cck 8 reagent  (Dojindo Labs)

Journal: Genes & Diseases

Article Title: Identification of PLXNC1 as a novel biomarker for consensus molecular subtype 4 in colorectal cancer

doi: 10.1016/j.gendis.2025.101974

Figure Lengend Snippet: PLXNC1 promotes the proliferation, migration, and invasion of colorectal cancer (CRC) cells in vitro. (A) qRT-PCR analysis was conducted to examine the knockdown efficiency of PLXNC1 in the negative control (NC)-siRNA- or PLXNC1-siRNA-transfected CRC cells. NC-siRNA was used as a negative control. GAPDH was a normalization control. (B) CCK-8 assay was performed to assay the viability of control and PLXNC1-silenced CRC cells. (C) After 48 h of transfection with NC-siRNA or PLXNC1-siRNA, the migration of CRC cells in Transwell chambers was determined. (D) After 48 h of transfection with NC-siRNA or PLXNC1-siRNA, CRC cells invading the Matrigel in Transwell chambers were performed. Note: Scale bars = 200 μm. (E) Representative images of EdU-stained (red) cells and the quantification of cell proliferation ratio normalized to Hoechst-stained (blue) cells. Scale bars = 75 μm. (F) qRT-PCR data of the PLXNC1 expression in LoVo cells following transfection with PLXNC1 plasmids or controls. GAPDH was a normalization control. (G) CCK-8 assay results show the viability of LoVo cells following transfection with PLXNC1 plasmids or controls. (H, I) Transwell assay was employed to count the number of migrated (H) and invaded (I) LoVo cells following transfection with PLXNC1 plasmids or controls. ∗∗∗ p < 0.001; ∗∗ p < 0.01, and ∗ p < 0.05.

Article Snippet: CCK-8 reagent (10 μL, DOJINDO, Kumamoto, Japan) was added to each well at 0, 24, 48, and 72 h after transfection and incubated at 37 °C for 4 h. Absorbance at 450 nm was measured using a microplate reader (PerkinElmer EnVision, Massachusetts, USA).

Techniques: Migration, In Vitro, Quantitative RT-PCR, Knockdown, Negative Control, Transfection, Control, CCK-8 Assay, Staining, Expressing, Transwell Assay

Journal: Materials Today Bio

Article Title: Hepatic cavernous hemangioma decellularized extracellular matrix/GelMA composite hydrogel promotes angiogenesis via the ITGA9–FAK–ERK1/2 axis

doi: 10.1016/j.mtbio.2026.102976

Figure Lengend Snippet: Biological responses of HUVECs to HCH dECM. (A) Live/dead staining of HUVECs cultured on HCH dECM/GelMA composite hydrogels (HCH gel) with varying dECM concentrations (scale bars = 200 μm). (B) Quantification of cell viability from graph A. (C) CCK-8 assay assessing HUVEC proliferation in response to HCH gel. (D) Scratch wound assay demonstrating HUVEC migration (scale bars = 200 μm). (E) Transwell migration assay further evaluating HUVEC migration (scale bars = 200 μm). (F) Tube formation assay assessing the angiogenic potential of HUVECs (scale bars = 200 μm). (G) Wound closure rate quantified from graph D. (H) Number of migrating cells quantified from graph E. (I) Total tube length of vessel-like structures quantified from graph F. (n = 5, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001).

Article Snippet: After 1, 2, and 3 days, the culture medium was replaced with 100 μL of fresh medium containing 10% (v/v) CCK-8 reagent (Solarbio, China) and incubated for 2 h at 37 °C.

Techniques: Staining, Cell Culture, CCK-8 Assay, Scratch Wound Assay Assay, Migration, Transwell Migration Assay, Tube Formation Assay

Journal: Materials Today Bio

Article Title: Hepatic cavernous hemangioma decellularized extracellular matrix/GelMA composite hydrogel promotes angiogenesis via the ITGA9–FAK–ERK1/2 axis

doi: 10.1016/j.mtbio.2026.102976

Figure Lengend Snippet: Mechanism underlying the regulation of HUVEC behavior by the HCH gel. (A) Western blot analysis of ITGA9 expression and the phosphorylation status of FAK and ERK1/2. (B) Quantification of Western blot results (n = 3). (C) CCK-8 assay detecting the effect of ITGA9 knockdown (KD) on the proliferation of HUVECs cultured on the HCH gel (n = 5). (D) Transwell migration assay evaluating the effect of ITGA9 KD on HUVEC migration (scale bars = 200 μm). (E) Quantification of the number of migrating cells from graph D (n = 5). (F) Tube formation assay assessing the effect of ITGA9 KD on the angiogenic capacity of HUVECs (incubation for 12 h, scale bars = 200 μm). (G) Quantification of the total tube length from graph F (n = 5). (∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001).

Article Snippet: After 1, 2, and 3 days, the culture medium was replaced with 100 μL of fresh medium containing 10% (v/v) CCK-8 reagent (Solarbio, China) and incubated for 2 h at 37 °C.

Techniques: Western Blot, Expressing, Phospho-proteomics, CCK-8 Assay, Knockdown, Cell Culture, Transwell Migration Assay, Migration, Tube Formation Assay, Incubation

Journal: IBRO Neuroscience Reports

Article Title: TNKS1 mediates the PTEN-PI3K/AKT pathway to regulate glycolysis and proliferation in gliomas

doi: 10.1016/j.ibneur.2026.01.007

Figure Lengend Snippet: TNKS1 can activate the PI3K/AKT pathway by inhibiting the expression of PTEN in glioma cells.Western blotting was used to detect the expression of PTEN in U87 and U251 cell lines (A); the CCK-8 assay was used to measure the viability of U87 and U251 glioma cells treated with different concentrations of LY294002 and 740 Y-P (B); Western blotting was also used to detect the expression of PI3K, p-AKT/AKT in U87 and U251 cell lines (C).*P < 0.05 vs si-NC，@P < 0.05 vs si-NC+Agonist，#P < 0.05 vs si-TNKS1，&P < 0.05 vs OE-TNKS1.

Article Snippet: Subsequently, 10 μL of CCK-8 reagent (Batch no. KGA317, KeyGen Biotech, Nanjing, China) was added to each well.

Techniques: Expressing, Western Blot, CCK-8 Assay