Overexpression of p42.3 promotes cell proliferation, migration, and invasion in human gastric cancer cells.

As a newly discovered tumor-specific gene, p42.3 is overexpressed in most of human gastric cancers (GC). However, the role of p42.3 in GC progression remains unclear. To assess the role of p42.3 in gastric cancers, immunohistochemistry and western blot were performed to detect the p42.3 expression in human GC tissues and cells. We also investigated the role of p42.3 in GC cell proliferation, migration, and invasion. Our results showed that the p42.3 expression was increased dramatically in human GC tissue and cells. In addition, we found that overexpression of p42.3 promotes GC cell proliferation, migration, and invasion abilities. Furthermore, p42.3 expression suppressed the E-cadherin protein level and promoted the ß-catenin and p-ERK protein level. Taken together, overexpressed p42.3 is correlated with gastric cancer cell proliferation, migration, and invasion, suggesting its use as a biological marker in gastric cancer.

p21-Activated kinase 5 affects cisplatin-induced apoptosis and proliferation in hepatocellular carcinoma cells.

p21-Activated kinase 5 (PAK5) is the last identified member of the PAK family. The PAKs are highly conserved serine/threonine and effector proteins for Cdc42 and Rac and are essential in regulating cell motility and survival. Previous studies have demonstrated that PAK5 played a pivotal role in apoptosis, proliferation, cancer migration, and invasion. However, the biological function of PAK5 in hepatocellular carcinoma, as well as its underlying mechanism, still remains to be fully elucidated. In the present study, we demonstrated that PAK5 markedly inhibited cisplatin-induced apoptosis and promoted cell proliferation in hepatocellular carcinoma cells. Moreover, our results showed that overexpression of PAK5 contributed to cell cycle regulation. In order to elucidate the underlying mechanism of PAK5 on cisplatin-induced apoptosis and cell cycle regulation, we also examined the protein expressions of chk2 and p-chk2. In summary, our study investigated the role of PAK5 in cisplatin-induced cellular processes and provided evidence of its underlying mechanism.

[Seasonal Distribution Characteristics and Health Risk Assessment of Heavy Metals in Surface Water of Qingjiang River].

In order to assess the health risks of heavy metals in surface water of Qingjiang River, surface water samples were taken at designed cross-sections of the river and analyzed for Cr, Cu, Zn, Pb, Cd, As, and Mn. Health risks from these heavy metals for adults and children in wet and dry seasons were compared by water environmental health risk assessment model of the USEPA. It found that the main excessive element is Mn, concentrating in the Danshui, Yantouxi, and Pingluoxi, the slightly excessive element is As, the concentration of Mn was above national standard, and it mainly distributed in Danshui, Yantouxi, and Pingluoxi, As was slightiy over the standard, and it concentrated in Wujiahe, The content of heavy metals during wet season were all higher than those during dry season. Cr, Cu, Zn, and Cd are mainly originated from the nature, Pb and As are separately mainly originated from traffic and agriculture, Mn originated from mining mainly in the downstream, while it has natural source from upper to middle. The health risks of heavy metals in surface water to adults and children in wet season are higher than those in dry season. The main health risk area was the midstream. As was the highest health risk element and children were the most preventive group. Specially, people in towns who drink the water from midstream should pay more attention.

p42.3: An abductor of cell cycle.

As a newly discovered tumor-associated gene, p42.3 was originally ascertained in gastric cancer cell line BGC823 and has been confirmed as a cell cycle-dependent gene that is overexpressed in many human tumor cell lines and embryonic tissues. p42.3 can regulate the level of relevant cycle-dependent proteins and promote malignant transformation of cells. A variety of cellular functions, including cell proliferation, cell invasion and cell migration, are under control of p42.3. Our review, namely the introduction of the structure of p42.3, underlying activity regulation mechanisms of p42.3 as well as the role p42.3 plays in malignant cellular transformation process, are accompanied by the presentation of potential directions of further researches of cancer prevention and therapy in which p42.3 is inevitable.

p42.3 promotes cell proliferation and invasion in human Renal-Cell Carcinoma.

p42.3 is a tumor-specific gene and found to be over-expressed in many tumor cell lines and primary tumor tissues. It plays a significant role in neoplastic transformation and tumor progression. To date, the association between p42.3 and Renal-Cell Carcinoma (RCC) has not been reported. This study investigated the biological effects and mechanisms of p42.3 in RCC progression. In this study, we found that p42.3 is overexpressed in various kinds of RCC cells, and knockdown of p42.3 dramatically reduced cell proliferation and invasion in vitro. Our studies revealed that overexpression of p42.3 accelerates the epithelial-mesenchymal transition (EMT) progression and induces RCC cells proliferation and invasion. Further studies show that p42.3 may involve in activation of ß-catenin and participate in RCC cell invasion. Combined, these data indicate that p42.3 contributes to promoting RCC cells proliferation and invasion through accelerates the EMT progression and ß-catenin activation.