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OBJECTIVE To investigate the neuroprotective effects of umbilical cord-derived mesenchymal stem cells (UC-MSCs) on radiation-induced brain injury (RIBI). METHODS Thirty female C57BL/6 mice were randomly divided into three groups control (CON), whole brain irradiation (WBI), and the cell therapy (MSC) group. Mice in the WBI and MSC groups received a single, whole brain irradiation treatment with 15 Gy of 60Co. Learning and memory were evaluated in the mice using the step-down avoidance test. The neuronal changes in the hippocampal cornu ammonis (CA) 1 region were observed using hematoxylin eosin (H&E) staining. The changes in astrocytes were visualized with glial fibrillary acidic protein immunohistochemistry, and the expression of TNF-α, IL-6, and IL-10 was detected by quantitative polymerase chain reaction (qPCR) along with Enzyme linked immunosorbent assay (ELISA). RESULTS Compared with mice in the WBI group, learning and memory in the MSC mice were significantly increased (P less then 0.05), neuronal degeneration and necrosis were significantly decreased (P less then 0.05), and the number of astrocytes was significantly increased (P less then 0.05). The levels of the in˙ammatory cytokines, TNF-α and IL-6, were significantly decreased (P less then 0.05), however, the inhibitory factor IL-10 was significantly increased (P less then 0.05). CONCLUSIONS UC-MSCs play a neuroprotective role by inhibiting brain cell injury and neuroinflammation. © 2020 by the Association of Clinical Scientists, Inc.OBJECTIVE Pancreatic ductal carcinoma has a 5-year survival rate of 9%. This makes it the 4th leading cause of cancer-related death in the United States. Advanced-stage diagnosis and limited treatment options contribute to poor prognosis. Thus, there is an urgent need for new approaches to treatment. Enhancer of Zeste 2 (EZH2), a catalytic subunit of the multi-protein histone methyltransferase, known as the polycomb repressive complex, has been implicated in carcinogenesis. E2H2's downregulation has been shown to have a therapeutic effect in B cell lymphomas. MATERIALS AND METHODS We examined the effect of EZH2 downregulation in combination with irradiation on the proliferation and apoptosis of pancreatic cancer cells (PANC-1 and MIA PaCa-2) in vitro. EZH2 downregulation was accomplished by treatment of cells with small interfering RNA (siRNA) or EPZ. To do this, cell survival was assessed over a 96 hr (short-term) by ATP measurement and immunohistochemical assessment of Phosphohistone 3 (PHH3), Ki-67 and CC3 over two weeks (long-term) by clonogenic assay. RESULTS EZH2 downregulation resulted in the decreased proliferation of PANC-1 and MIA PaCa-2 cells within short-term assays with maximal reduction at 72 hr. Irradiation reduced cell proliferation beginning at 96 hr and continued over the long-term. Irradiation with EZH2 downregulation reduced cell proliferation between 48 and 72 hr. This combined treatment reduced cell proliferation by 3 to 14% as compared to those treated with irradiation alone at two weeks. PANC-1 and MIA PaCa-2 cells exhibited similar responses to EZH2 downregulation and irradiation, but to different degrees. siRNA or EPZ were equally effective in EZH2 downregulation. CONCLUSIONS EZH2 downregulation in combination with irradiation reduces PANC-1 and MIA PaCa-2 cell proliferation more than irradiation alone. This study affirms the role of EZH2 downregulation for radiosensitization in pancreatic cancer treatment. © 2020 by the Association of Clinical Scientists, Inc.The microbiome has recently become a key interest for cancer research. Anti-tumor effects of reinforced clostridium media (RCM) were investigated for all ingredients of RCM, which showed that yeast extract could be a candidate for this phenomenon. MTT assay, cell counting, cell death analysis, cell cycle analysis, and Western blotting were done on colorectal cancer cells with or without 5-fluorouracil resistance (SNU-C5 and SNU-C5/5-FUR). Yeast extract treatment showed dose- and time-dependent anti-tumor effects on SNU-C5 and SNU-C5/5-FUR. Anti-tumor effects were related to G0/G1 phase arrest with increased p21, reactive oxygen species scavenger activities, and decreased free iron. Yeast extract treatment significantly increased apoptosis, which was effectively blocked with the PARP inhibitor. Anti-tumor effects of yeast extract were correlated with the increased phosphorylation of p38 and p53. These results suggest that yeast extract might inhibit the proliferation of colorectal cancer cells via the activation of the p38-p53-p21 cascade. © 2020 by the Association of Clinical Scientists, Inc.OBJECTIVE Calpain 6 (CAPN6) is one of the calcium-dependent intracellular nonlysosomal proteases that are dysregulated in uterine leiomyomas (UtLMs). However, its function and mechanism in UtLMs is still unknown. METHODS The correlation between CAPN6 expression and UtLMs was analyzed by the Gene Expression Omnibus (GEO). The expression of CAPN6 and Rac1 was detected by quantitative real-time PCR (qPCR) and western blot analysis. Cell proliferation ability was analyzed by a Cell Counting Kit-8 (CCK-8) assay. Cell apoptosis was detected by flow cytometry. RESULTS CAPN6 was overexpressed in UtLMs compared with uterine smooth muscle cells (UtSMCs). The downregulation of CAPN6 resulted in decreased cell proliferation and increased apoptosis of UtLMs. Furthermore, mechanical investigations revealed that these inhibitory effects were correlated with Rac1/PAK1 signaling pathways. Silencing the expression of CAPN6 resulted in decreased Rac1 and phospho-PAK1. On the other hand, upregulated Rac1 expression could reverse the reduced phosphorylation of PAK1 induced by CAPN6 silencing. CONCLUSIONS This data suggests that CAPN6 regulates UtLMs proliferation and apoptosis while being mediated through the Rac1/PAK1 signaling pathway. © 2020 by the Association of Clinical Scientists, Inc.FZD8, a G protein-coupled receptor protein belonging to the Frizzled family, is considered to play an important role in cancer invasion and metastasis. However, the function of FZD8 in the invasion and metastasis of gastric cancer (GC) has not been elucidated. In this study, we first confirm that FZD8 protein expression was significantly upregulated in gastric cancer tissue and has a potential to be an independent predictor of poor prognosis for patients with GC. In vivo and in vitro evidences were provided that support the idea of FZD8 being able to suppress GC cell invasion and metastasis. Further studies show that FZD8 promotes the markers expression related to invasion and metastasis. FZD8 exerts biological function through the β-catenin pathway which plays an important role in invasion and metastasis of gastric cancer cells. SNX-5422 mw Finally, FZD8 could activate the β-catenin pathway and its target gene's expression. In conclusion, our findings show that FZD8 promotes GC invasion and metastasis via the β-catenin pathway.
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