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Accumulating evidence has demonstrated that long non-coding RNAs (lncRNAs) function as essential regulators in the development and progression of multiple tumors. However, the molecular mechanisms of MIR31HG in regulating ESCC progression remain unknown. Here, we confirmed that MIR31HG facilitated ESCC cells proliferation in vivo. Besides, MIR31HG knockdown increases the percentage of cells at the G1 phase, along with reduced arrest in S phase and MIR31HG overexpression exhibits the opposite effects. Overexpressed MIR31HG decreases the percentage of apoptotic ESCC cells. Interestingly, MIR31HG can function as a competing endogenous RNA by sponging miR-34a. The rescue experiments demonstrated that MIR31HG function is partially reversed by inhibiting miR-34a. In addition, we found c-Met is a target gene of miR-34a and is indirectly regulated by MIR31HG. Taken together, our findings revealed that MIR31HG promotes ESCC progression by regulating miR-34a/ c-Met axis and may provide a new prospective for exploration and understanding of the biological effects of esophageal squamous cell carcinoma.

// Yunhui Qu 1, 2, * , Hongtao Liu 3, * , Xinquan Lv 1 , Yuqiong Liu 1 , Xiaojuan Wang 1 , Min Zhang 1 , Xiaqing Zhang 3 , Yuenan Li 3 , Qianqian Lou 3 , Shenglei Li 1 and Huixiang Li 1 1 Department of Pathology, School of Basic Medical Sciences, Zhengzhou University and The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450001, Henan, P.R. China 2 Clinical Laboratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450001, Henan, P.R. China 3 Laboratory for Cell Biology, College of Life Sciences of Zhengzhou University, Zhengzhou, 450001, Henan, P.R. China * These authors contributed equally to this work Correspondence to: Huixiang Li, email: lhx20170220@126.com Keywords: microRNA-16-5p, breast carcinoma, HIF-α, VEGFA, tumor growth Received: March 03, 2017 Accepted: August 07, 2017 Published: August 23, 2017 ABSTRACT MicroRNAs (miRNAs), a class of small noncoding RNA molecules, can manipulate the expressions of endogenous tumor-related genes, and are implicated in the development and progression of a wide type of tumors. In this study, the investigation from real-time quantitative PCR revealed that miRNA-16-5p was downregulated in breast carcinoma tissues and cells, coupled with the elevations of HIF-α and VEGFA protein expressions, compared with normal tissues. Lentiviral armed with miR-16-5p markedly increased the miR-16-5p levels in MCF-7 and MDA-MB-231 cells, compared to blank and NC groups, and miR-16-5p overexpression significantly inhibited the proliferation and colony formation in MCF-7 and MDA-MB-231 cells. Besides, miR-16-5p upregulation markedly induced apoptosis and reduced invasion ability in MCF-7 and MDA-MB-231 cells. Notably, VEGFA was direct target of miR-16-5p. Stepwise investigation from in vitro and in vivo experiments demonstrated that miR-16-5p overexpression suppressed tumor growth and reduced HIF-α and VEGFA expressions in breast carcinoma cells and nude mice tumor tissues. These findings provide novel insights into molecular mechanism involved in the roles of miR-16-5p in tumor development and progression of breast carcinoma, and thus manipulation of miR-16-5p may be a novel potential therapeutic target for future therapies of the patients with breast carcinoma.

Exosomes derived from human umbilical cord mesenchymal stem cells (HUCMSCs) expressing microRNAs (miRs) have been highlighted as important carriers for gene or drug therapy. Hence, this study aimed to explore the role of exosomal miR-148b-3p from HUCMSCs in breast cancer. Clinical samples subjected to RT-qPCR detection revealed that miR-148b-3p was poorly expressed, while tripartite motif 59 (TRIM59) was highly expressed in breast cancer tissues. Online analyses available at miRanda, TargetScan, and miRbase databases revealed that miR-148b-3p could bind to TRIM59, while dual-luciferase reporter gene assay further verified that TRIM59 was a target gene of miR-148b-3p. Next, miR-148b-3p mimic or inhibitor and siRNA against TRIM59 were delivered into the breast cancer cells (MDA-MB-231) to alter the expression of miR-148b-3p and TRIM59 so as to evaluate their respective effects on breast cancer cellular processes. Evidence was obtained demonstrating that miR-148b-3p inhibited cell proliferation, invasion, and migration, but promoted cell apoptosis in breast cancer by down-regulating TRIM59. Next, MDA-MB-231 cells were co-cultured with the exosomes derived from HUCMSCs expressing miR-148b-3p. The results of co-culture experiments demonstrated that HUCMSCs-derived exosomes carrying miR-148b-3p exerted inhibitory effects on MDA-MB-231 progression in vitro. In vivo experimentation further confirmed the anti-tumor effects of HUCMSCs-derived exosomes carrying miR-148b-3p. Taken together, HUCMSC-derived exosomes carrying miR-148b-3p might suppress breast cancer progression, which highlights the potential of exosomes containing miR-148b-3p as a promising therapeutic approach for breast cancer treatment.

