肺癌小鼠MDSC和T细胞变化

目的：探讨肺癌小鼠CD4＋T细胞、CD8＋T细胞和骨髓源性抑制细胞（ MDSC）的比例和数量变化。方法：采用LLC细胞皮下接种制备小鼠肺癌肿瘤模型,流式细胞仪检测肿瘤小鼠骨髓、脾脏、淋巴结内CD4＋T细胞、CD8＋T细胞和MDSC的数量变化。结果：与正常对照小鼠相比,肿瘤小鼠脾脏、淋巴结内CD4＋T细胞、CD8＋T细胞的比例和数量显著降低,骨髓CD4＋T细胞变化不明显,但CD8＋T细胞显著减少。 MDSC 在肿瘤小鼠骨髓、脾脏和淋巴结内的比例和数量则显著增加。结论：肺癌小鼠T细胞数量降低而MDSC细胞数量增加,诱导对肿瘤细胞的免疫耐受。     

表观遗传修饰和代谢重编程对乳腺癌干细胞的调控

概乳腺癌已居我国女性恶性肿瘤死亡率首位。近来研究表明,乳腺肿瘤组织内有少量具有自我更新和分化潜能的肿瘤干细胞,这些肿瘤干细胞在乳腺癌发生、发展、转移及复发过程中起关键作用。深入研究乳腺癌干细胞的调控机制对乳腺癌的预防和治疗具有十分重要意义。本文综合近期的研究成果,概括了表观遗传修饰和代谢重编程对上皮间质转化及乳腺癌干细胞的调控机制,且系统地分析与总结了表观遗传修饰、代谢重编程、上皮间质转化和乳腺癌干细胞之间的相互关系。     

Up-regulation of mitochondrial antioxidation signals in ovarian cancer cells with aggressive biologic behavior

Objective  

Recently, a high frequency of mutations in mitochondrial DNA (mtDNA) has been detected in ovarian cancer. To explore the alterations of proteins in mitochondria in ovarian cancer, a pair of human ovarian carcinoma cell lines (SKOV3/SKOV3.ip1) with different metastatic potentials was examined.     

Influence of CO2 pneumoperitoneum on intracellular pH and signal transduction in cancer cells

Object: The authors studied the influence of CO2 pneumoperitoneum on intracellular pH and signal transduction arising from cancer cell multiplication in laparoscopic tumor operation. Method: They set up a simulation of pneumoperitoneum under different CO2 pressure, and then measured the variation of intracellular pH (pHi) at different time and the activity of protein kinase C (PKC) and protein phosphatase 2a (PP2a) at the end of the pneumoperitoneum. After 1 week, the concentration of cancer cells in the culture medium was calculated. Result: When the pressure of CO2 pneumoperitoneum was 0, 10, 20, 30 mmHg respectively, the average pHi was 7.273, 7.075, 6.783, 6.693 at the end of the pneumoperitoneum; PKC activity was 159.4, 168.5, 178.0, 181.6 nmol/(g-min) and PP2a was 4158.3,4066.9, 3984.0, 3878.5 nmol/(g-min) respectively. After 1 week, the cancer cells concentration was 2.15×105, 2.03×105, 2.20×105, 2.18×105 L-1. Conclusion: CO2 pneumoperitoneum could promote acidosis in cancer cells, inducing the activation of protein kinase C and deactivation of protein phosphatase 2a, but it could not accelerate the mitosis rate of the cancer cells.     

Effect of siRNA-mediated knockdown of eIF3c gene on survival of colon cancer cells

Eukaryotic initiation factor subunit c(eIF3c) has been identified as an oncogene that is over-expressed in tumor cells and,therefore,is a potential therapeutic target for gene-based cancer treatment.This study was focused on investigating the effect of small interfering RNA(siRNA)-mediated eIF3c gene knockdown on colon cancer cell survival.The eIF3c gene was observed to be highly expressed in colon cancer cell models.The expression levels of the gene in eIF3c siRNA infected and control siRNA infected cells were compared via real-time polymerase chain reaction(PCR) and western blotting analysis.Cell proliferation levels were analyzed employing 3-(4,5-dimethylthiazol 2-yl)-2,5-diphenyltetrazolium bromide(MTT) and colony formation assays.Furthermore,the effects of eIF3c gene knockdown on the cell cycle and apoptosis were analyzed using flow cytometry.The results showed that suppression of eIF3c expression significantly(P<0.001) reduced cell proliferation and colony formation of RKO colon cancer cells.The cell cycle was arrested by decreasing the number of cells entering S phase.Further,apoptosis was induced as a result of eIF3c knockdown.Collectively,eIF3c deletion effectively reduced the survival of colon cancer cells and could be used as a therapeutic tool for colon cancer therapy.     

