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1.  The Correlation between miRNA and Lymph Node Metastasis in Gastric Cancer 
BioMed Research International  2015;2015:543163.
Lymph node metastasis (LNM) in gastric cancer is associated with higher rate of cancer recurrence and poor prognosis. As a result, a reliable biomarker for the prediction of LNM is important and would be valuable in the clinical practice. MiRNA microarray revealed that ten miRNAs were expressed significantly different among patients with or without LNM. A total of 46 gastric cancer patients were enrolled and divided into two groups (23 in each group) according to the presence or absence of LNM. RT-PCR of these 10 miRNAs was investigated and compared between the two groups. MiR-1207-5p was significantly upregulated in gastric cancer patients without LNM compared with those with LNM. Patients with upregulated miR-1207-5p had less scirrhous stromal reaction, less lymphovascular invasion, and earlier pathological T category, N category, and TNM stage, compared with those with downregulated or unchanged miR-1207-5p. Multivariate analysis showed that stromal reaction type, lymphovascular invasion, pathological T category and TNM stage, and expression of miR-1207-5p were independent risk factors of LNM. MiR-1207-5p could serve as a useful biomarker in the prediction of LNM in gastric cancer.
doi:10.1155/2015/543163
PMCID: PMC4320935
2.  Molecular and Survival Differences between Familial and Sporadic Gastric Cancers 
BioMed Research International  2013;2013:396272.
Mismatch repair (MMR) and germline E-cadherin (CDH1) mutations are two of the major pathways of carcinogenesis in familial gastric cancer (GC). A total of 260 sporadic and 66 familial GC patients were enrolled and molecular and survival differences were compared. Familial GC patients had earlier onset and were diagnosed at an earlier stage and had both a better 5-year overall survival rate and 3-year disease-free survival rate compared with sporadic GC patients. Only in diffuse type GC, the MSI-H phenotype and abnormal MMR protein expression were significantly higher in familial GC than in sporadic GC. In MSI-H GC, MLH1 promoter methylation was slightly higher in sporadic GC than familial GC (50% versus 23.1%), while the frequency of MMR gene mutation was slightly higher in familial GC than in sporadic GC (15.4% versus 3.1%). All of the patients with MMR gene mutation had diffuse type GC. Among familial GC patients with CDH1 mutation, most patients (72.3%) had diffuse type GC. In summary, for familial GC patients, we recommend screening of MSI status and CDH1 mutation especially for diffuse type GC. Because of the low incidence, mutation analysis of MMR gene might be considered in MSI-H familial GC with diffuse type only.
doi:10.1155/2013/396272
PMCID: PMC3603157  PMID: 23555086
3.  Analysis of Adiponectin Gene Polymorphisms in Chinese Population with Systemic Lupus Erythematosus 
Systemic lupus erythematosus (SLE) is a prototypic systemic autoimmune disease. Adiponectin is an adipocyte-derived cytokine with anti-inflammatory, antidiabetic, and antiatherogenic properties. No study has reported on the association between adiponectin (ADIPOQ) gene and SLE. Our aim is to investigate the association between single-nucleotide polymorphisms in ADIPOQ gene and SLE. We examined 179 SLE patients and 237 age- and gender-matched controls from Sichuan province in China. Genotypes were determined using polymerase chain reaction-restriction fragment length polymorphism and DNA sequencing. Results show that there was no significant difference in the allele frequencies of rs1501299 (P = .311, OR = 1.17, 95% CI: 0.86–1.59) and rs2241766 (P = .929, OR = 0.99, 95% CI: 0.74–1.33) in ADIPOQ gene between SLE patients and controls. The same results were seen in their genotypes (P < .05). The allele frequencies of rs1501299 and rs2241766 polymorphisms of ADIPOQ may not be associated with SLE risk.
doi:10.1155/2010/401537
PMCID: PMC2856039  PMID: 20414354
4.  Comparison of the Operative Outcomes and Learning Curves between Laparoscopic and Robotic Gastrectomy for Gastric Cancer 
PLoS ONE  2014;9(10):e111499.
Background
Minimally invasive surgery, including laparoscopic and robotic gastrectomy, has become more popular in the treatment of gastric cancer. However, few studies have compared the learning curves between laparoscopic and robotic gastrectomy for gastric cancer.
Methods
Data were prospectively collected between July 2008 and Aug 2014. A total of 145 patients underwent minimally invasive gastrectomy for gastric cancer by a single surgeon, including 73 laparoscopic and 72 robotic gastrectomies. The clinicopathologic characteristics, operative outcomes and learning curves were compared between the two groups.
Results
Compared with the laparoscopic group, the robotic group was associated with less blood loss and longer operative time. After the surgeon learning curves were overcome for each technique, the operative outcomes became similar between the two groups except longer operative time in the robotic group. After accumulating more cases of robotic gastrectomy, the operative time in the laparoscopic group decreased dramatically.
