Journal: Oncology Letters

Article Title: Exosomal-miR-32-5p directly targets FOXN2 to regulate the proliferation, migration and apoptosis of uterine corpus endometrial carcinoma via the PI3K/AKT/BCL-2 pathway

doi: 10.3892/ol.2026.15574

Figure Lengend Snippet: Effects of miR-32-5p on the proliferative capacities, migratory abilities and apoptotic rate of UCEC cells. (A) The expression of miR-32-5p in HEC-1-A and Ishikawa cells were then determined using quantitative reverse transcription-PCR. ***P<0.001 vs. HEC-1-A cells. (B) The expression of miR-32-5p in HEC-1-A cells after transfection of miR-32-5p inhibitor or in Ishikawa cells after transfection of miR-32-5p mimic. (C) The viability of UCEC cell lines were measured using the CCK-8 assay. (D) Relative colony formation efficiency of UCEC cell lines was evaluated using the colony formation assay. (E) EdU-positive cells were measured through EdU proliferation assay. (Scale bar, 100 µm). (F) The migratory potential of UCEC cell lines were determined via Transwell migration assay. (Scale bar, 100 µm). (G) Flow cytometry was used to detect apoptosis. * P<0.05, **P<0.01, ***P<0.001 vs. miR-32-5p inhibitor-NC or miR-32-5p mimic-NC. UCEC, uterine corpus endometrial carcinoma; miRNA, microRNA; NC, negative control; EdU, 5-ethynyl-2′-deoxyuridine.

Article Snippet: HEC-1-A or Ishikawa cells (3×10 3 cells/ml) were grown in 96-well plates for 0, 24, 48 and 72 h before adding the CCK-8 solution (15 μl; Dojindo Laboratories, Inc.).

Techniques: Expressing, Reverse Transcription, Transfection, CCK-8 Assay, Colony Assay, Proliferation Assay, Transwell Migration Assay, Flow Cytometry, Negative Control

Journal: Oncology Letters

Article Title: Exosomal-miR-32-5p directly targets FOXN2 to regulate the proliferation, migration and apoptosis of uterine corpus endometrial carcinoma via the PI3K/AKT/BCL-2 pathway

doi: 10.3892/ol.2026.15574

Figure Lengend Snippet: Exo-miR-32-5p regulates the proliferation, migration and apoptosis of UCEC cells through regulating FOXN2 expression and PI3K/AKT/Bcl-2 pathway. The impact of Exo-miR-32-5p on the proliferation, migration and apoptosis of UCEC cells were examined utilizing a co-culture model. (A) Exo-miR-32-5p expression in HEC-1-A cells transfected with miR-32-5p-inhibitor or in Ishikawa cells transfected with miR-32-5p-mimic was determined through qRT-PCR. (B) The viability of UCEC cell lines were measured using the CCK-8 assay. (C) Relative colony formation efficiency of UCEC cell lines was evaluated using the colony formation assay. (D) EdU-positive cells were measured through EdU proliferation assay. (Scale bar, 100 µm). (E) The migratory potential of UCEC cell lines were determined via the Transwell migration assay. (F) Flow cytometry was used to detect apoptosis. (G) The mRNA expression of AKT, PI3K, Bcl-2 and FOXN2 was detected by qRT-PCR. (H) The protein levels of AKT, PI3K, p-PI3K, Bcl-2, FOXN2 and the ratio of p-AKT/AKT were measured by western blotting. **P<0.01, ***P<0.001 vs. Exo-miR-32-5p inhibitor-NC or Exo-miR-32-5p mimic-NC. UCEC, uterine corpus endometrial carcinoma; miRNA, microRNA; NC, negative control; NS, not significant; WT, wild-type; MUT, mutant; qRT-PCR, quantitative reverse transcription-PCR; p-, phosphorylated; FOXN2, Forkhead Box N2; EdU, 5-ethynyl-2′-deoxyuridine.

Article Snippet: HEC-1-A or Ishikawa cells (3×10 3 cells/ml) were grown in 96-well plates for 0, 24, 48 and 72 h before adding the CCK-8 solution (15 μl; Dojindo Laboratories, Inc.).

