Wu T.,Ningbo University |
Du Y.,Ningbo Institute of Medical Science
International Journal of Biological Sciences | Year: 2017
This review aimed to summarize the current research contents about long noncoding RNAs (lncRNAs) and some related lncRNAs as molecular biomarkers or therapy strategies in human cancer and cardiovascular diseases. Following the development of various kinds of sequencing technologies, lncRNAs have become one of the most unknown areas that need to be explored. First, the definition and classification of lncRNAs were constantly amended and supplemented because of their complexity and diversity. Second, several methods and strategies have been developed to study the characteristic of lncRNAs, including new species identifications, subcellular localization, gain or loss of function, molecular interaction, and bioinformatics analysis. Third, based on the present results from basic researches, the working mechanisms of lncRNAs were proved to be different forms of interactions involving DNAs, RNAs, and proteins. Fourth, lncRNA can play different important roles during the embryogenesis and organ differentiations. Finally, because of the tissue-specific expression of lncRNAs, they could be used as biomarkers or therapy targets and effectively applied in different kinds of diseases, such as human cancer and cardiovascular diseases. © Ivyspring International Publisher.
Zhang C.,Zhejiang University |
Li M.,Zhejiang University |
Li M.,Ningbo Institute of Medical science |
Zhao J.,Zhejiang University
Chinese Journal of Biomedical Engineering | Year: 2017
The limited ability of the body to fully repair large bone defects beyond critical sizes often necessitates the implantation of replacement material to promote healing. While the current clinical strategies to address such bone defects generally carry associated limitations, bone-tissue engineering approaches seek to minimize any adverse effects and facilitatecomplete regeneration of the lost tissue. Extracellular matrix, due to its excellent biocompatibility, unique biomechanical properties and biological activities, has been widely investigated as a scaffold in regenerative medicine. This review focused on hybrid constructs and modification on ECM materials, as well as its biological effects in vitro and in vivo. Application prospects in bone regeneration were also discussed.
du Y.,Ningbo Institute of Medical Science |
Chen Y.,Ningbo Institute of Medical Science |
Wang F.,Ningbo Institute of Medical Science |
Gu L.,Peking University
Tumor Biology | Year: 2016
Aberrant expression of miR-137 has been reported in many kinds of cancers, but its mechanisms seem to be diversely. In the present study, we compared the expression level of miR-137 in 18 paired gastric cancer (GC) samples and surgical margin (SM) samples by RNA extraction and quantitative real-time PCR (QRT-PCR). Then, we investigated the effects of miR-137 on cell proliferation, cell cycle, and cell migration separately by cell growth counting assay, cell cycle analysis, and transwell assay. Candidate targets of miR-137 were selected by biological information analysis from the intersection of miRDB, Pictar, and TarScan. Finally, mRNA and protein expression level of Krűppel-like factor 12 (KLF12) and Myosin 1C (MYO1C) were tested by QRT-PCR and western blotting assay, followed by the Luciferase reporter assay to investigate the direct interaction between them and miR-137. The results showed that miR-137 was down-regulated in GC samples than in SM samples. The expression level of miR-137 was significantly higher in patients without the vascular embolus than those with vascular embolus. And the overall survival time of patients with high miR-137 expression was longer than those with low miR-137 expression. Over expression of miR-137 could inhibit the cell migration, proliferation, and promote cell cycle arrest in G0/G1 stage in BGC-823 and SGC-7901 cell lines. KLF12 and MYO1C might be the candidate target genes of miR-137 with direct interactions between them and miR-137. In conclusion, miR-137 plays tumor suppressor roles in gastric cancer cell lines by targeting KLF12 and MYO1C. © 2016 International Society of Oncology and BioMarkers (ISOBM)
PubMed | Ningbo Institute of Medical Science and Peking University
Type: Journal Article | Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine | Year: 2016
Aberrant expression of miR-137 has been reported in many kinds of cancers, but its mechanisms seem to be diversely. In the present study, we compared the expression level of miR-137 in 18 paired gastric cancer (GC) samples and surgical margin (SM) samples by RNA extraction and quantitative real-time PCR (QRT-PCR). Then, we investigated the effects of miR-137 on cell proliferation, cell cycle, and cell migration separately by cell growth counting assay, cell cycle analysis, and transwell assay. Candidate targets of miR-137 were selected by biological information analysis from the intersection of miRDB, Pictar, and TarScan. Finally, mRNA and protein expression level of Krppel-like factor 12 (KLF12) and Myosin 1C (MYO1C) were tested by QRT-PCR and western blotting assay, followed by the Luciferase reporter assay to investigate the direct interaction between them and miR-137. The results showed that miR-137 was down-regulated in GC samples than in SM samples. The expression level of miR-137 was significantly higher in patients without the vascular embolus than those with vascular embolus. And the overall survival time of patients with high miR-137 expression was longer than those with low miR-137 expression. Over expression of miR-137 could inhibit the cell migration, proliferation, and promote cell cycle arrest in G0/G1 stage in BGC-823 and SGC-7901 cell lines. KLF12 and MYO1C might be the candidate target genes of miR-137 with direct interactions between them and miR-137. In conclusion, miR-137 plays tumor suppressor roles in gastric cancer cell lines by targeting KLF12 and MYO1C.
