Abstract:Abstract. Endostar, a modified recombinant human endostatin, inhibits the growth of a variety of tumors by suppressing neovascularization. Vascular endothelial growth factor (VEGF) has an important role in malignant ascites formation. In order to determine whether Endostar can suppress the formation of ascites and prolong survival times, mouse models of malignant ascites were established using S180 and H22 tumor cells. The experimental mice were randomly divided into four groups: The three treatment groups rec… Show more
“…When combined with cisplatin, Endostar showed enhanced anti-cancer effect in esophageal cancer and lung cancer (Xu et al, 2014;Fan et al, 2015). Furthermore, Endostar inhibits ascites formation and prolongs survival in malignant ascites mouse models (Wei et al, 2015) and acquired 45%~100% effective rates in MSE patients when Endostar was admmonistrated through intraperitoneal perfusion combined with platinum (Yan et al, 2012). However, the related studies are single center RCTs with small sample size, and among each study, the treatment programs were confused and had no reference standard and consistent observation index.…”
“…When combined with cisplatin, Endostar showed enhanced anti-cancer effect in esophageal cancer and lung cancer (Xu et al, 2014;Fan et al, 2015). Furthermore, Endostar inhibits ascites formation and prolongs survival in malignant ascites mouse models (Wei et al, 2015) and acquired 45%~100% effective rates in MSE patients when Endostar was admmonistrated through intraperitoneal perfusion combined with platinum (Yan et al, 2012). However, the related studies are single center RCTs with small sample size, and among each study, the treatment programs were confused and had no reference standard and consistent observation index.…”
“…Cells were then resuspended in saline at a concentration of 1 × 10 6 cells/mL. BALB/c mice received 0.2 mL of the cell suspension (5 × 10 5 cells per mouse) in the left peritoneal cavity, as previously described [ 45 , 46 ]. H22 tumor-bearing mice were randomly divided into five groups ( n = 16 per group): cyclophosphamide group, in which the mice were treated with cyclophosphamide (20 mg/kg), control group, in which the mice were given the same volume of physiological saline, and the PRP-treated groups, in which the mice were treated with 75, 150, or 300 mg/kg PRP.…”
Malignant ascites is a highly severe and intractable complication of advanced or recurrent malignant tumors that is often immunotherapy-resistant. Rhizoma Pleionis is widely used in traditional medicine as an antimicrobial and anticancer agent, but its effectiveness in treating malignant ascites is unclear. In the current study, we investigated the effect of polysaccharides isolated from Rhizoma Pleionis (PRP) on murine hepatocarcinoma H22 cells in an ascites model. We have found that the main components of PRP, that presented a relative molecular weight of 383.57 kDa, were mannose and glucose. We also found that PRP reduced the occurrence of abdominal ascites and increased survival in our mouse model. An immune response in the ascites tumor model was observed by performing a lymphocytes proliferation experiment and an E-rosette test. The ratios of CD8+ cytotoxic T cells and NK cells in the spleen were examined by flow cytometry, and the mRNA expression of Foxp3+in CD4+CD25+ (T regulatory Tregs) was measured by RT-PCR (reverse transcription-polymerase chain reaction). The levels of the cytokines TNF-α (tumor necrosis factor), VEGF (vascular endothelial growth factor), IL-2 (interleukin), and IFN-γ (interferon) in the serum and ascites supernatants were measured by ELISA. The expression of Foxp3 and Stat3 in peritoneal cells in the mouse model was measured by immunocytochemistry. The results indicated that PRP increased H22 tumor cell apoptosis in vivo by activating and enhancing the immune response. Furthermore, the effects of PRP on the proliferation of H22 cells were assessed by the CCK8 assay, Hoechest 33258, and TUNEL staining in vitro. We found that PRP suppressed the proliferation of H22 tumor cells but had no effect on BRL (Big rat liver) -3A rat hepatoma normal cells in vitro. Next, we investigated the underlying immunological mechanism by which PRP inhibits malignant ascites. PRP induced tumor cell apoptosis by inhibiting the Jak1–Stat3 pathway and by activating Caspase-3 and Caspase-8 to increase the Bax/Bcl-2 ratio. Collectively, our results indicate that PRP exhibits significant antitumor properties in H22 cells in vivo and in vitro, indicating that PRP may be used as a new therapeutic drug for cancer treatment.
“…The average progression-free survival (PFS) time for patients with MPE who received treatment with endostar in combination with cisplatin was 95 days, which was significantly longer than that of patients treated with cisplatin alone (PFS, 53 days; P=0.039) ( 57 ). Endostar has also been demonstrated to inhibit ascites formation and prolong survival in mouse models of malignant ascites established using S180 and H22 tumor cells ( 58 ). The tumor cells collected from the ascites in endostar-treated mice demonstrated a decrease in the expression of VEGF mRNA ( 58 ).…”
Section: Vegf-targeted Strategies For the Management Of Mpe In Patienmentioning
confidence: 99%
“…Endostar has also been demonstrated to inhibit ascites formation and prolong survival in mouse models of malignant ascites established using S180 and H22 tumor cells ( 58 ). The tumor cells collected from the ascites in endostar-treated mice demonstrated a decrease in the expression of VEGF mRNA ( 58 ). In addition, treatment of S180 and H22 tumor cells with endostar revealed a significant inhibition of VEGF protein secretion and VEGF mRNA expression, but no effect on cellular proliferation ( 58 ).…”
Section: Vegf-targeted Strategies For the Management Of Mpe In Patienmentioning
confidence: 99%
“…The tumor cells collected from the ascites in endostar-treated mice demonstrated a decrease in the expression of VEGF mRNA ( 58 ). In addition, treatment of S180 and H22 tumor cells with endostar revealed a significant inhibition of VEGF protein secretion and VEGF mRNA expression, but no effect on cellular proliferation ( 58 ). The inhibitory effects of recombinant human endostatin/endostar on tumor growth have also been reported in other cancer types, including ovarian cancer, malignant melanoma and colon cancer, and in liver transplantation-associated angiogenesis ( 59 ).…”
Section: Vegf-targeted Strategies For the Management Of Mpe In Patienmentioning
Malignant pleural effusion (MPE) is a severe medical condition, which can result in breathlessness, pain, cachexia and reduced physical activity. It can occur in almost all types of malignant tumors; however, lung cancer is the most common cause of MPE, accounting for ~1/3 of clinical cases. Although there are numerous therapeutic approaches currently available for the treatment of MPE, none are fully effective and the majority can only alleviate the symptoms of the patients. Vascular endothelial growth factor (VEGF) has now been recognized as one of the most important regulatory factors in tumor angiogenesis, which participates in the entire process of tumor growth through its function to stimulate tumor angiogenesis, activate host vascular endothelial cells and promote malignant proliferation. Novel drugs targeting VEGF, including endostar and bevacizumab, have been developed and approved for the treatment of various tumors. Data from recent clinical studies have demonstrated that drugs targeting VEGF are effective and safe for the clinical management of MPE. Therefore, VEGF-targeting represents a promising novel strategy for the diagnosis and treatment of MPE. The present review summarized recent advances in the role of VEGF in the pathogenesis, diagnosis and clinical management of MPE in patients with non-small cell lung cancer.
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