Techniques: Migration, Expressing, Co-Culture Assay, Transfection, Quantitative RT-PCR, CCK-8 Assay, Colony Assay, Proliferation Assay, Transwell Migration Assay, Flow Cytometry, Western Blot, Negative Control, Mutagenesis, Reverse Transcription

Journal: Bioactive Materials

Article Title: Revolutionizing Mg-based guided bone regeneration mesh derived from endogenous dentoalveolar bone augmentation

doi: 10.1016/j.bioactmat.2026.04.003

Figure Lengend Snippet: In vitro cytocompatibility assessment . (a) CCK-8 assay results of MC3T3-E1 cells and HUVECs cultured with mesh extracts. (b) Representative live/dead staining images of MC3T3-E1 cells and HUVECs after 1 and 3 days of culture. (c) Representative phalloidin (cytoskeleton) and DAPI (nucleus) staining images of MC3T3-E1 cells and HUVECs after 24 h of culture. (d) SEM images of MC3T3-E1 cells and HUVECs directly cultured on mesh surfaces for 1 day. (e) Optical images of scratch wound-healing assays for MC3T3-E1 cells cultured in different extracts for 0 h, 12 h, and 24 h. (f) Migration rates of MC3T3-E1 cells cultured in different extracts for 0 h, 12 h, and 24 h. n.s.>0.05, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Article Snippet: On days 1, 3, and 5 of culture, the existing culture medium was substituted with 100 μL of CCK-8 working solution (Cell Counting Kit-8, Beyotime Biotech, China), prepared by mixing fresh α-MEM and CCK-8 reagent at a volume ratio of 10:1.

Techniques: In Vitro, CCK-8 Assay, Cell Culture, Staining, Migration

Journal: Current Therapeutic Research, Clinical and Experimental

Article Title: The Berberine Derivative BBR684 Inhibits VDAC Oligomerization to Suppress Ferroptosis in Acute Kidney Injury

doi: 10.1016/j.curtheres.2026.100825

Figure Lengend Snippet: The berberine derivative BBR684 is superior to berberine in (BBR) in protecting against Erastin-induced ferroptosis in HK-2 cells. (A-C)Representative phase-contrast microscopy images showing the morphological changes of HK-2 cells treated with the indicated compounds for 24 hours. (D) Quantification of cell death by flow cytometry using propidium iodide (PI) staining. HK-2 cells were pre-treated with BBR684 or BBR for 1 hour, followed by co-incubation with Erastin for 12 hours. (E) Cells viability assessed by the CCK-8 assay after treating HK-2 cells with increasing concentrations of BBR684 for 24 hours. (F) Flow cytometry analysis of cell death (PI-positive cells) in HK-2 cells treated with Erastin in the presence or absence of BBR684.

Article Snippet: Subsequently, the medium was replaced with fresh medium, and 10 μl of CCK-8 solution (Catalog #KGA1606-1000, KeyGen Biotech) was added to each well.

Techniques: Microscopy, Flow Cytometry, Staining, Incubation, CCK-8 Assay

Journal: Current Therapeutic Research, Clinical and Experimental

Article Title: The Berberine Derivative BBR684 Inhibits VDAC Oligomerization to Suppress Ferroptosis in Acute Kidney Injury

doi: 10.1016/j.curtheres.2026.100825

Figure Lengend Snippet: Overexpression of VDAC abolishes the protective effects of BBR684 against ferroptosis.(A) Western blot analysis validating the overexpression of VDAC1 in HEK293T cells. (B) Representative phase-contrast microscopy images showing the morphology of HEK293T cells with or without VDAC1 overexpression after the indicated treatments for 24 hours. (C) Quantification of cell death by flow cytometry (propidium iodide staining) in HEK293T cells treated with Erastin and BBR684. (D) Cells viability assessed by the CCK-8 assay in HEK293T cells treated with increasing concentrations of BBR684 for 24 hours. (n = 3, 3 biological replicates). (E, F) Levels of malondialdehyde (MDA, F) and reduced glutathione (GSH, E) in cell lysates. (n = 3, 3 biological replicates). (G) Intracellular Fe²⁺ levels measured by a colorimetric assay. (n = 3, 3 biological replicates).

Article Snippet: Subsequently, the medium was replaced with fresh medium, and 10 μl of CCK-8 solution (Catalog #KGA1606-1000, KeyGen Biotech) was added to each well.

Techniques: Over Expression, Western Blot, Microscopy, Flow Cytometry, Staining, CCK-8 Assay, Colorimetric Assay