Increasing evidence has demonstrated that histone deacetylase 2 (HDAC2) participates in the regulation of a variety of biological processes in numerous tumors. However, the potential role of HDAC2 in the development and progression of esophageal squamous cell carcinoma (ESCC) remains elusive. Immunohistochemistry was utilized to detect the expression of HDAC2, Cell Counting Kit-8 was used to determine the cell proliferation, and flow cytometry was employed to investigate cell cycle and cell apoptosis. Finally, western blotting was employed to detect the protein expression of cyclin D1, p21, B cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax). The present study found that expression of HDAC2 protein in ESCC tissues was significantly increased compared with atypical hyperplasia tissues and normal esophageal mucosa (P0.05), but was closely associated with the histological grade, invasion depth, tumor-node-metastasis stage and lymph node metastasis, respectively (all P

Background Long non-coding RNAs (lncRNAs) are powerful factors influencing the tumorigenesis and metastasis of multiple carcinomas. LncRNA MNX1-AS1 plays critical roles in the progression of tumor formation according to recent research, while its roles in esophageal squamous cell carcinoma (ESCC) remains unknown. Methods The expression levels of lncRNA MNX1-AS1 were examined in ESCC tissues by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). The role of lncRNA MNX1-AS1 was performed by WST-1 proliferation assays, migration and invasion assays. Besides, the molecular mechanism of lncRNA MNX1-AS1 was verified by online bioinformatics, qRT-PCR and rescue assays. Results MNX1-AS1 was signifcantly upregulated in ESCC tissues. It was conformed that high MNX1-AS1 expression was associated with ESCC lymph node metastasis. Moreover, we found that knockdown of MNX1-AS1 apparently suppressed the cell proliferation, migration, and invasion capacity. Flow cytometry analysis showed MNX1-AS1 regulated ESCC cell cycle and apoptosis progression. Mechanism analysis revealed that miR-34a inhibitor could rescue the influence of inhibiting MNX1-AS1 on ESCC cells migration by serving as competing endogenous RNA (ceRNAs). Furthermore, we found that miR-34a specifically targeted SIRTI. Conclusions Taken together, we demonstrated that lncRNA MNX1-AS1/miR-34a/SIRT1 regulatory axis could play an important role in ESCC progression, and MNX1-AS1 may act as a novel potential biomarker for esophageal squamous cell carcinoma.

To explore the expression of S100A7 in esophageal squamous cell carcinoma (ESCC) and examine the effect of S100A7 down-regulated expression mediated via RNA interfering on cell proliferation and invasion.The expressions of S100A7 mRNA and protein were analyzed by in situ hybridization and immunohistochemistry.S100A7 siRNA was transfected into ESCC cell line EC9706 and the expressions of S100A7 mRNA and protein were detected by real-time polymerase chain reaction (PCR) and Western blot.Furthermore, the effects of down-regulated of S100A7 on cell proliferation and invasion were examine by Cell Counting Kit-8 (CCK-8) and Boyden chamber respectively.Finally the effect of down-regulated expression of S100A7 on matrix metalloproteinase-2 (MMP-2) protein was analyzed by Western blot.Positive expression ratios of S100A7 mRNA and protein expressions in ESCC tissues (72.0% and 69.3%) were significantly higher than those in normal esophageal tissues (10.7% and 8.0%) (χ² = 58.174 and 59.483, both P = 0.000). The expressions of S100A7 mRNA and protein in S100A7 siRNA group were markedly lower than those in untreated group (mRNA: 0.235 ± 0.056 vs 1, protein: 0.119 ± 0.025 vs 0.518 ± 0.129, both P0.05). Additionally, the down-regulated expression of S100A7 resulted in the proliferation inhibition and the decreased invasiveness in EC9706 cells. And it was coupled with a down-regulation of MMP-2 protein.S100A7 may play an essential role in the occurrence and development of ESCC and the decreased invasiveness of EC9706 cells mediated by the down-regulated expression of S100A7 may be closely associated with the down-regulation of MMP-2 protein.