An in vitro study to explore the role of prolylcarboxypeptidase in non-small cell lung cancer

Prolylcarboxypeptidase (PRCP) belongs to the S28 family of proteases, which is also a dipeptidyl peptidase.In this study, we demonstrate the expression pattern of PRCP in Non-small cell lung cancer (NSCLC). We found thatthe repression of PRCP expression by small interfering RNA successfully inhibited cell proliferation, migration, andinvasion. Further, we explored the involvement of PRCP in the regulation of epithelial-mesenchymal transition (EMT).The epithelial marker E-cadherin was significantly increased, meanwhile mesenchymal markers MUC1, vimentin, andSNAIL were markedly decreased in PRCP knockdown cells. Moreover, the downregulation of PRCP in the NSCLCcells induced the expression of apoptosis-related proteins in vitro. We performed RT-PCR in 30 pairs of clinical NSCLCtissues and adjacent non-cancerous tissues, which revealed significantly higher PRCP expression levels in cancer tissuesthan in adjacent non-cancerous tissues. Collectively the results from our study suggest a possible cancer promotion roleof PRCP in NSCLC.     

3-<i>epi</i>-bufotalin suppresses the proliferation in colorectal cancer cells through the inhibition of the JAK1/STAT3 signaling pathway

Traditional Chinese medicine (TCM) has been increasingly employed in the last decades in China for both preventing and treating a variety of cancers. 3-epi-bufotalin is an active ingredient of TCM “Chanpi” with anti-tumor potential. However, the effect and mechanism of 3-epi-bufotalin on colorectal cancers were not well disclosed. The present study demonstrated that 3-epi-bufotalin could reduce viability, trigger apoptosis, and block the cell cycle at the G₂/M stage in colorectal cancer cell lines HT29, RKO, and COLO205 in vitro. Moreover, 3-epi-bufotalin inhibited the JAK1/STAT3 signaling pathway. These results indicated the anti-proliferation ability of 3-epi-bufotalin in colorectal cancer cells.     

流式细胞仪检测甘草多糖对小鼠S-180肉瘤的凋亡诱导作用

随着单克隆抗体及标记技术的发展,流式细胞术(FlowCytometry,FCM)检测细胞凋亡技术已广为使用,为探讨中药甘草多糖抑瘤作用及其机制,本文应用流式细胞术(FCM)检测细胞凋亡,结果表明甘草多糖抑制肿瘤生长可能与诱导细胞凋亡有关。     

Application of confocal scanning laser microscopy in experimental pathology

Confocal scanning laser microscopy (CSLM) represents an exciting new tool for scientific disciplines which focus on mechanistic studies such as experimental pathology. Enhanced resolution in the specimen plane and rejection of out-of-focus fluorescence flare allow analysis of specific nucleic acid sequences, enzymes, structural macromolecules, and cellular homeostasis utilizing fluorescent probes. Four different experimental applications are discussed which utilize CSLM to evaluate pathological processes at the subcellular, cellular, and tissue levels. Programmed cell death, or apoptosis, is a natural process of significance both during development and as a response to toxic stimuli. CSLM-imaging of nuclei of human B lymphoblastoid cells following exposure to a monofunctional alkylating agent suggests that the degradation of chromatin characteristic of apoptosis may occur in asymmetric patterns. Surfactant apoprotein-A is the major non-serum protein component of pulmonary surfactant and is essential for the extracellular function of surfactant. CSLM of alveolar type II cells suggests that apoprotein-A is present in both the cytoplasm, predominantly in lamellar bodies, and in the nucleus. The tumor promoter, phorbol myristate acetate, rapidly stimulated the formation of vacuoles in human neutrophils. CSLM using Lucifer Yellow as a probe suggests that cylindrical vacuoles are formed by fluid-phase pinocytosis. The blood-nerve barrier (BNB) in peripheral nerves may be an important target during toxin-induced neuropathies. Ricin-induced permeability of the BNB in the rat was rapidly visualized by CSLM as leakage of fluorescein isothiocynate (FITC)-dextran into the endoneurial compartment.     

Polyphenol-rich seaweed (Eucheuma cottonii) extract suppresses breast tumour via hormone modulation and apoptosis induction

The edible red seaweed Eucheuma cottonii is abundantly cultivated for carrageenan production. This study investigated the effects of dietary E. cottonii polyphenol-rich extract (ECME) on breast cancer. In vitro assays showed that ECME was antiproliferative against oestrogen-dependent MCF-7 and oestrogen-independent MB-MDA-231 human breast-cancer cells (IC₅₀ values of 20 and 42 μg/ml, respectively) but was non-toxic to normal cell lines. The ECME (150 and 300 mg/kg BW) was fed to female rats and, after 4 weeks, rat mammary tumour was induced using LA7 cells (inoculated subcutaneously). The ECME inhibited tumour development and erythrocyte lipid peroxidation in the cancer-induced rats, dose-dependently. It showed anti-oestrogenic effects on the rat estrous cycle and serum hormone levels. Electron microscopy and histopathology observations confirmed apoptosis in the rat mammary tumours. The polyphenol-rich ECME was tumour-suppressive via apoptosis induction, downregulating the endogenous oestrogen biosynthesis, and improving antioxidative status in the rats.     

姬松茸多糖对糖尿病大鼠脑组织保护作用及其机制

目的:探讨姬松茸多糖对糖尿病大鼠脑组织保护作用及其作用机制。方法:将Wistar大鼠随机分为5组,A:正常对照组;B:模型组;C:2%姬松茸多糖组;D:4%姬松茸多糖组;E:8%姬松茸多糖组。8周后,HE染色观察脑组织病理变化,琼脂糖凝胶电泳检测细胞凋亡,RT-PCR观察p53基因的表达。结果:与模型组相比,姬松茸多糖治疗组脑组织形态明显改善,脑组织细胞凋亡量明显减少,p53基因的表达明显减少。结论:姬松茸多糖对糖尿病大鼠脑组织有明显保护作用,其机制可能与抑制细胞凋亡及p53基因的表达有关。     

The potential of sphingomyelin as a chemopreventive agent in AOM-induced colon cancer model: wild-type and p53+/- mice

A protective effect of sphingolipids on colorectal cancer (CRC) has been reported in certain mouse strains. It is unknown if sphingolipids are protective in a p53 deficiency mouse model of CRC. This study investigated the effect of sphingomyelin (SM) on intestinal sphingomyelinase (SMase) activity, colonic epithelial biology and azoxymethane (AOM)-induced CRC. Groups of wild-type (C57BL/6J) and p53+/- mice were fed 0.1% SM diet for 4 wk, administered a single AOM injection and then killed 6 h later to measure apoptosis and proliferation. Separately, both mouse types were fed 0.05% SM diet, administered three AOM injections and killed 33-38 wk later to measure tumour formation. SM significantly increased SMase activity and reduced proliferation (p < 0.05) in wild-type and p53+/- mice. SM did not regulate baseline apoptosis, apoptotic response to AOM or apoptosis in tumours, nor did it restore defective apoptosis in p53+/- mice. There was a nonsignificant trend to reduced tumour incidence with SM in wild-type (p = 0.15) and p53+/- (p = 0.12) mice. In conclusion, while increasing intestinal SMase activity and suppressing proliferation, SM did not promote any form of apoptosis and failed to achieve significant protection in these mice. Further investigation to understand the variable effect of SM in preventing CRC is warranted.