Cui J.,Jinan Stomatologic Hospital |
Shen L.,Jinan Stomatologic Hospital |
Wang Y.,Shandong University
Asian Pacific Journal of Cancer Prevention | Year: 2012
Background: The Cyclin D1(CCND1) G870A polymorphism may be associated with breast cancer, but the evidence from individual studies is inconclusive. The aim of this study was to investigate the correlation between the CCND1 G870A polymorphism and breast cancer risk in a meta-analysis. Materials and Methods: We searched Pubmed and analysed 11 articles on 5,528 cases and 5,353 controls before February 1, 2012. Results: we found there are significant association for AA versus GG and AA versus GA/GG. No significant associations were found for GA versus GG, GA/AA versus GG. There are significant association for AA versus GG ,and AA versus GA/GG in Caucasians. We didn't find any significant main effects for G870Apolymorphism on breast cancer risk either in recessive or dominant models in Asians. Conclusion: This meta-analysis suggests that AA of the CCND1 G870A polymorphism is associated with breast cancer susceptibility.
Wen Y.,Shandong University |
Wen Y.,Shandong Provincial Key Laboratory of Oral Biomedicine |
Gu W.,Shandong University |
Cui J.,Jinan Stomatologic Hospital |
And 10 more authors.
Archives of Oral Biology | Year: 2014
Objectives To evaluate the effects of platelet-rich plasma (PRP) on the proliferation and differentiation of umbilical cord mesenchymal stem cells (UC-MSCs) and explore the possibility that PRP combined with UC-MSCs may be useful for bone tissue regeneration in vivo. Methods The proliferation potential of UC-MSCs was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay. The pluripotent differentiation capacity and alkaline phosphatase (ALP) expression were further determined by ALP staining. The expression of osteoblast-associated genes was evaluated by real-time PCR. In addition, rat critical-sized calvarial defects were examined to evaluate bone regeneration in vivo. Results PRP enhanced UC-MSC proliferation, and 10% PRP caused the strongest ALP and Alizarin red staining. At 7 days, the expression levels of ALP, Collagen 1 (COL-1) and Runt-related transcription factor 2 (RUNX2) in the PRP group were higher than those in the FBS group. Newly regenerated bone was observed in the defect areas, and PRP combined with UC-MSCs can accelerate bone regeneration at an early stage. Conclusions Our current data suggest that UC-MSCs may be utilized in alternative stem cell-based approaches for the reconstruction and regeneration of bone defects, and PRP combined with UC-MSCs can enhance bone regeneration in vivo. © 2014 Elsevier Ltd.
Hu J.,The Military General Hospital of Beijing PLA |
Zhang N.,General Hospital of the Second Artillery |
Wang R.,Jinan Stomatologic Hospital |
Huang F.,Navy General Hospital |
Li G.,General Hospital of the Second Artillery
Oncology Letters | Year: 2015
Oral cavity cancer is common worldwide. Furthermore, the epidermal growth factor receptor (EGFR) signaling pathway is considered to be constitutively activated in oral cancers. Paclitaxel is widely accepted as an antitumor drug as it effectively inhibits the cell cycle. This study predominantly explores the possible molecule mechanism of paclitaxel on oral cancer treatment. Cell viability was first detected using an MTT assay. Cell apoptosis was examined by Hoechst staining and flow cytometry using an annexin‑V and propidium iodide kit. Specific EGFR signaling pathways were further explored through western blot analysis. Abnormal protein expression levels were determined via immunofluoresence. Additionally, the protein levels of matrix metalloproteinase (MMP)‑2 and 9 were determined using ELISA. Paclitaxel significantly inhibited oral cancer cell viability in a time‑ and dose‑dependent manner. Paclitaxel also enhanced oral cancer cell apoptosis via increased Bim and Bid protein expression. Furthermore, paclitaxel was observed to inhibit oral cancer cell proliferation through increased MMP‑2 and MMP‑9 protein levels. Paclitaxel inhibited the growth of the oral cancer cell line, tea8113 malignant proliferation and enhanced tea8113 cell apoptosis through inhibiting the EGFR signaling pathway. © 2015 Spandidos Publications. All rights reserved.
Cui J.,Jinan Stomatologic Hospital |
Cui J.,Shandong University |
Li D.,Jinan Stomatological Hospital |
Zhang W.,Jinan Stomatological Hospital |
And 2 more authors.
Oncology Letters | Year: 2014
MicroRNAs (miRNAs) are important in the regulation of cell growth, differentiation, apoptosis and carcinogenesis. The overexpression of oncogenic miRNAs or the underexpression of tumor suppressor miRNAs exhibits a critical function in the tumorigenesis of oral cancer. The aim of the present study was to identify differentially expressed miRNAs (DE-miRNAs), which may differentiate oral cancer from normal tissues, as well as the molecular signatures that differ in tumor histology. The miRNA expression profiles of GSE28100 [the Gene Expression Omnibus (GEO) accession number] were downloaded from the GEO database and an independent sample t-test was used to identify statistical differences between the DE-miRNAs of the oral cancer patients and the healthy control subjects. The target genes of DE-miRNA were retrieved from the miRecords database. Furthermore, a protein-protein interaction network was constructed using the Search Tools for the Retrieval of Interacting Genes database and Cytoscape software. A total of 15 DE-miRNAs were identified and among them, hsa-miR-15a drew specific attention. Gene Ontology analysis revealed that the target genes of fibroblast growth factor (FGF)2 are involved in the progression of oral cancer. Furthermore, functional analysis indicated that the FGF-receptor signaling pathway was significantly upregulated in oral cancer. hsa-miR-15a is important in the regulation of oral cancer and thus, may present a potential biomarker for the prediction of oral cancer progression.
Sun J.,Shandong University |
Liu X.,Jinan Stomatologic Hospital |
Jiang G.,Shandong University |
Qi Q.,Shandong University
Antimicrobial Agents and Chemotherapy | Year: 2015
Candida albicans persisters constitute a small subpopulation of biofilm cells and play a major role in recalcitrant chronic candidiasis; however, the mechanism underlying persister formation remains unclear. Persisters are often described as dormant, multidrug-tolerant, nongrowing cells. Persister cells are difficult to isolate and study not only due to their low levels in C. albicans biofilms but also due to their transient, reversible phenotype. In this study, we tried to induce persister formation by inducing C. albicans cells into a dormant state. C. albicans cells were pretreated with 5-fluorocytosine (planktonic cells, 0.8 μgml-1; biofilm cells, 1 μgml-1) for 6 h at 37°C, which inhibits nucleic acid and protein synthesis. Biofilms and planktonic cultures of eight C. albicans strains were surveyed for persisters after amphotericin B treatment (100 μgml-1 for 24 h) and CFU assay. None of the planktonic cultures, with or without 5-fluorocytosine pretreatment, contained persisters. Persister cells were found in biofilms of all tested C. albicans strains, representing approximately 0.01 to 1.93% of the total population. However, the persister levels were not significantly increased in C. albicans biofilms pretreated with 5-fluorocytosine. These results suggest that inhibition of nucleic acid synthesis did not seem to increase the formation of amphotericin B-tolerant persisters in C. albicans biofilms. Copyright © 2015, American Society for Microbiology. All Rights Reserved.