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Wang Y.,Shandong University | Zhang P.,Shandong University | Liu Z.,The Fifth Peoples Hospital | Wang Q.,Shandong University | And 4 more authors.
Molecular Cancer | Year: 2015

Background: CUL4A has been proposed as oncogene in several types of human cancer, but its clinical significance and functional role in human non-small cell lung cancer (NSCLC) remain unclear. Methods: Expression level of CUL4A was examined by RT-PCR and Western blot. Forced expression of CUL4A was mediated by retroviruses, and CUL4A silencing by shRNAs expressing lentiviruses. Growth capacity of lung cancer cells was measured by MTT in vitro and tumorigenesis in vivo, respectively. Results: We found that CUL4A was highly expressed in human lung cancer tissues and lung cancer cell lines, and this elevated expression positively correlated with disease progression and prognosis. Overexpression of CUL4A in human lung cancer cell lines increased cell proliferation, inhibited apoptosis, and subsequently conferred resistance to chemotherapy. On other hand, silencing CUL4A expression in NSCLC cells reduced proliferation, promoted apoptosis and resulted in tumor growth inhibition in cancer xenograft model. Mechanistically, we revealed CUL4A regulated EGFR transcriptional expression and activation, and subsequently activated AKT. Targeted inhibition of EGFR activity blocked these CUL4A induced oncogenic activities. Conclusions: Our results highlight the significance of CUL4A in NSCLC and suggest that CUL4A could be a promising therapy target and a potential biomarker for prognosis and EGFR target therapy in NSCLC patients. © 2014 Wang et al.; licensee BioMed Central Ltd. Source


Zhang M.-X.,Renmin University of China | Xu X.-M.,Renmin University of China | Zhang P.,Hubei University | Han N.-N.,Renmin University of China | And 5 more authors.
Tumor Biology | Year: 2015

To investigate the expression level of NEK2 in 40 tissue specimens of primary liver cancer and to search for clues whether the effect of NEK2 depletion plays a role on biological behaviors of HepG2 cells and the relevant molecular mechanism are the objectives of this study. Real-time PCR and immunohistochemistry assessed expression level of NEK2 in specimens of cancerous tissues and carcinoma-adjacent tissues. The NEK2 expression level in HepG2, Huh7, SMMC, and 7402 cells was detected by real-time PCR and western blot to screen experimental cell line. To assess the expression levels of NEK2 mRNA and protein, an effective siRNA transfected into the HepG2 cells was designed. CCK8 and colony-forming assays were performed to verify short-term and long-term proliferative activities, respectively. Capacity of apoptosis and cell cycle changes were assessed by flow cytometry. Ability of transference and invasion was measured by Transwell Chambers. Western blot approach was used to determine the protein expression levels. There was significantly high expression level of NEK2 in cancerous tissues compared to adjacent tissues. The expression of NEK2 was higher in HepG2 cells than other cell lines. Real-time PCR and western blot shown there were obviously down-regulated NEK2 expression in the NEK2-siRNA group compared to control groups. The capacity of amplification and invasion was inhibited distinctly, and FCM revealed the apoptosis rate was increased and G1 phase was arrested in NEK2-siRNA group. Western blot indicated that low expression of NEK2 in HepG2 cells could increase the expression levels of Bax, caspase-3, P21, and TIMP-1, but significantly suppressed the c-myc, c-jun, Bcl-2, cyclinD1, CDK4, MMP2, and MMP9 expression levels and the phosphorylation levels of ERK, JNK, and P38 compared with the control groups. Our findings demonstrated that NEK2 could be a valuable carcinogenic factor and a promising therapeutic target for primary liver cancer; NEK2 may regulate proliferation, apoptosis, and other biological behaviors of HepG2 cells via MAPK signal pathway. © 2015 International Society of Oncology and BioMarkers (ISOBM) Source


Wang Y.,Shandong University | Zhang P.,Shandong University | Liu Z.,The Fifth Peoples Hospital | Wang Q.,Shandong University | And 4 more authors.
Molecular Cancer | Year: 2014

