Journal: Materials Today Bio

Article Title: Enhanced oral nanomedicine utilizing biomineralized oncolytic virus for synergistic gastrointestinal cancer therapy

doi: 10.1016/j.mtbio.2025.102583

Figure Lengend Snippet: CaCO 3 @CM-OA suppresses CRC growth and epithelial–mesenchymal transition (EMT). (A) Mice bearing orthotopic colorectal tumors received oral administration every other day for 14 days. (B) Body weight monitoring. (C) Fecal occult blood test results. (D) Endoscopic images of the intestinal tract. (E) Tumor images from each treatment group. (F) Fluorescence imaging of major organs and colorectal tissue. (G) Serum IL-6 levels in each group. (H) H&E staining of tumors. (I) TUNEL assay on paraffin-embedded tumors. (J) IHC staining of Ki67, Bcl2, Vimentin, and LC3A/B. (K–N) Western blot analyses of Ki67, P62, Beclin1, LC3A/B, Bcl2, Bax, Cytochrome-c, N-cadherin, Vimentin, Collagen III, and α-SMA in tumor tissues. Data are presented as mean ± SD. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001.

Article Snippet: The antibodies used in western blot, immunofluorescence and immunohistochemistry experiments were as follows: CRT (Bioss, 5913R), HMGB1 (Beytime, AF1174), Anti-Adenovirus Type 5 Hexon (abcam, ab816352), Ki67 (Proteintech, 27309-1-AP), p53 (MCE, HY- P80938 ), p-p53 (Affinity, AF3075), p21 (Affinity, AF6290), CyclinB1 (Proteintech, 28603-1-AP), Bcl2 (Proteintech, 26593-1-AP), Bax (Proteintech, 50599-2-Ig), Caspase3 (Proteintech, 19677-1-AP), cleaved-Caspase3 (CST, 9661S), Cytochrome c (Proteintech, 10993-1-AP), p62 (HuaBio, HA721171), Beclin1 (CST, 3495S), LC3A/B (CST, 12741T), p-MLKL (MCE, HY-P81878), MLKL (HuaBio, ET1601-25), N-cadherin (Affinity, AF5239), E-cadherin (Affinity, AF0131), α-SMA (HuaBio, ET1607-53), Vimentin (Affinity, AF7013), Collegen-I (Proteintech, 66761-1-Ig), Collegen-III (Abcam, ab7778).

Techniques: Fluorescence, Imaging, Staining, TUNEL Assay, Immunohistochemistry, Western Blot

Journal: Materials Today Bio

Article Title: Enhanced oral nanomedicine utilizing biomineralized oncolytic virus for synergistic gastrointestinal cancer therapy

doi: 10.1016/j.mtbio.2025.102583

Figure Lengend Snippet: CaCO 3 @CM-OA inhibits pancreatic cancer (PCC) progression and EMT. (A) Mice bearing PCC xenografts were treated orally every other day for 14 days. (B) Body weight monitoring. (C) Tumor volume measurements. (D) Fluorescence imaging of tumors. (E) Tumor photographs. (F) Serum IL-6 levels. (G) H&E staining. (H) TUNEL assay. (I) IHC staining of Ki67, Bcl2, Vimentin, and LC3A/B. (J–M) Western blot results for Ki67, P62, Beclin1, LC3A/B, Bcl2, Bax, FL-Cas3, CL-Cas3, Cytochrome-c, E-cadherin, Vimentin, Collagen I, and α-SMA. Data are presented as mean ± SD. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001.

Article Snippet: The antibodies used in western blot, immunofluorescence and immunohistochemistry experiments were as follows: CRT (Bioss, 5913R), HMGB1 (Beytime, AF1174), Anti-Adenovirus Type 5 Hexon (abcam, ab816352), Ki67 (Proteintech, 27309-1-AP), p53 (MCE, HY- P80938 ), p-p53 (Affinity, AF3075), p21 (Affinity, AF6290), CyclinB1 (Proteintech, 28603-1-AP), Bcl2 (Proteintech, 26593-1-AP), Bax (Proteintech, 50599-2-Ig), Caspase3 (Proteintech, 19677-1-AP), cleaved-Caspase3 (CST, 9661S), Cytochrome c (Proteintech, 10993-1-AP), p62 (HuaBio, HA721171), Beclin1 (CST, 3495S), LC3A/B (CST, 12741T), p-MLKL (MCE, HY-P81878), MLKL (HuaBio, ET1601-25), N-cadherin (Affinity, AF5239), E-cadherin (Affinity, AF0131), α-SMA (HuaBio, ET1607-53), Vimentin (Affinity, AF7013), Collegen-I (Proteintech, 66761-1-Ig), Collegen-III (Abcam, ab7778).

