Fig 2: Artificial upregulation of miR-520a inhibits NSCLC progression. (a) Viability of A549 and H460 cells determined by the EdU labeling assay (*p < 0.05, two-way ANOVA). (b) Proliferation of A549 and H460 cells after miR-520a transfection determined by the MTT assay (*p < 0.05, two-way ANOVA). (c, d) Changes in number of migrating (c) and invading cells (d) detected using the transwell assays (*p < 0.05, two-way ANOVA). (e) The apoptosis rate of A549 and H460 cells determined by flow cytometry (*p < 0.05, two-way ANOVA). (f) Protein levels of apoptosis-related factors Bcl-2, Bax, caspase-3, and cleaved caspase-3 determined by western blot analysis (*p < 0.05, two-way ANOVA).

Fig 3: Efficacy of intra-arterial chemotherapy versus intravenous chemotherapy against retinoblastoma xenograft vitreous seeds in the rabbit model. This figure shows immunohistochemical staining with cleaved caspase-3, a marker for apoptosis. In this immunohistochemistry figure, brown-stained cells are undergoing apoptosis, and blue cells (i.e., cells that are not stained brown) are not undergoing apoptosis. (A) All vitreous seeds were significantly regressed in the IAC treated eye, with all retinoblastoma cells staining positively for cleaved caspase-3 via immunohistochemistry, indicating that they were all already undergoing apoptosis. In contrast, immunohistochemistry for cleaved caspase-3 revealed no positivity for retinoblastoma vitreous seed cells following administration of the same dose of melphalan intravenously (B) or following standard intravenous CEV administration (C).

Fig 4: Representative images and histological analysis of caspase-3 in the corneal epithelium, conjunctival epithelium, and lacrimal gland on day 14. Control experiment showed no positive stained cells in the corneal epithelium (A, B), conjunctival epithelium (F, G), and lacrimal gland (K, I) in the control group and the dry group. On day 14, in the control group, there were little apoptotic cells in the corneal epithelium (C), conjunctival epithelium (H), and lacrimal gland (M). In the dry group, the caspase-3-positive cells in the cornea (D, E) and conjunctiva (I, J) were more significantly increased than in the control group (cornea, **P < 0.01, n = 3 [6 eyes] per group; conjunctiva, *P < 0.05, n = 3 [6 eyes] per group). There were no statistically significant differences in the lacrimal glands (N, O) between these two groups (P > 0.05, n = 3 [6 eyes] each group). Data are shown as mean ± SD (error bars). Magnification, × 400.

Fig 5: Expression of Bcl-2, Bax and Caspase-3 proteins determined by western blot analysis. (A) Results normalized relative to ß-actin in the ASCI rats at day 7 and (B) in spinal neuron culture scratch models following 24 h culture. Data are presented as mean ± standard error of the mean, n=4 per group. (A) *P<0.05 vs. ACSI group; #P<0.05 vs. TIIA + MP group. (B) *P<0.05 vs. ASCI group; #P<0.05 vs. TIIA + MP group and MP group. Bcl-2, B-cell lymphoma-2; Bax, Bcl-2 associated protein X; ASCI, acute spinal cord injury; MP, methylprednisolone; TIIA, tanshinone IIA; TIIA + MP, TIIA and MP combined treatment; Sham, sham-operated, no treatment.