Conclusions
After overcoming the learning curves, the operative outcomes became similar between laparoscopic and robotic gastrectomy. The experience of robotic gastrectomy could affect the learning process of laparoscopic gastrectomy.
doi:10.1371/journal.pone.0111499
PMCID: PMC4216064  PMID: 25360767
5.  Yin Yang 1 is a target of microRNA-34 family and contributes to gastric carcinogenesis 
Oncotarget  2014;5(13):5002-5016.
Gastric cancer is the second leading cause of cancer-related death worldwide. Herein, we investigated the role of transcription factor Yin Yang 1 (YY1), a multi-functional protein, in tumorigenesis of gastric cancer cells. Results showed that YY1 contributed to gastric carcinogenesis of SC-M1 cells including growth, viability, and abilities of colony formation, migration, invasion, and tumorsphere formation. Levels of pluripotency genes CD44, Oct4, SOX-2, and Nanog were also up-regulated by YY1 in SC-M1 cells. Additionally, the 3'-untranslated region (3'-UTR) of YY1 mRNA was the target of microRNA-34 (miR-34) family consisting of miR-34a, miR-34b, and miR-34c. Overexpression of miR-34 family suppressed carcinogenesis through down-regulation of YY1 in NUGC-3 gastric cancer cells scarcely expressing miR-34 family. Alternatively, knockdown of miR-34 family promoted tumorigenesis via up-regulation of YY1 in SC-M1 and AZ521 gastric cancer cells with higher levels of miR-34 family. The miR-34 family also affected tumorsphere ultra-structure and inhibited the xenografted tumor growth as well as lung metastasis of SC-M1 cells through YY1. Expressions of miR-34a and miR-34c in gastric cancer tissues of patients were lower than those in normal tissues. Taken together, these results suggest that miR-34 family-YY1 axis plays an important role in the control of gastric carcinogenesis.
PMCID: PMC4148117  PMID: 24970812
YY1; miR-34 family; gastric cancer; carcinogenesis; pluripotency
6.  Transcriptional regulation of miR-196b by ETS2 in gastric cancer cells 
Carcinogenesis  2012;33(4):760-769.
E26 transformation-specific sequence (ETS)-2 is a transcriptional modulator located on chromosome 21, alterations in its expression have been implicated with a reduced incidence of solid tumors in Down syndrome patients. MicroRNAs (miRNAs) are thought to participate in diverse biological functions; however, the regulation of miRNAs is not well characterized. Recently, we reported that miR-196b is highly expressed in gastric cancers. Herein, we demonstrate that miR-196b expression was significantly repressed by ETS2 during gastric cancer oncogenesis. We demonstrate that knockdown of endogenous ETS2 expression increases miR-196b expression. A genomic region between −751 and −824 bp upstream of the miR-196b transcriptional start site was found to be critical for the repression activity. This putative regulatory promoter region contains three potential ETS2-binding motifs. Mutations within the ETS2 binding sites blocked the repression activity of ETS2. Furthermore, knockdown of ETS2 or overexpression of miR-196b significantly induced migration and invasion in gastric cancer cells. In addition, alterations in ETS2 and miR-196b expression in gastric cancer cell lines affected the expression of epithelial–mesenchymal transition-related genes. The levels of vimentin, matrix metalloproteinase (MMP)-2 and MMP9 were drastically induced, but levels of E-cadherin were decreased in shETS2- or miR-196b-transfected cells. Our data indicate that ETS2 plays a key role in controlling the expression of miR-196b, and miR-196b may mediate the tumor suppressor effects of ETS2. We demonstrated that miR-196b was transcriptionally regulated by ETS2 and there was an inverse expression profile between miR-196b and ETS2 in clinical samples. This finding could be beneficial for the development of effective cancer diagnostic and alternative therapeutic strategies.
doi:10.1093/carcin/bgs023
PMCID: PMC3324441  PMID: 22298639
7.  Aberrant hypermethylation of miR-9 genes in gastric cancer 
Epigenetics  2011;6(10):1189-1197.
Carcinogenesis of the stomach involves multiple steps including genetic mutation or epigenetic alteration of tumor suppressor genes or oncogenes. Recently, tumor suppressive miRNAs have been shown to be deregulated by aberrant hypermethylation during gastric cancer progression. In this study, we demonstrate that three independent genetic loci encoding for miR-9 (miR-9-1, miR-9-2 and miR-9-3) are simultaneously modified by DNA methylation in gastric cancer cells. Methylation-mediated silencing of these three miR-9 genes can be reactivated in gastric cancer cells through 5-Aza-dC treatment. Subsequent analysis of the expression levels of miR-9 showed that it was significantly downregulated in gastric cancers compared with adjacent normal tissues (p value < 0.005). A similar tendency toward a tumor-specific DNA methylation pattern was shown for miR-9-1, miR-9-2 and miR-9-3 in 72 primary human gastric cancer specimens. Ectopic expression of miR-9 inhibited cell proliferation, migration and invasion, suggesting its tumor suppressive potential in gastric cancer progression.
doi:10.4161/epi.6.10.16535
PMCID: PMC3225840  PMID: 21931274
miR-9; DNA methylation; CpG islands; gastric cancer

Results 1-7 (7)