Techniques: Fluorescence, Imaging, Staining, TUNEL Assay, Immunohistochemistry, Western Blot

Journal: Frontiers in Endocrinology

Article Title: Ultrasound combined with microbubbles promotes diabetic wound healing by regulating macrophage polarization

doi: 10.3389/fendo.2026.1781906

Figure Lengend Snippet: Immunohistochemical staining of wounds in diabetic rats. (A) Representative images of Ki67 immunohistochemical staining in healing tissues from three experimental groups; (B) Quantitative analysis of Ki67-positive cells across groups; (C) Immunohistochemical staining of CD31 in diabetic wounds; (D) Statistical results of CD31-positive expression. Data are presented as mean ± SD (n = 4); *p < 0.05, **p < 0.01, ***p < 0.001.

Article Snippet: After three washes with PBS, they were incubated overnight at 4 °C with anti-CD31 antibodies (1:1000, abcam) and anti-Ki67 antibodies (1:1000, Proteintech).

Techniques: Immunohistochemical staining, Staining, Expressing

Journal: NPJ Breast Cancer

Article Title: Targeting GD2 with naxitamab overcomes GD3 synthase-driven immune suppression in triple-negative breast cancer

doi: 10.1038/s41523-025-00843-7

Figure Lengend Snippet: A Analysis of GD3S ( ST8SIA1 ) mRNA expression in METABRIC and TCGA (pan cancer) BC patient datasets shows significant correlation with immune checkpoint inhibitors. In the METABRIC dataset, Pearson’s correlation coefficients indicate significant correlations of GD3S mRNA expression with CTLA-4 ( r = 0.4; P < 0.001), LAG3 ( r = 0.33; P < 0.001), PD1 ( r = 0.3; P < 0.001), CD25 ( r = 0.38; P < 0.001), and SIRPα ( r = 0.36; P < 0.001). Similarly, in the TCGA dataset, GD3S mRNA expression was significantly correlated with CTLA-4 ( r = 0.47; P < 0.001), LAG3 ( r = 0.33; P < 0.001), PD1 ( r = 0.38; P < 0.001), CD25 ( r = 0.45; P < 0.001), and SIRPα ( r = 0.56; P < 0.001). B Representative IHC images obtained by sequential multiplex immunofluorescence images (Lunaphore COMET) from FFPE samples of TNBC patients with high or low GD3S expression ( n = 20 total) were used to compare immune infiltration patterns, showing distinct fluorescence intensities for PANK, Ki67, CD163, CD86, CD56, CD8, CD4, FOXP3, and GD3S within tumor tissues. C H-scores for GD3S expression in BC patients categorized into high and low GD3S expression groups ( ****P < 0.0001). Immune cell counts using Visiopharm IHC image analysis software show differences in the expression of CD8, CD4, CD86, and CD56 between the high and low GD3S expression groups ( ****P < 0.0001; **P < 0.01). Scale bar in IHC images represents 55 µm with 20x magnification. Bar graphs display means ± standard deviations.

