[Clinical efficacy and mechanism of total glucosides from white paeony for radioactive liver damage].

To discuss the effects of total glucosides from white paeony on preventing and treating radioactive liver damage, and explore its possible mechanisms. Thirty-six patients with primary hepatic carcinoma from 105th Hospital of Chinese PLA were treated with 3-dimensional conformal radiotherapy and randomly divided into simple irradiation group, total glucosides from white paeony group, and control group. The levels of AST, ALT, HA, LN, PCⅢ, CIV and TGF-ß1 in serum of various groups were determined by using ELISA method. As compared with the simple irradiation group and control group, total glucosides from white paeony could obviously decrease the levels of AST, ALT, HA, LN, PCⅢ, CIV and TGF-ß1(P<0.05, P<0.01). The results showed that the total glucosides from white paeony could effectively prevent and treat radioactive liver damage, and its mechanism might be associated with decreasing the levels of TGF-ß1, and inhibiting the synthesis of collagen synthesis.

USP18 contributes to the proliferation and migration of ovarian cancer cells by regulating the AKT/mTOR signaling pathway.

Ubiquitin-specific peptidase (USP)18 is elevated in tumor tissues and is associated with tumor malignancy. USP18 functions as an oncogene in different cancers. However, the role of USP18 in ovarian cancer was poorly understood. TCGA database showed that USP18 was elevated in ovarian cancer tissues. Additionally, USP18 mRNA and protein expression was also up-regulated in tumor tissues. The functional assays were then designed via siRNA-mediated knockdown of USP18. The results showed that knockdown of USP18 reduced cell viability and ovarian cancer proliferation. Furthermore, cell apoptosis was promoted by USP18 silencing, and interference of USP18 suppressed cell migration and invasion. The expression of phosphorylated AKT (p-AKT) and p-mTOR protein was decreased in ovarian cancer cells by USP18 knockdown. Inhibition of AKT attenuated the decrease in cell apoptosis induced by USP18 overexpression and increased cell viability and migration. In conclusion, USP18 promoted the proliferation and migration of ovarian cancer cells by activating AKT/mTOR signaling.

Paeoniflorin exerts protective effect on radiation-induced hepatic fibrosis in rats via TGF-ß1/Smads signaling pathway.

AIM: This study aimed to investigate the protective effects of paeoniflorin (PAE) on radiation-induced hepatic fibrosis in a rat model. METHODS: Fifty healthy male Sprague-Dawley rats were randomly assigned to normal control group, hepatic fibrosis group, and PAE treatment groups. X-ray exposure was employed to establish radiation-induced hepatic fibrosis model. PAE was administered once daily, and rats were sacrificed at week 26 after irradiation. The liver histopathology was evaluated under a light microscope after HE staining and Masson staining. Meanwhile, the protein expression of transforming growth factor-beta 1 (TGF-ß1), Smad3/4 and Smad7 was detected by immunohistochemistry. RESULTS: Radiation-induced liver damage and collagen deposition were observed in the model group as compared to normal control group, but PAE treatment significantly attenuated the liver injury and reduce collagen deposition (P<0.05 or 0.01). The hepatic hydroxyproline content and serum levels of TGF-ß1, hyaluronic acid, ro-collagen type III and laminin markedly increased in model group as compared to control group (P<0.01), but they decreased dramatically after PAE treatment. The expression of TGF-ß1, Smad3/4 and Smad7 in the liver increased significantly in model group as compared to control group (P<0.01), and PAE could down-regulate the expression of Smad3/4 and up-regulate Smad7 expression (P<0.05 or 0.01). The activities of serum amino-transferase and aspartate aminotransferase were significantly higher in hepatic fibrosis group than in normal control group, but PAE treatment markedly reduced them (P<0.05). CONCLUSION: PAE can inhibit the radiation induced hepatic fibrosis via regulating TGF-ß1/Smads signaling pathway.

Iris metastasis from esophageal squamous cell carcinoma: A case report.

Carcinoma metastatic to the eye is a rare condition, typically associated with a poor prognosis. Breast and lung cancers are the most common sources of intraocular metastases, and the majority of metastatic lesions involve the posterior uvea, with <8% of reported cases arising in the iris. Intraocular metastasis as the presenting form of esophageal carcinoma is highly uncommon. In the present report, a rare case of metastatic iris tumor resulting from esophageal squamous cell carcinoma is discussed. A 64-year-old patient presented with a progressively distending pain in the right eye, with associated blurred vision. Local and systemic evaluation was performed, followed by treatment. Multiple examinations identified a neoplasm in the right iris and postoperative pathology revealed that the iris lesion was a metastasis of esophageal squamous cell cancer origin. The patient was treated with adjuvant radiation. To the best of our knowledge, this was only the second reported case of esophageal squamous cell carcinoma metastasizing to the iris.

Activation of STAT3 in human gastric cancer cells via interleukin (IL)-6-type cytokine signaling correlates with clinical implications.

BACKGROUND: The signal transducers and activators of transcription 3 (STAT3) signaling pathway plays important roles in oncogenesis, angiogenesis, immunity, and tumor cell invasion. In the present study, we investigated the association of interleukin (IL)-6/STAT3 signaling pathway with T lymphocytes and clinical implication in patients with gastric cancer. METHODS: Seventy one patients who underwent gastrectomy due to gastric adenocarcinoma were studied. Blood samples were collected before and after surgical gastrectomy to quantify the levels of IL-6, IL-10 and VEGF using an enzyme-linked immunosorbent assay, as well as T lymphocyte subsets (CD3(+), CD4(+), CD8(+), CD4(+)/CD8(+)) and natural killer (NK) cells by a flow cytometry. Furthermore, the expression of IL-6, survivin, STAT3, STAT3 phosphorylation (p-STAT3), and VEGF were determined in human gastric cancer and adjacent normal mucosa through Western blot and immunohistochemistry. RESULTS: Postoperative levels of IL-6, IL-10 and VEGF in serum were significantly lower than preoperative levels. Percentages of T-cell subsets and NK cells in blood were significantly increased after postoperative-week 1 as compared to preoperative group, which was further augmented at 1 month after gastrectomy. In addition, the expression of IL-6, survivin, STAT3, p-STAT3, and VEGF were increased in human gastric cancer tissues as compared to adjacent normal mucosa. Their expression was associated with TNM stage of gastric cancer. The level of STAT3 activation in clinical samples was correlated with IL-6 expression. All gastric tumor samples, which expressed p-STAT3, also expressed IL-6 with weak expression detected in adjacent normal mucosa. CONCLUSION: Increased IL-6-induced activation of STAT3 was observed in neoplastic gastric tissue, which positively correlated with tumor progression. Moreover, IL-6 and STAT3 downstream signals such as IL-10 and VEGF were reduced in patients after removal of gastric cancer as compared to pre-operation. Therefore, inhibition of the IL-6/STAT3 signaling pathway may provide a new therapeutic strategy against gastric cancer.