Journal: bioRxiv

Article Title: Breast cancer interactions with osteoclasts generate osteoclast-tumor hybrid-like cells through dynamic non-canonical cell fusion and cell-in-cell processes

doi: 10.64898/2026.04.05.716538

Figure Lengend Snippet: a,b, Fluorescent snapshot image for osteoclast-tumor hybrid-like cells formed between RAW264.7-GFP and other solid tumor cell lines. Hybrids containing tumor nuclei derived from (a) B16F10-H2B-mRFP melanoma and hybrids with tumor nuclei derived from (b) CT26-H2B-mRFP colon cancer.

Article Snippet: RAW264.7, 4T1, EO771, B16F10, and CT26 cell lines were obtained from ATCC.

Techniques: Derivative Assay

Journal: RSC Advances

Article Title: Exploring an azo-uracil based nickel( ii ) complex for anticancer and phosphatase like activities

doi: 10.1039/d6ra01587e

Figure Lengend Snippet: Cytotoxic and anti-cancer activity of the N1: (A) dose-dependent inhibition of cell proliferation in murine colon carcinoma cell lines (CT26 and MC-38) and human colorectal cancer cell line (HCT-15) upon treatment with increasing concentrations of N1, determined by MTT assay; (B) cell viability of normal murine fibroblast cells (NIH-3T3) following treatment with N1 at indicated concentrations, demonstrating minimal cytotoxicity; (C–E) dose–response curves showing percentage growth inhibition and corresponding IC 50 values for CT26 (C), MC-38 (D), and HCT-15 (E) cells. IC 50 values are calculated by nonlinear regression analysis using GraphPad Prism. Data are expressed as mean ± SD ( n = 3).

Article Snippet: Murine colon carcinoma cell lines CT26 and MC-38, human colorectal carcinoma cell line HCT-15, and normal murine fibroblast cell line NIH-3T3 were procured from the ATCC, USA.

Techniques: Activity Assay, Inhibition, MTT Assay

Journal: RSC Advances

Article Title: Exploring an azo-uracil based nickel( ii ) complex for anticancer and phosphatase like activities

doi: 10.1039/d6ra01587e

Figure Lengend Snippet: N1 induced apoptosis in colon cancer cells: (A) representative bright-field and fluorescence micrographs of CT26 cells treated with N1 (0.04 and 0.08 µg mL −1 ) for 12 h and stained with Annexin V-FITC (green) and propidium iodide (PI, red); merged images indicate apoptotic cell populations; (B–E) flow cytometric dot plots of Annexin V-FITC/PI staining showing viable (Q4, Annexin V − /PI − ), early apoptotic (Q3, Annexin V + /PI − ), late apoptotic (Q2, Annexin V + /PI + ), and necrotic (Q1, Annexin V − /PI + ) cell populations in untreated control (B), doxorubicin-treated positive control (0.25 µM) (C), and N1-treated cells at 0.04 µg mL −1 (D) and 0.08 µg mL −1 (E); (F) overlay histogram showing fluorescence intensity shifts in the FITC channel for control, doxorubicin, and N1-treated cells; (G) quantitative analysis of percentage dead/apoptotic cells under different treatment conditions (mean ± SD, n = 3; *** p < 0.001 vs. control).

Article Snippet: Murine colon carcinoma cell lines CT26 and MC-38, human colorectal carcinoma cell line HCT-15, and normal murine fibroblast cell line NIH-3T3 were procured from the ATCC, USA.

Techniques: Fluorescence, Staining, Control, Positive Control

Journal: RSC Advances

Article Title: Exploring an azo-uracil based nickel( ii ) complex for anticancer and phosphatase like activities

doi: 10.1039/d6ra01587e

Figure Lengend Snippet: Mechanistic insights into N1-induced apoptosis: caspase dependence, ROS generation, and mitochondrial perturbation: (A) representative flow cytometric dot plots of Annexin V-FITC/PI staining in CT26 cells treated with N1 (0.04 and 0.08 µg mL −1 ) for 12 h, showing viable (Annexin V − /PI − ), early apoptotic (Annexin V + /PI − ), late apoptotic (Annexin V + /PI + ), and necrotic (Annexin V − /PI + ) populations; (B) effect of pan-caspase inhibitor Z-VAD-FMK (20 µM, 1 h pre-treatment) on N1-induced apoptosis, showing reduced Annexin V-positive cell populations; (C) flow cytometric histograms of intracellular ROS levels measured using CellROX Green (total ROS) and MitoSOX Red (mitochondrial superoxide) in untreated, doxorubicin-treated (0.25 µM), and N1-treated cells (0.04 and 0.08 µg mL −1 ), indicating predominant induction of total ROS; (D) assessment of mitochondrial membrane potential (Δ Ψ m) using JC-1 staining, showing changes in red (JC-1 aggregates) and green (JC-1 monomers) fluorescence in control, N1-treated, and doxorubicin-treated cells, indicative of moderate mitochondrial depolarization. All experiments were performed in CT26 cells and analysed by flow cytometry. Data shown are representative of three independent experiments.

Article Snippet: Murine colon carcinoma cell lines CT26 and MC-38, human colorectal carcinoma cell line HCT-15, and normal murine fibroblast cell line NIH-3T3 were procured from the ATCC, USA.

Techniques: Staining, Membrane, Fluorescence, Control, Flow Cytometry

Journal: RSC Advances

Article Title: Exploring an azo-uracil based nickel( ii ) complex for anticancer and phosphatase like activities

doi: 10.1039/d6ra01587e

Figure Lengend Snippet: Effect of ROS scavenging and phosphatase inhibition on N1-induced cytotoxicity: (A) percentage cytotoxicity in CT26 cells treated with N1 (0.04 and 0.08 µg mL −1 ) in the presence or absence of N -acetyl cysteine (NAC, 5 mM) and PhosSTOP phosphatase inhibitor (1×); (B) corresponding cytotoxicity in HCT-15 cells under similar treatment conditions. NAC pre-treatment significantly reduces N1-induced cytotoxicity, indicating the involvement of ROS, while PhosSTOP treatment partially attenuates cytotoxicity, suggesting a possible contribution of phosphate-related processes. Data are expressed as mean ± SD ( n = 3; *** p < 0.001, **** p < 0.0001 vs. N1-treated group).

Article Snippet: Murine colon carcinoma cell lines CT26 and MC-38, human colorectal carcinoma cell line HCT-15, and normal murine fibroblast cell line NIH-3T3 were procured from the ATCC, USA.

Techniques: Inhibition