Article Snippet: We also purchased the following antibodies: pan-Cytokeratin (Proteintech, cat. #26411-1-AP, rabbit host) along with GD3S (Proteintech, cat. #24918-1-AP, rabbit host), CD45 (Fortislife, clone BL-178-1267, cat. #A700-012, rabbit host), Ki67 (Bethyl, clone BLR021E, cat. #A700-021CF, rabbit host), CD3 (Fortislife, clone BL-298-5012, cat. #A700-016F, rabbit host), CD8 (Fortislife, clone c8/144B, cat. #A500-012A, mouse host), CD4 (Bethyl, clone BL-155-1C11, cat. #A700-015, rabbit host), FOXP3 (Bethyl, clone BLR034F, cat. #A700-034, rabbit host), CD68 (Fortislife, cat. #A500-018ACF, mouse host), CD163 (Invitrogen, clone I0D6, cat. #MA5-11458, mouse host), CD86 (CST, clone E2G8P, cat. #76755SF, rabbit host), CD56 (Fortislife, clone BLR152J, cat. #A700-152, rabbit host) and human IgG1 Kappa antibody (hIgG, cat. #0151K-14, SouthernBiotech).

Techniques: Expressing, Multiplex Assay, Immunofluorescence, Fluorescence, Software

Journal: Cell stem cell

Article Title: Melanocyte Stem Cell Activation and Translocation Initiate Cutaneous Melanoma in Response to Ultraviolet Exposure

doi: 10.1016/j.stem.2017.09.001

Figure Lengend Snippet: (A) MCSC translocation by topical TPA treatment shown by tdTomato lineage tracing. (B) Experimental scheme. (C) Macroscopic phenotypes in TBP mice with/without topical TPA treatment, and quantification of epidermal pigmentation. n = 10 TPA-treated control, n = 7 non-TPA TBP and n = 7 TPA-treated TBP mice. (D) Histological phenotypes of TPA-induced melanoma during quiescent MCSC, telogen period, and co-immunostaining for Sox10, a melanocyte stem cell/melanoma marker, with Ki67, a marker of proliferation. (E) Experimental scheme. Dex., dexamethasone. (F) Relative number of MCSC migration was quantified via tdTomato lineage tracing in TT mice, compared to the total number of hair follicles (≥ 500 hair follicles / each). Mean ± SEM, n = 10 / group. (G) Experimental scheme. (H) Macroscopic phenotypes with the quantification of epidermal pigmentation. n = 6 low-dose (80 mJ cm−2) UVB, n = 10 per each group (UVB only or UVB + Dex.). Data are represented as Mean ± SEM. Also see Figures S5 and S6.

Article Snippet: Rabbit monoclonal anti-Ki-67 , Rockland , Cat#900-C01-B38; RRID:AB_2142230.

Techniques: Translocation Assay, Immunostaining, Marker, Migration

Journal: Cell stem cell

Article Title: Melanocyte Stem Cell Activation and Translocation Initiate Cutaneous Melanoma in Response to Ultraviolet Exposure

doi: 10.1016/j.stem.2017.09.001

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: Rabbit monoclonal anti-Ki-67 , Rockland , Cat#900-C01-B38; RRID:AB_2142230.

Techniques: Plasmid Preparation, Recombinant, DNA Ligation, SYBR Green Assay, BIA-KA, Ab Array, Software, CRISPR

Journal: Frontiers in Molecular Biosciences

Article Title: Antimetastatic and antitumor activities of oncolytic NDV AMHA1 in a 3D culture model of breast cancer

doi: 10.3389/fmolb.2024.1331369

Figure Lengend Snippet: Analysis of the expressions of caspase-3, P21, and Ki67 by immunofluorescence assay in the 3D spheroids of the breast cancer metastasis model and normal tissue spheroids. Spheroids were infected with NDV (MOI 10) for 24 h; the spheroids were stained with anti-caspase-3, anti-P21, and anti-KI67 antibodies. Caspase-3 and P21 proteins exhibit a high expression of green fluorescence, while there is no expression in untreated spheroids (control). Furthermore, KI67 was absent in cancer spheroids treated with NDV. Normal tissue spheroids (hATMSCs) were not affected by the presence of virus as there were no notable changes in the expression of these proteins between treated and untreated spheroids, again confirming the safety of the virus.

Article Snippet: Cells were then treated with 1 μgmL −1 of each of the primary markers, KI67 (mouse monoclonal antibody, dilution 1:200; Elabscience, China), caspase-3 (mouse monoclonal antibody, dilution 1:200; Elabscience, China), and P21 (mouse monoclonal antibody, dilution 1: 500, Santa Cruz, CA, United States), which were diluted in blocking buffer and incubated for 1:30 h or overnight at 4°C.

