr68), and SKA2. (E) Western blotting analysis of P38, p-P38 (Thr180/Tyr182), ERK, p -ERK1/2 (Thr202/Tyr204), JNK, p -JNK (Thr183/Tyr185), and SKA2 expression in SNU638 and NUGC3 SKA2-knockdown cell lines. (F) Western blotting analysis of the rescue effect of SKA2 overexpression on MAPK pathway markers (ERK, p -ERK1/2, JNK, and p -JNK) in SNU638 and NUGC3 SKA2-knockdown cell lines. (G) Western blotting analysis of JNK-IN-8 treatment in SNU638 SKA2-knockdown cell lines using antibodies against PARP, cleaved-caspase3, JNK, p -JNK (Thr183/Tyr185), and SKA2. α-Tubulin was used as the internal control for all blots. Representative blotting images are shown from 3 independent experiments.
Article Snippet:
Techniques: Western Blot, Expressing, Knockdown, Over Expression, Control
Journal: iScience
Article Title: CGF induces ROS-mediated metabolic reprogramming and mitochondrial dysfunction to suppress colorectal cancer progression
doi: 10.1016/j.isci.2026.115273
Figure Lengend Snippet: CGF’s effect on cell cycle and apoptosis in CRC (A) Flow cytometry was used to analyze how CGF affects the cell cycle of HCT116 and HT29 cells at certain concentrations, with the percentage of cells in G1, S, and G2 phases shown in each panel. (B) Western blot analysis of the changes in cell cycle-related proteins CDK1, p-CDK1, and cyclin B1 in HCT116 and HT29 cells after CGF treatment. (C) RT-qPCR analysis of the relative expression levels of PUMA and NOXA genes in HCT116 and HT29 cells treated with different concentrations of CGF. (D) Western blot analysis of the changes in apoptosis-related proteins BCL2, PUMA, Noxa, C-caspase 9, and C-caspase 3 in HCT116 and HT29 cells after CGF treatment. (E) Flow cytometry was used to analyze apoptosis in HCT116 and HT29 cells treated with CGF. On the left is a representative plot showing apoptosis, utilizing Annexin V-FITC and PI double staining. Right: Analysis of early and late apoptosis in cells from each group using quantitative methods. (A–C and E) Data presentation is in the form of mean ± SEM. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001.
Article Snippet:
Techniques: Flow Cytometry, Western Blot, Quantitative RT-PCR, Expressing, Double Staining