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.

Expression of Elf-1 and survivin in non-small cell lung cancer and their relationship to intratumoral microvessel density.

Abstract: BACKGROUND AND OBJECTIVE The expression of transcription factor Elf-1 and inhibitor of apoptosis survivin in non-small cell lung cancer (NSCLC) is correlated with the angiogenic factor vascular endothelial growth factor (VEGF), and are both factors affecting the cell cycle. This study investigated the expression of Elf-1, survivin, and intratumoral microvessel density (iMVD) assessed by monoclonal antibody CD105 in NSCLC, and explored their correlations with clinicopathologic features and angiogenesis of NSCLC. METHODS PowerVision(TM)-9000 immunohistochemistry was used to evaluate the expression of Elf-1, survivin, and CD105 in tissue microarrays containing 60 specimens of NSCLC and 9 specimens of normal tissue. Western blot analysis was used to evaluate the protein levels of Elf-1 and survivin in 17 specimens of NSCLC and 5 specimens of normal tissue. RESULTS Elf-1 and survivin were detected in 1 of the 9 normal tissues. The positive rates of Elf-1 and survivin in NSCLC were 70.0% and 65.0%, respectively. The expression levels of both Elf-1 and survivin were significantly related to tumor differentiation, lymphatic metastasis, clinical stage, and postoperative survival time (P < 0.05). Overexpression of both were related to poor prognosis: the survival rates were significantly lower in patients with positive expression than in those with negative expression (P < 0.01). Elf-1 expression was positively correlated with survivin expression (r = 0.769, P < 0.01). Elf-1 and survivin expressions were positively correlated with iMVD (r = 0.446, P < 0.01; r = 0.435, P < 0.01). CONCLUSIONS The expression of Elf-1 and survivin in NSCLC is related to differentiation, lymphatic metastasis, clinical stage, and prognosis, and both are positively correlated with iMVD. Detection their combined expression can help to predict the malignant behavior of NSCLC. Blocking the activity of Elf-1 and survivin may be a new way to inhibit angiogenesis in NSCLC.

Robo1 promotes angiogenesis in hepatocellular carcinoma through the Rho family of guanosine triphosphatases’ signaling pathway

Abstract: Robo1 is a member of the Robo immunoglobulin superfamily of proteins, and it plays an important role in angiogenesis and cancer. In this study, we investigate the role of roundabout 1 (Robo1) in tumor angiogenesis in hepatocellular carcinoma (HCC). Firstly, the relationship between Robo1 expression on tumors and patient’s survival and endothelial cells in tumor blood vessels and patient’s survival was studied. Secondly, Robo1 was overexpressed or knocked down in human umbilical vein endothelial cells (HUVECs). Cell proliferation, motility, and tube formation were compared in HUVEC with different Robo1 expression. Also, HUVECs with different Robo1 expression were mixed with HCCLM3 and HepG2 hepatoma cells and then implanted in a nude mouse model to examine the effects of Robo1 in endothelial cells on tumor growth and angiogenesis. Cell motility-related molecules were studied to investigate the potential mechanism how Robo1 promoted tumor angiogenesis in HCC. The disease-free survival of the patients with high Robo1 expression in tumoral endothelial cells was significantly shorter than that of those with low expression (P = 0.021). Overexpression of Robo1 in HUVECs resulted in increased proliferation, motility, and tube formation in vitro. In the implanted mixture of tumor cells and HUVECs with an increased Robo1 expression, tumor growth and microvessel density were enhanced compared with controls. Robo1 promoted cell division cycle 42 (Cdc42) expression in HUVECs, and a distorted actin cytoskeleton in HUVECs was observed when Robo1 expression was suppressed. In conclusion, Robo1 promoted angiogenesis in HCC mediated by Cdc42.

Actual long-term survival in HCC patients with portal vein tumor thrombus after liver resection: a nationwide study

Abstract: Liver resection for hepatocellular carcinoma (HCC) patients with portal vein tumor thrombus (PVTT) offers a chance of cure, although survival is often limited. The actual 3-year survival and its associated prognostic factors have not been reported. A nationwide database of HCC patients with PVTT who underwent liver resection with ‘curative’ intent was analyzed. The clinicopathologic characteristics, the perioperative, and survival outcomes for the actual long-term survivors were compared with the non-long-term survivors (patients who died within 3 years of surgery). Univariable and multivariable regression analyses were performed to identify predictive factors associated with long-term survival outcomes. The study included 1590 patients with an actuarial 3-year survival of 16.6%, while the actual 3-year survival rate was 11.7%. There were 171 patients who survived for at least 3 years after surgery and 1290 who died within 3 years of surgery. Multivariable regression analysis revealed that total bilirubin > 17.1 μmol/l, AFP > 400 ng/ml, types of hepatectomy, extent of PVTT, intraoperative blood loss > 400 ml, tumor diameter > 5 cm, tumor encapsulation, R0 resection, liver cirrhosis, adjuvant TACE, postoperative early recurrence (< 1 year), and recurrence treatments were independent prognostic factors associated with actual long-term survival. One in nine HCC patients with PVTT reached the long-term survival milestone of 3 years after resection. Major hepatectomy, controlling intraoperative blood loss, R0 resection, adjuvant TACE, and ‘curative’ treatment for initial recurrence should be considered for patients to achieve better long-term survival outcomes.

L-arginine administration ameliorates serum and pulmonary cytokine response after gut ischemia-reperfusion in immature rats.

Abstract: L-arginine administration ameliorates serum and pulmonary cytokine response after gut ischemia-reperfusion in immature rats

Licochalcone B Arrests Cell Cycle Progression and Induces Apoptosis in Human Breast Cancer MCF-7 Cells

Abstract: Background: Recent patent of licochalcone B (LCB) as an antiinflammatory agent has been developed. Emerging evidence shows that LCB may be a promising alternative compound with anti-cancer activities. However, the anticancer mechanism of LCB in MCF-7 cells has not been fully investigated. Objective: We aimed to unearth the anti-cancer effect and mechanism of LCB in MCF-7 cells. Method: Cell proliferation activity and cell-cycle progression were determined by sulforhodamine B assay and flow cytometry, respectively. The mRNA and protein levels of cell cycle-related proteins and apoptosis-associated proteins were examined by RT-qPCR and western blot, respectively. Mitochondrial membrane potential (MMP) was measured by flow cytometry after JC-1 staining. Results: We found that LCB inhibited MCF-7 cells proliferation in a concentration- and time-dependent manner. Moreover, LCB-treatment led to S phase arrest in MCF-7 cells, which could be elucidated by the decreased mRNA and protein levels of Cyclin A, Cdk2 and Cdc25 A, and the increased protein level of p21. LCB also induced such apoptosis morphology as phosphatidylserine externalization, chromatin condensation and DNA fragmentation. Moreover, LCB led to the loss of MMP, resulting in the release of cytochrome C. The above apoptotic events were supported by the fact that LCB upregulated the mRNA and protein levels of Caspase 3, Caspase 9 and Bax, and downregulated the mRNA and protein level of Bcl-2, which was triggered by the increased p53 protein level in LCB-treated MCF-7 cells. Conclusion: These findings suggested that LCB could be a promising agent for treatment of human breast cancer.