Techniques: Immunofluorescence, Infection, Staining, Expressing, Fluorescence, Control, Virus

Journal: Frontiers in Pediatrics

Article Title: Neurogenesis Is Reduced at 48 h in the Subventricular Zone Independent of Cell Death in a Piglet Model of Perinatal Hypoxia-Ischemia

doi: 10.3389/fped.2022.793189

Figure Lengend Snippet: Fluorescent microphotographs of Ki67 [cell proliferation, (A,B) ], Sox2/Ki67 [neural stem/progenitor cell proliferation, (C,D) ], and DAPI [nuclei, (E,F) ] immune-stained samples from control and HI piglets. Ki67 positive cells (green) are abundant in the control piglet (A) , whereas HI (B) significantly reduced its counts by half in L-SVZ and DL-SVZ (both *** p < 0.001). Double Sox2 (red) + /Ki67 (green) + cells are observed in control animals; again, HI reduced neural stem/progenitor cell counts in L-SVZ and DL-SVZ (both *** p < 0.001). DAPI immunostaining reveals total nuclei. LV, lateral ventricle; SVZ, subventricular zone; CDT, caudate nucleus; PvWM, periventricular white matter. Original magnification 400×. Scale bar: 100 μm.

Article Snippet: For single labeling, radial-glia/neural stem cells were identified using an anti-glial fibrillary acidic protein (GFAP) antibody to assess neurogenic activity close to the ventricular wall (mouse anti-GFAP, 1:100, MA5-12023, Thermo Fisher, United States); an anti-doublecortin (DCX) antibody was used to identify young neurons/neuroblasts (mouse anti-DCX, 1:50, sc-271390, Santa Cruz Biotechnology, United States); cell proliferation was identified by an anti-Ki67 antibody (mouse anti-Ki67; 1:50, STJ96966, St Johns Labs, United Kingdom).

Techniques: Staining, Control, Immunostaining

Journal: Molecular Medicine Reports

Article Title: ER-α36 knockdown is associated with lysosomal dysfunction and proliferation inhibition in liver cancer cells

doi: 10.3892/mmr.2025.13649

Figure Lengend Snippet: ER-α36 knockdown suppresses the malignant proliferation of liver cancer cells and induces lysosomal membrane permeabilization. (A) Representative images of liver tumors from nude mice intrahepatically injected with HepG2 cells expressing different ER-α36 levels, harvested at 28 days post-injection. (B) Quantitative analysis of liver tumor volume, liver weight, body weight and the ratio of liver weight to body weight. (C) Representative H&E staining images showing pathological karyomitosis changes. Scale bar, 50 µm. (D) Immunohistochemical staining of LC3, p62, LAMP1 and Ki67 with corresponding IOD values. Scale bar, 50 µm. (E) Immunofluorescence staining of Gal-3 in the tumors formed from the transfected HepG2 cells. Scale bar, 10 µm. (F) Western blotting results showing the levels of LC3-II and LC3-II, p62, LAMP1, p-AKT and t-AKT in the tumors, and (G) quantitative analyses of the LC3-II/LC3-I and p-AKT/t-AKT ratios, and p62 and LAMP1 expression levels. β-actin was used as the internal loading control. Data are presented as the mean ± SEM. **P<0.01. ER, estrogen receptor; H&E, hematoxylin and eosin; LC3, microtubule-associated protein 1 light chain 3; LAMP1, lysosome-associated membrane protein 1; Gal-3, galectin-3; IOD, integrated optical density; p-, phosphorylated; t-, total; Sh36, transfected with ER-α36 specific short hairpin RNA expression vector; Vector, transfected with empty vector.

Article Snippet: The Ki67 antibody (cat. no. bs-2130R) was purchased from Biosynthesis Biotechnology Co., Ltd. Chloroquine (CQ; cat. no. HY-17589A) and the AKT inhibitor MK-2206 (cat. no. HY-108232) were obtained from MedChemExpress.

Techniques: Knockdown, Membrane, Injection, Expressing, Staining, Immunohistochemical staining, Immunofluorescence, Transfection, Western Blot, Control, shRNA, Plasmid Preparation