PubMed | P.A. College, Ningbo Institute of Medical science, The Ningbo No 2 Hospital and Shanghai University
Type: Journal Article | Journal: Oncology letters | Year: 2016
The aim of the present study was to establish a model of tumor cell growth and visualize HIF-1 overexpression in a nude mouse xenograft model of colorectal cancer (CRC). In the study, HIF-1 lentiviral vector and helper plasmid were co-transfected into 293T packaging cells using a liposome method, and the virus was collected following transfection and used to infect CRC SW480, SW620, LoVo and HCT116 cells. Puromycin was used for the selection and large-scale amplification of the stable HIF-1 expression of green fluorescent protein (GFP)-positive cells. HIF-1-expressing cells were injected intraperitoneally into a nude mouse xenograft model, and resulting tumor nodules was separated and confirmed using an inverted fluorescence microscope. The results demonstrated that HIF-1 was not expressed in CRC cells in normoxic conditions. When treated with CoCl
Wu T.,Zhejiang University |
Xu Y.-H.,Shanghai JiaoTong University |
Ye X.-L.,Ningbo Institute of Medical science
Tumor Biology | Year: 2013
There were many studies performed to assess the association between X-ray repair cross-complementing group 1 (XRCC1) Arg194Trp polymorphism and lung cancer risk in Chinese Han population, but contradictory results were reported. To provide a comprehensive and objective assessment of the association, a meta-analysis of all eligible case-control studies was carried out. After searching the databases and reading the abstracts, 12 case-control studies on the association between XRCC1 Arg194Trp polymorphism and lung cancer risk were finally included into this meta-analysis. Those 12 studies included a total of 4,385 cases and 4,545 controls. XRCC1 Arg194Trp polymorphism was associated with increased risk of lung cancer in Chinese Han population under three main models (allele contrast model, odds ratio (OR) = 1.12, 95 % confidence interval (CI) 1.00-1.26, P = 0.049; homozygote model, OR = 1.27, 95 % CI 1.09-1.48, P = 0.003; recessive model, OR = 1.26, 95 % CI 1.09-1.46, P = 0.003). However, there was no obvious association between XRCC1 Arg194Trp polymorphism and lung cancer risk under the dominant model (OR = 1.06, 95 % CI 0.98-1.16, P = 0.146). Sensitivity analysis suggested the stability and liability of this meta-analysis. Therefore, this meta-analysis suggests that XRCC1 Arg194Trp polymorphism is associated with increased risk of lung cancer in Chinese Han population. © 2013 International Society of Oncology and BioMarkers (ISOBM).
Ye X.,Ningbo Institute of Medical science |
Zhang C.,Changzhou University |
Chen Y.,Ningbo Institute of Medical science |
Zhou T.,The Ningbo No 2 Hospital
Journal of Cancer | Year: 2015
Background: The expression of acetylcholinesterase (AChE) could be induced during apoptosis in various cell types. And reduced AChE expression either by siRNA could prevent apoptosis. However, the detailed mechanisms underlying the AChE regulation are largely unknown in human breast cancer cell. Material and methods: MCF-7 cells were cultured and treated by cisplatin in the absence or presence of p53 siRNA. Results: In this study, the regulation of AChE expression during apoptosis induced by cisplatin, a current used anticancer drug, was investigated in human breast cancer cell line MCF-7. Exposure of MCF-7 cells to cisplatin resulted in apoptosis in a time- and concentration-dependent manner. Meanwhile, the upregulated AChE and p53 were also observed during apoptosis. Silencing interfering RNA directed against p53 blocked the expression of AChE. Conclusion: Taken together, these results suggested that AChE expression could be upregulated by the activation of p53 during apoptosis induced by cisplatin in MCF-7 cells. © Ivyspring International Publisher.
