Binzhou Medical College

About: Binzhou Medical College is a education organization based out in Yantai, China. It is known for research contribution in the topics: Apoptosis & Cancer. The organization has 959 authors who have published 619 publications receiving 7642 citations.

Gelsolin Promotes Radioresistance in Non-Small Cell Lung Cancer Cells Through Activation of Phosphoinositide 3-Kinase/Akt Signaling

Abstract: Gelsolin is an actin-binding protein and acts as an important regulator of cell survival. This study aimed to determine the function of gelsolin in the radioresistance of non-small cell lung cancer cells. We examined the expression of gelsolin in radioresistant A549 and H460 cells and their parental cells. The effects of gelsolin overexpression and knockdown on the clonogenic survival and apoptosis of non-small cell lung cancer cells after irradiation were studied. The involvement of phosphoinositide 3-kinase/Akt signaling in the action of gelsolin was checked. We found that gelsolin was significantly upregulated in radioresistant A549 and H460 cells. Overexpression of gelsolin significantly ( P < .05) increased the number of colonies from irradiated A549 and H460 cells compared to transfection of empty vector. In contrast, knockdown of gelsolin significantly ( P < .05) suppressed colony formation after irradiation. Gelsolin-overexpressing cells displayed reduced apoptosis in response to irradiation, which was coupled with decreased levels of cleaved caspase-3 and poly adenosine diphosphate-ribose polymerase. Ectopic expression of gelsolin significantly ( P < .05) enhanced the phosphorylation of Akt compared to nontransfected cells. Pretreatment with the phosphoinositide 3-kinase inhibitor LY294002 (20 μmol/L) significantly decreased clonogenic survival and enhanced apoptosis in gelsolin-overexpressing A549 and H460 cells after irradiation. Taken together, gelsolin upregulation promotes radioresistance in non-small cell lung cancer cells, at least partially, through activation of phosphoinositide 3-kinase/Akt signaling.

Clinicopathological features and survival of early stage breast cancer in northwest China: A population-based retrospective study of 1287 patients.

Abstract: Background Breast cancer (BC) displays different clinicopathological features and outcomes based on patient age, molecular subtype, and treatment. However, such features in BC patients in northwest China are unclear. This study investigated the clinicopathological features and overall survival (OS) of early stage BC patients using a population-based study. Methods Patients who were newly diagnosed with BC at the First Affiliated Hospital of Xi'an Jiaotong University between January 2001 and June 2012 were included. Clinicopathological features and OS were assessed. Results The median age of 1287 patients was 50 years, with an average tumor size of 2.65 cm. Additionally, 42.7% were luminal A, 25.6% luminal B, 9.3% Her2 overexpression, and 17.7% triple negative. The cut-off age was 35 years, and young patients (< 35) tended to have larger tumors, ≥ 4 positive lymph nodes, grade 2 or 3 histology, non-luminal types, high Ki67, and poor outcomes. Patients with luminal A tumors showed moderate features: 50.6% had tumors < 2 cm, 56.7% had negative lymph nodes. Patients with Her2 overexpression tumors showed aggressive features and the poorest survival (5-year OS 67.6%). Patients with triple negative tumors were the youngest (average 48.4 years), but had the largest proportion of grade 3 histology and poor outcomes. Conclusion Our results are consistent with those in other provinces in China, but showed an earlier age at diagnosis and more aggressive pathological features compared to developed countries. Additionally, each molecular subtype showed specific features and different survival outcomes.

PAR-2 promotes cell proliferation, migration, and invasion through activating PI3K/AKT signaling pathway in oral squamous cell carcinoma.

Abstract: Objective: This research aimed to explore the function of PAR-2 in oral squamous cell carcinoma (OSCC) development and progression, as well as underlying molecular mechanism. Methods: Tissue samples were collected from 115 OSCC patients. Quantitative real time polymerase chain reaction (qRT-PCR) was performed to measure the expression of PAR-2 mRNA in OSCC tissues and cells. MTT and Transwell assays were used to detect the proliferation, migration and invasion of OSCC cells, respectively. Western blot was performed to determine protein expression. Results: The expression of PAR-2 mRNA was up-regulated in OSCC tissue and cells ( P <0.01), and its mRNA level was obviously correlated to tumor differentiation and TNM stage in OSCC ( P <0.05 for both). The activation of PAR-2 with PAR-2AP ( PAR-2 agonist) significantly promoted the proliferation, migration and invasion of OSCC cells, while its knockout could inhibit malignant behaviors of OSCC cells ( P <0.05). Excessive activation of PAR-2 enhanced phosphorylation level of PI3K, AKT and mTOR, revealing the activation of PI3K/AKT pathway. Moreover, LY294002, the inhibitor of PI3K/AKT pathway, could reverse oncogenic action caused by PAR-2 activation. Conclusion: PAR-2 can promote OSCC growth and progression via activating PI3K/AKT signaling pathway.

Effects of PDTC on NF-κB expression and apoptosis in rats with severe acute pancreatitis-associated lung injury.

Abstract: We investigated the effects of pyrrolidine dithiocarbamate (PDTC) on intrapulmonary expression of nuclear factor-κB (NF-κB), and apoptosis in rats with severe acute pancreatitis (SAP). We induced SAP, then used immunohistochemistry, TUNEL staining, quantitative PCR assays and western blotting to examine PDTC effects. Treatment with PDTC resulted in interstitial edema and widening of the basement membrane, with swollen mitochondria and aggregation of nuclear chromatin. Expression of NF-κB, Fas, Bcl-2 and TNF-α in lung tissues of SAP rats was increased, with NF-κB, Fas and TNF-α levels maximal after 6 h. PDTC appeared to ameliorate pathological changes, with low levels of NF-κB, Fas, TNF-α, and Caspase-3 mRNA observed and a lower apoptosis index compared with that seen in SAP rats. Expression of NF-κB could be involved in lung tissue apoptosis during SAP. We postulate that PDTC inhibits the activation of NF-κB and apoptosis, effectively alleviating the severity of lung injury.

Protective effects of Danshensu on liver injury induced by omethoate in rats

Abstract: This study was to evaluate the protective effects of Danshensu on liver injury induced by omethoate in Sprague Dawley rats. The acute omethoate poisoning model was established by administrating subcutaneously with omethoate at a single dose of 60 mg/kg. Danshensu treatment markedly inhibited the increases of aspartate aminotransferase, alanine aminotransferase, cyclooxygenase-2, tumor necrosis factor-alpha, thromboxane B(2), and thromboxane B(2)/6-keto-PGF1alpha ratio induced by omethoate. The histopathological examination further confirmed that administration with Denshensu ameliorated liver injury. The results demonstrated that Danshensu possesses protective action on hepatic injury induced by omethoate and the pharmacological mechanism was related to the anti-inflammatory effect and circulation improvement of Danshensu, at least in part.