Comparative study of the cytotoxicity of the nanosized and microsized tellurium powders on HeLa cells

To compare the cytotoxicity on HeLa cells induced by nanosized and microsized tellurium powders, HeLa cells were exposed to different concentrations of tellurium powders (0, 50, 100, 150 and 200 μg/mL) for 12 h. In this study, detection of a series of biomarkers, including reactive oxygen species (ROS), glutathione (GSH), 8-hydroxy-2′-deoxyguanosine (8-OHdG), in addition to DNA and protein crosslink (DPC) and MTTassay, were conducted to evaluate the cytotoxicity. It is indicated that compared with the control group, there was no significant difference in the induced cytotoxicity at concentrations lower than 50 μg/mL for both nanosized and microsized tellurium powders. While there appears a significant difference in the induced cytotoxicity for nanosized tellurium powders when the concentration is higher than 100 μg/mL as well as for microsized tellurium powders when the concentration is higher than 200 μg/mL. Moreover, it is found that the cytotoxicity induced on HeLa cells exhibits a certain dose-effect relationship with the concentration of tellurium powders. A conclusion has been reached that the toxicity on HeLa cells can be induced by both nanosized and microsized tellurium powders, and the toxicity of the nanosized tellurium powders is significantly greater than the microsized one.     

CHIP facilitates ubiquitination of inducible nitric oxide synthase and promotes its proteasomal degradation

Inducible nitric oxide synthase (iNOS) is responsible for nitric oxide (NO) synthesis from l-arginine in response to inflammatory mediators. It is reported that iNOS is degraded mainly by the ubiquitin-proteasome pathway in RAW264.7 cells and human embryonic kidney (HEK) 293 cells. In this study, we showed that iNOS was ubiquitinated and degraded dependent on CHIP (COOH terminus of heat shock protein 70-interacting protein), a chaperone-dependent ubiquitin ligase. The results from overexpression and RNAi experiments demonstrated that CHIP decreased the protein level of iNOS, shortened the half-life of iNOS and attenuated the production of NO. Furthermore, CHIP promoted ubiquitination and proteasomal degradation of iNOS by associating with iNOS. These results suggest that CHIP plays an important role in regulation iNOS activity.     

纳米管和镉对蚕豆幼苗根系的毒害效应

以蚕豆幼苗为实验材料,采用水培法研究不同浓度(0、2、4、8、16 mg·L~(-1))羟基化多壁碳纳米管(MWCNTs-OH)与10μmol·L~(-1)镉(Cd)单一和联合作用对蚕豆幼苗根系生长、生理及Cd含量的影响。结果表明:(1)单一MWCNTs-OH处理下,随着MWCNTs-OH浓度(2～8 mg·L~(-1))的增加,蚕豆的根长度增加,且■产生速率增加的同时会伴随着SOD、POD活性升高。(2)单一Cd处理的幼苗根系MDA含量和■产生速率均高于对照,其中■产生速率较对照增加了1.98倍。(3)MWCNTs-OH联合处理诱导了蚕豆根■的产生和MDA含量增加,16 mg·L~(-1) MWCNTs-OH和Cd共同作用对蚕豆幼苗根的损伤最大,会促使部分根尖细胞受损脱落,Cd含量明显下降。研究发现,低浓度MWCNTs-OH可促进蚕豆的根生长,降低Cd的毒性;高浓度MWCNTs-OH(16 mg·L~(-1))和Cd对蚕豆幼苗根的致毒性表现为协同效应。     

Functional roles of PC‐PLC and Cdc20 in the cell cycle,proliferation, and apoptosis

Phosphatidylcholine‐specific phospholipase C (PC‐PLC) is the major enzyme in the Phosphatidylcholine (PC) cycle and is involved in many long‐term cellular responses such as activation, proliferation, and differentiation events. Cell division cycle 20 homolog (Cdc20) is an essential cell‐cycle regulator required for the completion of mitosis. Our previous studies identified the interaction between PC‐PLC and Cdc20. Through the interaction, Cdc20 could mediate the degradation of PC‐PLC by Cdc20‐mediated ubiquitin proteasome pathway (UPP). In this study, we found that PC‐PLC might not be involved in cancer metastasis. Inhibition of PC‐PLC by D609 could cause cell proliferation inhibition and apoptosis inhibition in CBRH‐7919 cells. Inhibition of PC‐PLC could also influence the cell cycle by arresting the cells in G1 phase, and Cdc20 might be involved in these processes. Taken together, in this report, we provided new evidence for the functional roles of PC‐PLC and Cdc20 in the cell cycle, proliferation, and apoptosis in CBRH‐7919 cells. Copyright © 2010 John Wiley & Sons, Ltd.     

醛固酮对心室成纤维细胞分泌内皮素的影响

用细胞培养、内皮素放射免疫测定和RT-PCR的方法,探讨醛固酮对心室成纤维细胞分泌内皮素的影响。结果显示,醛固酮(1×10     

Short exposure to paclitaxel induces multipolar spindle formation and aneuploidy through promotion of acentrosomal pole assembly

Paclitaxel is a widely used microtubule drug and cancer medicine. Here we report that by short exposure to paclitaxel at a low dose, multipolar spindles were induced in mitotic cells without centrosome amplification. Both TPX2 depletion and Aurora-A overexpression antagonized the multipolarity. Live cell imaging showed that some paclitaxel-treated cells accomplished multipolar cell division and a portion of the daughter cells went on to the next round of mitosis. The surviving cells grew into clones with varied genome content. The results indicated that an aneuploidy population could be induced by short exposure to paclitaxel at a low dose, implicating potential side effects of paclitaxel.     

Circular RNA circDVL1 inhibits clear cell renal cell carcinoma progression through the miR-412-3p/PCDH7 axis

Clear cell renal cell carcinoma (ccRCC) is a primary kidney cancer with high aggressive phenotype and extremely poor prognosis. Accumulating evidence suggests that circular RNAs (circRNAs) play pivotal roles in the occurrence and development of various human cancers. However, the expression, clinical significance and regulatory role of circRNAs in ccRCC remain largely unclear. Here we report that circDVL1 to be reduced in the serums and tissues from ccRCC patients, and to negatively correlate with ccRCC malignant features. Overexpression of circDVL1 inhibits proliferation, induces G1/S arrest, triggers apoptosis, and reduces migration and invasion in different ccRCC cells in vitro. Correspondingly, circDVL1 overexpression suppresses ccRCC tumorigenicity in a mouse xenograft model. Mechanistically, circDVL1 serves as a sponge for oncogenic miR-412-3p, thereby preventing miR-412-3p-mediated repression of its target protocadherin 7 (PCDH7) in ccRCC cells. Collectively, our results demonstrate that circDVL1 exerts tumor-suppressive function during ccRCC progression through circDVL1/miR-412-3p/PCDH7 axis, and suggest that circDVL1 could be a novel diagnostic and prognositc marker and therapeutic target for ccRCC.