Down-regulation of eIF5A-2 prevents epithelial-mesenchymal transition in non-small-cell lung cancer cells

Background

Epithelial-mesenchymal transition (EMT) is believed to be the critical process in malignant tumor invasion and metastases, and has a great influence on improving the survival rate in non-small-cell lung cancer (NSCLC) patients. Recent studies suggested that eukaryotic initiation factor 5A-2 (eIF5A-2) might serve as an adverse prognostic marker of survival. We detected eIF5A-2 in NSCLC A549 cells, and found that the invasive capability correlates with the eIF5A-2 expression.

Methods

Transforming growth factor (TGF)-β1 was used to induce EMT in A549 cells. Western blotting, immunofluorescence, wound healing assay, and transwell-matrigel invasion chambers were used to identify phenotype changes. Western blotting was also used to observe changes of the expression of eIF5A-2. We down-regulated the eIF5A-2 expression using an eIF5A-2 siRNA and identified the phenotype changes by western blotting and immunofluorescence. We tested the change of migration and invasion capabilities of A549 cells by the wound healing assay and transwell-matrigel invasion chambers.

Results

After stimulating with TGF-β1, almost all A549 cells changed to the mesenchymal phenotype and acquired more migration and invasion capabilities. These cells also had higher eIF5A-2 protein expression. Down-regulation of eIF5A-2 expression with eIF5A-2 siRNA transfection could change the cells from mesenchymal to epithelial phenotype and decrease tumor cell migration and invasive capabilities significantly.

Conclusions

The expression of eIF5A-2 was up-regulated following EMT phenotype changes in A549 cells, which correlated with enhanced tumor invasion and metastatic capabilities. Furthermore, in the A549 cell line, the process of EMT phenotype change could be reversed by eIF5A-2 siRNA, with a consequent weakening of both invasive and metastatic capabilities.     

A novel anticancer property of Lycium barbarum polysaccharide in triggering ferroptosis of breast cancer cells

Journal of Zhejiang University-SCIENCE B - Breast cancer is one of the most malignant tumors and is associated with high mortality rates among women. Lycium barbarum polysaccharide (LBP) is an...     

Traditional Chinese medicines and their active ingredients sensitize cancer cells to TRAIL-induced apoptosis

The rapidly developing resistance of cancers to chemotherapy agents and the severe cytotoxicity of such agents to normal cells are major stumbling blocks in current cancer treatments.Most current chemotherapy agents have significant cytotoxicity,which leads to devastating adverse effects and results in a substandard quality of life,including increased daily morbidity and premature mortality.The death receptor of tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)can sidestep p53-dependent pathways to induce tumor cell apoptosis without damaging most normal cells.However,various cancer cells can develop resistance to TRAIL-induced apoptosis via different pathways.Therefore,it is critical to find an efficient TRAIL sensitizer to reverse the resistance of tumor cells to TRAIL,and to reinforce TRAIL’s ability to induce tumor cell apoptosis.In recent years,traditional Chinese medicines and their active ingredients have shown great potential to trigger apoptotic cell death in TRAIL-resistant cancer cell lines.This review aims to collate information about Chinese medicines that can effectively reverse the resistance of tumor cells to TRAIL and enhance TRAIL’s ability to induce apoptosis.We explore the therapeutic potential of TRAIL and provide new ideas for the development of TRAIL therapy and the generation of new anticancer drugs for human cancer treatment.This study involved an extensive review of studies obtained from literature searches of electronic databases such as Google Scholar and PubMed."TRAIL sensitize"and"Chinese medicine"were the search keywords.We then isolated newly published studies on the mechanisms of TRAIL-induced apoptosis.The name of each plant was validated using certified databases such as The Plant List.This study indicates that TRAIL can be combined with different Chinese medicine components through intrinsic or extrinsic pathways to promote cancer cell apoptosis.It also demonstrates that the active ingredients of traditional Chinese medicines enhance the sensitivity of cancer cells to TRAIL-mediated apoptosis.This provides useful information regarding traditional Chinese medicine treatment,the development of TRAIL-based therapies,and the treatment of cancer.     

Study on interleukin-18 gene transfer into human breast cancer cells to prevent tumorigenicity

INTRODUCTIONInterleukin-18(IL-18),originallydescribedasinterferon(IFN)-g-inducingfactor,isan18.3-kDaproinflammatorycytokineproducedbyactivatedmacrophagesanddendriticcells,andplaysanim-portantroleintheTh1response,primarilybasedonitsabilitytoinduceIFN-gproductioninTcellsandNKcells.IL-18inducesproliferationofactivatedTcells,secretionofseveralcytokines,andpartici-patesinbothinnateandacquiredimmunity.TheroleofIL-18inantitumorimmunitywassuggestedinmanystudies.Genetransferofcytokinesisani…     

Study on interleukin-18 gene transfer into human breast cancer cells to prevent tumorigenicity

