In both tumor lines (A549 and H1299), co-transplantation of RGE cells resulted in faster growth rates [maximal tumor diameter of 20 mm after 22 (± 1.2) as compared to 45 (± 1.8) days, p < 0.001], higher microvessel density (MVD) determined histologically after CD-31 staining [171.4 (± 18.9) as compared to 110.8 (± 11) vessels per mm<sup>2</sup>, p = 0.002], and higher perfusion as indicated by the number of beads [1.3 (± 0.1) as compared to 1.1 (± 0.04) beads per field of view, p = 0.001].
The tumor inhibition rate was calculated, α-smooth muscle actin (α-SMA) and cluster of differentiation 31 (CD31) were detected via immunohistochemistry, and the vascular maturity index (VMI) and microvessel density (MVD) were also detected.
High CD31 expression was found in poorly differentiated tumours (p=0.0006), and high p53 expression was found in poorly differentiated cancers (p<0.0001), high clinical stage (p<0.0001), non-radical surgery (p<0.0001) and high serum CA-125 values (p<0.0001).
Tumors were examined by immunostaining with antibodies against proteins associated tumor proliferation (Ki‑67), angiogenesis [CD31 and vascular endothelial growth factor (VEGF)], anti‑immunity (CD204) and epithelial‑mesenchymal transition (EMT; E‑cadherin).
CD31 staining revealed that sFlt-1-loaded exosomes significantly reduced the vascular density of experimental mice. sFlt-1-loaded exosomes markedly induced tumor apoptosis and inhibited tumor cell proliferation in mice.
After sacrifice histologic staining, including hematoxylin and eosin (H&E), CD31, and Oil Red O (ORO) were performed on tumor and liver samples to evaluate necrosis, microvascular density (MVD), and Lipiodol retention over time.
By immunoperoxidase stains, the tumor cells are positive with the vascular markers CD31 and CD34 but negative with the epithelial marker cytokeratin AE1/AE3.
In a murine breast cancer model of tumor cell 4T1 inoculation, subcutaneous injection of PS induced effective antitumor effect through reprogramming M2 macrophages in the tumor microenvironment to M1, increased CD4<sup>+</sup> and CD8<sup>+</sup> T cells, and decreased the expression of CD31 in the tumor mass, which together inhibited the tumor progression and the metastasis in lung and liver, leading to the prolong of the mice survival.
Tumor samples collected at baseline and at surgery were assayed for select epithelial mesenchymal transition and vascular density markers: E-cadherin, vimentin, and CD31 expression.
Immunohistochemical staining of tumor Ki-67 and vascular endothelial cell marker antigen (CD31) were used to evaluate the effects on tumor proliferation and angiogenesis.
Additionally, THZ1 reduced VEGF expression in human RCC cells (786-O and Caki-2), and THZ1 treatment inhibited tumor growth, vascularity, and angiogenic marker (CD31) expression in RCC xenografts.
More interestingly, results also demonstrated that cancer patients presented higher concentrations of circulating CD31+ endothelial-derived and tumour cancer stem cell-derived CD133 + CD326- EVs, when compared to healthy volunteers.
These findings imply that stable vessels supply anti-cancer immune cells, which are at least partially responsible for better OS in the CD31 high expressing tumors.
Based on immunohistochemical staining, the tumor xenografts in mice treated with 29dL showed time-dependent decreases in the intensity of CD31, a marker of blood vessels, whereas the intensity of γ-H2AX, a marker of DNA damage, increased.
The expression levels of PFKFB3, CD163 and CD31 were significantly increased in OSCC specimens as compared with normal oral mucosa (P<0.05), and PFKFB was signifcantly correlated with tumor differentiation and tumor size (P<0.05), and CD163 was significantly correlated with areca nut chewing habit among OSCC tissues (P<0.05).
C. butyricum combined with apatinib significantly inhibits tumour growth with decreased CD31, PCNA and Bcl-2 expressions, and increased cleaved caspase-3 expressions.