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ObjectiveMany studies have reported the prognostic predictive value of CD166 as a cancer stem cell marker in cancers of the digestive system; however, its predictive value remains controversial. Here, we investigate the correlation between CD166 positivity in digestive system cancers and clinicopathological features using meta-analysis.MethodsA comprehensive search in PubMed and ISI Web of Science through March of 2013 was performed. Only articles containing CD166 antigen immunohistochemical staining in cancers of the digestive system were included,including pancreatic cancer, esophageal cancer, gastric cancer and colorectal cancer. Data comparing 3- and 5-year overall survival along with other clinicopathological features were collected.ResultsNine studies with 2553 patients who met the inclusion criteria were included for the analysis. The median rate of CD166 immunohistochemical staining expression was 56% (25.4%–76.3%). In colorectal cancer specifically, the results of a fixed-effects model indicated that CD166-positive expression was an independent marker associated with a smaller tumor burden (T category; RR = 0.93, 95%, CI: 0.88–0.98) but worse spread to nearby lymph nodes (N category; RR = 1.17, 95% CI: 1.05–1.30). The 5-year overall survival rate was showed relationship with cytoplasmic positive staining of CD166 (RR = 1.47 95% 1.21–1.79), but no significant association was found in the pool or any other stratified analysis with 3- or 5- year overall survival rate.ConclusionBased on the published studies, different cellular location of CD166 has distinct prognostic value and cytoplasmic positive expression is associated with worse prognosis outcome. Besides, our results also find CD166 expression indicate advanced T category and N-positive status in colorectal cancer specifically.

Background To understand the effect of DNMT1-mediated MEG3 promoter methylation on breast cancer progression. Methods Expression of DNMT1, MEG3 and miR-494-3p was assayed by qRT-PCR and western blot. Methylation-specific PCR was used to examine MEG3 promoter methylation level. ChIP, RNA binding protein immunoprecipitation assay and dual-luciferase reporter gene assay were applied to verify interaction between DNMT1 and MEG3, miR-494-3p and MEG3 and OTUD4. CCK-8, wound healing and Transwell assays were used to detect biological functions of breast cancer cells. Tumor growth was observed by tumor xenograft model. Results DNMT1 and miR-494-3p were highly expressed while MEG3 and OTUD4 were lowly expressed in breast cancer cells. Knockdown of DNMT1 inhibited progression of breast cancer cells by enhance MEG3 expression through demethylation. MEG3 could downregulate miR-494-3p expression, and OTUD4 was a target of miR-494-3p. Upregulation of MEG3 and downregulation of miR-494-3p both inhibited malignant behavior of cells in vitro. In addition, high MEG3 expression restrained growth of breast cancer in vivo. Conclusion Briefly, our results demonstrated that, DNMT1 induced methylation of MEG3 promoter, and played a key role in breast cancer growth throughmiR-494-3p/OTUD4 axis. These findings provide new insights into molecular therapeutic targets for breast cancer.

Breast cancer is a malignancy harmful to physical and mental health in women, with quite high mortality. Copy number variations (CNVs) are vital factors affecting the progression of breast cancer. Detecting CNVs in breast cancer to predict the prognosis of patients has become a promising approach to accurate treatment in recent years. The differential analysis was performed on CNVs of long noncoding RNAs (lncRNAs) as well as the expression of lncRNAs, microRNAs (miRNAs) and mRNAs in normal tissue and breast tumor tissue based on The Cancer Genome Atlas (TCGA) database. The CNV-driven lncRNAs were identified by the Kruskal-Wallis test.Meanwhile, a competitive endogenous RNA (ceRNA) network regulated by CNVdriven lncRNA was constructed. As the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses revealed, the mRNAs in the dysregulated ceRNA network were mainly enriched in the biological functions and signaling pathways, including the Focal Adhesion-PI3K-Akt-mTOR-signaling pathway, the neuronal system, metapathway biotransformation Phase I and II and blood circulation, etc. The relationship between the CNVs of five lncRNAs and their gene expression in the ceRNA network was analyzed via a chi-square test, which confirmed that except for LINC00243, the expression of four lncRNAs was notably correlated with the CNVs.The survival analysis revealed that only the copy number gain of LINC00536 was evidently related to the poor prognosis of patients. The CIBERSORT algorithm showed that five lncRNAs were correlated with the abundance of immune cell infiltration and immune checkpoints. In a word, by analyzing CNV-driven lncRNAs and the ceRNA network regulated by these lncRNAs, this study explored the mechanism of breast cancer and provided novel insights into new biomarkers.

Background: Breast cancer is the most common cancer among women and the second most common cancer among newly diagnosed cancers worldwide. At present, long non-coding RNAs (lncRNAs) are widely reported to be involved in the occurrence and development of multiple cancers. As a newly discovered long non-coding RNA, the function of HLA complex group 11 (HCG11) remain uncertain in breast cancer. This article aims to examine the effect of HCG11 in breast cancer.Methods: RT-PCR was performed to detect the mRNA level of HCG11 in both breast cancer tissues and cell lines. HCG11 overexpression virus and siHCG11 were constructed and transfected to the breast cancer cell line MCF-7. The effect of HCG11 were evaluated by CCK-8 assay, colony formation assay, wound scratch assay, and cell invasion assay. Then we found and determined small RNA that may interact with HCG11 by bioinformatics analysis and luciferase report analysis. Next, we further researched the role of miR-330-3p in HCG11-mediated breast cancer by CCK-8 assay, colony formation assay, wound scratch assay, and cell invasion assay. At last, the above experimental methods and nude mouse experiments were used to confirm the role of HCG11/miR-330-3p/ FOXO1 in breast cancer process.Results: The results showed that the mRNA level of HCG11 was low-expressed in breast cancer tissues and cell lines. HCG11 overexpression inhibited cell proliferation, invasion and migration in MCF-7 cell line. Moreover, HCG11 could target miR-330-3p/FOXO1 and further suppressed the progression of breast cancer. Conclusion: In summary, lncRNA HCG11 suppressed the progression of breast cancer through cooperating with miR-330-3p/FOXO1 axis