PA-MSHA induces apoptosis and suppresses metastasis by tumor associated macrophages in bladder cancer cells

Abstract

BackgroundThe aim of the present study was to investigate effects of Pseudomonas aeruginosa-mannose-sensitive hemagglutinin (PA-MSHA) on the inhibition of the proliferation of bladder cancer cell lines and to further define its functional mechanisms.MethodsA rat model of bladder tumor was induced by intravesical N-methyl-N nitrosourea. The dynamic growth of tumor was measured by whole-body fluorescent imaging system. Morphological analysis was observed by hematoxylin–eosin staining and microscopic examination. The expression of Caspase 3 and E-Ca were detected by immunohistochemistry technique. Macrophages were separated by flow cytometry. The expression of cytokines was measured by qRT-PCR and western blot. Apoptosis ability was conducted by means of annexin V and propidium iodide. The abilities of invasion and migration were determined by transwell migration assay and scratch assay.ResultsPA-MSHA and PA-MSHA + Fisetin groups inhibited the growth of tumor and increased the ratio of M1/M2. For one thing, PA-MSHA suppressed the invasive ability of the bladder tumor cell and promoted bladder tumor cell apoptosis. For another, it facilitated the expression of M1 cytokines and reduced expression of M2 cytokines. Furthermore, treated with PA-MSHA, mouse M1 phagocytosis rates were higher than that of M2 macrophages for bladder cancer lines.ConclusionsThe data revealed that PA-MSHA might promote apoptosis and inhibit proliferation, invasion and migration of mouse bladder cancer cells by inducing M1 polarization.

Rapamycin-induced M2 macrophage autophagy promotes the migration and invasion of bladder cancer cells via increased IL-10 secretion

“…11 In addition, M2 macrophage polarization stimulated by BMP4 accelerated the progression of bladder cancer in vivo and in vitro, 12 whereas M1 macrophages inhibited proliferation and induced apoptosis of bladder cancer cells by increasing phagocytosis and M1-related cytokines. 13 The present study demonstrated that the presence of M2 macrophages was increased in bladder cancer tissues, and that rapamycin-induced M2 macrophage autophagy promoted the migration and invasion of bladder cancer cells. Conversely, the presence of M1 macrophages was decreased, and enhanced autophagy in these cells did not exhibit any notable effects on the bladder cancer.…”

Molecular Repolarisation of Tumour-Associated Macrophages

“…This treatment inhibited the proliferation and invasion of gastric cancer cells in vitro and demonstrated tumour growth inhibition in vivo [48]. Similarly, Liu and Duan reported that PA-MSHA increased M1 cell infiltration in a mouse model of bladder cancer and inhibited tumour growth [49]. Combination of PA-MSHA with EGF receptor antagonist gefitinib demonstrated a synergistic effect in a xenograft mouse model of NSCLC.…”

An HDAC9-associated immune-related signature predicts bladder cancer prognosis

“…However, the evaluation of specific immune cells through the CIBERSORT algorithm suggested that M0 and M2 macrophages and neutrophils were more enriched in the high-risk group, whereas CD8 T cells, activated memory CD4 T cells, follicular helper T cells, activated dendritic cells and plasma cells were more enriched in the low-risk group. M0 and M2 macrophages were positively correlated with a poor prognosis of BC [ 77 , 78 ], while a higher infiltration level of CD8 T cells was correlated with a good prognosis [ 79 , 80 ]. Therefore, the constructed risk score could appropriately assess immune cell infiltration, and it had an impact on immune cell infiltration.…”