PubMed | Fudan University, Ningbo Institute of Medical science, Yichun University, Ningbo Urinary Kidney Disease Hospital and Ningbo Clinical and Pathology Diagnostic Center
Type: Journal Article | Journal: Oncology reports | Year: 2016
Inflammation is emerging as a new hallmark of cancer. Arachidonic acid (AA) metabolism, the family of cyclooxygenases (COXs) and lipoxygenase (LOX) play important roles in AA-related inflammatory cascades. In 94 colorectal cancer samples collected from the Han population, the immunohistochemical results indicated that 68% of the patients with colorectal cancer had a co-expression of both COX-2 and 5-LOX, while both displayed low expression in the matched normal tissues. In cell lines, three colorectal cancer cell lines exhibited high expression of COX-2 and 5-LOX. During stable silencing of the expression of COX-2 or 5-LOX in LoVo cancer cells, we found that downregulation of either COX-2 or 5-LOX significantly diminished the growth, migration and invasion of the colon cancer cells and specifically, downregulation of COX-2 could elicit upregulation of 5-LOX protein and vice versa. The above results suggested that the simultaneous blocking of COX-2 and 5-LOX activity may bring more potential benefits in managing the progression of colon cancer. Therefore, we sought to explore the effectiveness of a dual COX-2/5-LOX inhibitor darbufelone on the proliferation, migration, invasion and apoptosis of colon cancer cells, as well as the underlying mechanism of action. The results indicated that darbufelone significantly decreased the proliferative and invasive abilities of the colon cancer cells, in a dose-dependent manner. During the study of the related mechanisms, we found an upregulation of p27 and downregulation of cyclin D1 as well as CDK4 after darbufelone treatment, which indicated that darbufelone could arrest the cell cycle of LoVo cells at the G0/G1 phase. Furthermore, the activation of caspase-3 and -9, upregulation of Bax and downregulation of Bcl-2 demonstrated the occurrence of apoptosis by darbufelone. Finally, darbufelone also prevented the migration and invasion of LoVo cells, which may be ascribed to the upregulation of E-cadherin and ZO-1. In summary, our data suggest that the inhibition of both COX-2/5-LOX may be an effective therapeutic approach for colon cancer management, particularly for those patients with high expression of COX-2/5-LOX.
PubMed | Ningbo Institute of Medical science, Ningbo University, Ningbo Medical Treatment Center Lihuili Hospital and Ningbo Yin Zhou Hospital
Type: Journal Article | Journal: Oncology letters | Year: 2016
Primary renal lymphoma (PRL) is a rare disease, with no more than 70 cases reported in the literature. The present study reports the case of a 70-year-old woman with PRL. The patient was asymptomatic, however, a mass on the right kidney was identified incidentally during routine physical examination. Computed tomography revealed a mass in the right kidney that was 3.6 cm in diameter. Subsequently, right nephrectomy was performed. The histological evaluation of the nephrectomy specimen showed diffuse large B-cell non-Hodgkins lymphoma. The patient was treated with 6-8 cycles of a cyclophosphamide, epirubicin, vindesine and dexamethasone regimen. Follow-up examination performed after 2 months of treatment revealed no evidence of local recurrence. The present study also reviewed 49 cases of PRL that have been reported since 1989. It was found that a shorter survival time was experienced by patients with bilateral PRL (mean, 21 months) compared with unilateral PRL (mean, 68 months). A shorter survival time was also experienced by patients who were treated with chemotherapy only (mean, 15.8 months) compared with those who were treated with combination chemotherapy and surgery (mean, 49.4 months).
PubMed | Fudan University, Ningbo Institute of Medical science, Southern Medical University and China Pharmaceutical University
Type: Journal Article | Journal: Oncology reports | Year: 2015
Vacuole membrane protein1 (VMP1) was recently found to be involved in the process of tumor metastasis and is also considered to play a vital role in balancing apoptosis and autophagy. In the present study, the expression of VMP1 in colorectal cancer and matched adjacent noncancerous tissues was evaluated by immunohistochemistry (IHC) for studying the role of VMP1 in the process of colorectal cancer. KaplanMeier analysis and the log-rank test were used to calculate the correlation of classic clinicopathological characteristics related to survival and the expression of VMP1. Invitro, a VMP1 stable gene silencing cell model was constructed using a lentiviral vector. The invasive ability and proliferation of colorectal cancer cells were evaluated by Transwell and MTT assays, respectively, and the underlying signaling pathway was explored by western blotting. Additionally, drug susceptibility to cisplatin, oxaliplatin and 5-FU was tested before and after VMP1 knockout. Finally, an animal model was constructed to explore the role of VMP1 in the physiopathologic process of colorectal cancer. Our results indicated that VMP1 showed increased expression in the adjacent non-cancer tissues compared with that in the colorectal cancer tissues. For different stages of colorectal cancer, expression of VMP1 had a negative correlation with the malignancy of the cancer. In clinical research, we also found that the median survival of patients with low VMP1 expression was much shorter than the survival of patients with high expression. Invitro, after infection with the lentivirus, cells with VMP1 knockout gained significant aggressive properties in regards to invasion and proliferation, and the mechanisms may be related to the activation of the PI3K/Akt/ZO-1/E-cadherin pathway. We also found that shVMP1 cells were more sensitive to 5-FU, but not cisplatin and oxaliplatin. Finally, we found a higher number of formed nodules in nude mice after intraperitoneal injection with shVMP1 cells in the invivo study.