Fig 1: Various responses between T cell clusters, and Tnull and TCR-TMART-1 to different levels of tumor PD-L1. (A) Cluster composition of Tnull and TCR-TMART-1. (B) The proportion distribution of T cell clusters with the increased tumor PD-L1. (C) The bar plot shows the proportion distribution of cells expressing CTLA4, HAVCR2 (TIM3), LAG3, PDCD1, TIGIT, and VSIR among the five T cell clusters, respectively (cutoff: UMI of the gene > 0). (D) The bubble plot shows the proportion distribution of T cells expressing BCL2L11, CASP3, CASP8, CASP9, MKI67, and TP53 in TCR-TMART-1 responding to differential proportions of PD-L1+ tumor, among the five clusters respectively. The size of the point shows the mean expression of genes in the corresponding T cell population. The violin shows the expression distribution of BCL2L11 among the five clusters. (E) Differentially expressed genes in TCR-TMART-1 responding to differential proportions of PD-L1+ tumor. (F) The expression distribution of XCL1, TNFRSF9, DUSP4, and MIF in TCR-TMART-1 responding to differential proportions of PD-L1+ tumor. (G) Bubble plot showing the top 10 pathways in Tnull (left) and TCR-TMART-1 (right) compared to the control group, respectively. The color represents pvalue and the size represents gene ratio.
Fig 2: Knockdown of lncRNA FAM225A inhibits ESCC xenograft tumor development in vivo. KYSE510 cells stably transfected with sh-FAM225A or mock control were transplanted into the right flank of nude mice to establish ESCC xenograft tumor model. (A) The representative images of nude mice in different groups at week 1 and weeks 5 were shown. (B) Tumor growth was monitored at indicated time points. (C) Tumor weights from different groups were analyzed. (D) The representative immunohistochemical staining of Ki-67 and H&E staining of xenograft tumor sections and the quantification of Ki-67 expression were analyzed. ** P < 0.01.
Fig 3: Cell distribution, histopathology, and tumor formation analysis in chronic toxicity experiment. Biodistribution of transplanted cells and whether they caused pathological damage or tumor formation to major organs were assessed. (A) STEM121 (red) immunofluorescence staining marks the human-derived cells transplanted into the lateral ventricle of SD rats. Scale bar is 100 µm, inset 50 µm. (B) H&E staining was used to evaluate the pathological changes of the main organs (heart, liver, spleen, kidney, thymus, spinal cord, testes, ovary, brain, and lungs) in rats. Scale bar is 100 µm. (C) Ki67 protein expression was detected by IF. Scale bar is 100 µm. (D) IOD of Ki67 fluorescence image was calculated. Bars represent means. Error bars show the standard error of the mean. H&E, hematoxylin and eosin; IF, immunofluorescence; IOD, integrated optical density; SD, Sprague–Dawley.
Fig 4: Culture and identification of hOPCs. The transplanted cells were identified based on their morphology and main markers. (A) Identification of the bright field morphology of hOPCs. Scale bar is 200 µm, inset 100 µm. (B) Flow cytometry to detect PDGFR-a, A2B5, NG2, and Ki67 of hOPCs. (C) Tissue immunofluorescence staining to detect PDGFR-a, A2B5, NG2, and Ki67 of transplanted hOPCs. Scale bar is 100 µm. A2B5, ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 1; hOPCs, human–derived oligodendrocyte precursor cells; PDGFR-a, platelet-derived growth factor receptor alpha; NG2, chondroitin sulfate proteoglycan 4.
Fig 5: Caudatin restrained the proliferation of OS cells in vivo. MG63 cells are injected to nude mice, and 2 weeks after cell injection mice were randomly divided into the sham (injected with PBS) and caudatin (injected with 50 mg/kg every three days) groups. (a) Tumor volume and (b) tumor weight are measured in the sham and caudatin groups. (c) The expression level of Ki-67 is measured via immunohistochemistry. */**P < 0.05/0.01, compared with sham.
Supplier Page from Abcam for Anti-Ki67 antibody [Ki-67] (PE)