Background: CUL4A has been proposed as oncogene in several types of human cancer, but its clinical significance and functional role in human non-small cell lung cancer (NSCLC) remain unclear. Methods: Expression level of CUL4A was examined by RT-PCR and Western blot. Forced expression of CUL4A was mediated by retroviruses, and CUL4A silencing by shRNAs expressing lentiviruses. Growth capacity of lung cancer cells was measured by MTT in vitro and tumorigenesis in vivo, respectively. Results: We found that CUL4A was highly expressed in human lung cancer tissues and lung cancer cell lines, and this elevated expression positively correlated with disease progression and prognosis. Overexpression of CUL4A in human lung cancer cell lines increased cell proliferation, inhibited apoptosis, and subsequently conferred resistance to chemotherapy. On other hand, silencing CUL4A expression in NSCLC cells reduced proliferation, promoted apoptosis and resulted in tumor growth inhibition in cancer xenograft model. Mechanistically, we revealed CUL4A regulated EGFR transcriptional expression and activation, and subsequently activated AKT. Targeted inhibition of EGFR activity blocked these CUL4A induced oncogenic activities. Conclusions: Our results highlight the significance of CUL4A in NSCLC and suggest that CUL4A could be a promising therapy target and a potential biomarker for prognosis and EGFR target therapy in NSCLC patients. © 2014 Wang et al.; licensee BioMed Central Ltd. Source


Zhao C.-M.,The Fifth Peoples Hospital | Shang C.-X.,The Fifth Peoples Hospital
World Chinese Journal of Digestology | Year: 2014

AIM: To investigate the quality of life, social support and self-care self-efficacy in patients with digestive system tumors, and to analyze their correlation.METHODS: A total of 153 patients with digestive system tumors were surveyed using the general information questionnaire, strategies used by people to promote health, social support rating scale and quality of life questionnaire-C30.RESULTS: The score of self-care self-efficacy was 86.03 ± 14.23, and the score of social support was 40.28 ± 6.63. There was a significant positive correlation between social support and quality of life (P < 0.05), and between self-care selfefficacy and quality of life (P < 0.05).CONCLUSION: Health care professionals should pay attention to making patients have high quality of cancer self-care self-efficacy and fully utilize the sources of social support to improve the quality of life of patients with digestive system tumors. © 2014 Baishideng Publishing Group Inc. All rights reserved. Source


Zhong B.,The Fifth Peoples Hospital | Wang Y.,The Fifth Peoples Hospital | Zhang G.,The Fifth Peoples Hospital
Cardiology Journal | Year: 2016

Background: The factors and the mechanism contributing to increases in cardiac troponin I (cTnI) in patients with chest pain, at least one cardiovascular risk factor, and no evidence of coronary heart disease remains elusive. Methods: Excluding patients with acute coronary syndrome and chronic myocardial ischemia, we selected 362 consecutive patients with normal coronary angiography or computed tomography coronary angiography results or lesions causing < 50% stenosis in any one of the coronary arteries from January 2012 to June 2015. Using a cut-off value of 0.01 ng/mL, patients with cTnI levels ≥ 0.01 ng/mL (164 patients) were compared with those with cTnI levels < 0.01 ng/mL. Logistic regression analysis was used to evaluate associations between elevated cTnI and patient characteristics. Results: Other than history of diabetes mellitus (DM) (18.90% vs. 8.08%, p = 0.002), the characteristics of the patients with and without elevated cTnI levels were similar. History of DM predicted elevation of cTnI level (OR 3.34, 95% CI 1.55–7.20, p = 0.002) in logistic regression analysis. Conclusions: In total, 45.30% of patients with chest pain had elevated cTnI levels with a mean level of 0.07 ± 0.10 ng/mL. History of DM rather than blood glucose level itself was associated with elevated cTnI levels, whereas female gender was protective against increases in cTnI levels. © 2016 Via Medica. Source

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