To study the effect of interleukin-18 gene transfection on the tumorigenesis of breast cancer cell line Bacp37, human breast cancer cell line Bcap37 were transfected with Lipofectamine and selected by G418. The biological expression of rhIL-18 was tested by RT-PCR and ELISA method; nude mice were injected with Bcap37 cell with or without the hIL-18 gene. The hIL-18 cDNA was successfully integrated into Bcap37 cell; 126.3±4.5 pg hIL-18 secreted by one million transduced cells in 24 hours. Nude mice injected with IL-18 gene engineered Bcap37 cell had no tumor growth. These findings indicated that human breast cancer cells were successfully modified by the gene of IL-18 cytokine; the IL-18 gene engineered Bcap37 cells secreted hIL-18 and lost their tumorigenicity. The Bcap37 cells transduced with IL-18 gene may be used as breast cancer vaccine.     

Induced pluripotent stem cell-related genes influence biological behavior and 5-fluorouracil sensitivity of colorectal cancer cells

Objective  

We aimed to perform a preliminary study of the association between induced pluripotent stem cell (iPS)-related genes and biological behavior of human colorectal cancer (CRC) cells, and the potential for developing anti-cancer drugs targeting these genes.     

Anti-migratory effects of Piper betle leaf aqueous extract on cancer cells and its microtubule targeting properties

Journal of Zhejiang University-SCIENCE B - 本文研究了槟榔 (Piper betle, PB)...     

As2O3纳米粒的制备、表征和体外治疗人肝癌细胞的研究

研究了As2O3 纳米粒的制备方法、表征及其抗肝癌细胞的作用.采用溶胶凝胶法制备As2O3 纳米粒,并用透射电镜、能谱仪和图像分析仪等方法对其进行表征及特性检测.通过MTT法和流式细胞仪法研究了不同浓度As2O3 纳米粒对人肝癌细胞株的影响,并与传统的As2O3 溶液进行了比较.实验中制备了2种粒径大小的As2O3 纳米粒子,其平均直径分别为80nm和40nm,通过能谱仪的测试证实所制备的纳米粒为As2O3,且无其他成分.体外细胞实验发现,As2O3 纳米粒处理细胞48 h后,人肝癌细胞的存活率明显低于同浓度的As2O3 溶液处理组(P<0.05).研究结果显示,通过溶胶凝胶法可将As2O3 制备成纳米粒子;体外细胞实验表明,与传统的As2O3 溶液相比,As2O3纳米粒子可对肿瘤细胞产生更强细胞毒作用.     

Knockdown of OLA1, a regulator of oxidative stress response, inhibits motility and invasion of breast cancer cells

To explore the role of a novel Obg-like ATPase 1 (OLA1) in cancer metastasis, small interference RNA (siRNA) was used to knockdown the protein, and the cells were subjected to in vitro cell migration and invasion assays. Knockdown of OLA1 significantly inhibited cell migration and invasion in breast cancer cell line MDA-MB-231. The knockdown caused no changes in cell growth but affected ROS production. In wound-healing assays, decreased ROS in OLA1-knockdown cells were in situ asso-ciated with the cells' decreased motile morphology. Further, treatment of N-acetylcysteine, a general ROS scavenger, blunted the motility and invasiveness of MDA-MB-231 cells, similar to the effect of OLA1-knockdown. These results suggest that knock-down of OLA1 inhibits breast cancer cell migration and invasion through a mechanism that involves the modulation of intracel-lular ROS levels.     

Ursolic acid inhibits proliferation and induces apoptosis of HT-29 colon cancer cells by inhibiting the EGFR/MAPK pathway

rectal cancer.     

Green tea polyphenols induce cell death in breast cancer MCF-7 cells through induction of cell cycle arrest and mitochondrial-mediated apoptosis

In order to study the molecular mechanisms of green tea polyphenols (GTPs) in treatment or prevention of breast cancer, the cytotoxic effects of GTPs on five human cell lines (MCF-7, A549, Hela, PC3, and HepG2 cells) were determined and the antitumor mechanisms of GTPs in MCF-7 cells were analyzed. The results showed that GTPs exhibited a broad spectrum of inhibition against the detected cancer cell lines, particularly the MCF-7 cells. Studies on the mechanisms revealed that the main modes of cell death induced by GTPs were cell cycle arrest and mitochondrialmediated apoptosis. Flow cytometric analysis showed that GTPs mediated cell cycle arrest at both G1/M and G2/M transitions. GTP dose dependently led to apoptosis of MCF-7 cells via the mitochondrial pathways, as evidenced by induction of chromatin condensation, reduction of mitochondrial membrane potential (ΔΨm), improvement in the generation of reactive oxygen species (ROS), induction of DNA fragmentation, and activations of caspase-3 and caspase-9 in the present paper.     

NEDD8-conjugating enzyme E2 UBE2F confers radiation resistance by protecting lung cancer cells from apoptosis

Journal of Zhejiang University-SCIENCE B -...