Epithelial-mesenchymal transition (EMT) is a key process in the tumor metastatic cascade that is characterized by the loss of cell-cell junctions and cell polarity, resulting in the acquisition of migratory and invasive properties. Recent evidence showed that altered microRNA-10b (miR-10b) expression was implicated in the occurrence of EMT of breast cancer. However, the exact role and underlying mechanisms of miR-10b in the EMT of breast cancer still remain unknown. In this study, miR-10b was found to be upregulated in breast cancer tissues and breast cancer cell lines and the expression of miR-10b was shown to be closely correlated with aggressiveness in breast cancer. Treating breast cancer cells with the miR-10b inhibitor increased E-cadherin expression while decreasing vimentin expression. At the same time, on inhibition of miR-10b, the invasion and proliferation ability of breast cancer cells also decreased. Transforming growth factor-b (TGF-b) is a multifunctional cytokine that induces EMT in multiple cell types. Here, we identified miR-10b as a target gene of TGF-b1. The expression of miR-10b increased during TGF-b1-induced EMT of breast cancer cells. Further study showed that inhibition of miR-10b expression partially reversed the EMT, invasion and proliferation induced by TGF-b1 in breast cancer cells. Taken together, these results demonstrated a novel function for miR-10b in TGF-b1-induced EMT in breast cancer and increased their metastatic potential. MiR-10b might become a possible target for gene therapy in breast cancer.Cancer Gene Therapy (2014) 21, 60-67; doi:10.1038/cgt.2013.82; published online 24 January 2014Keywords: miR-10b; TGF-b1; EMT; E-cadherin; invasion Breast cancer is one of the most common types of malignant cancers worldwide. Even though there has been considerable progress in the early detection and surgical therapy of breast cancer, there are B350 000 women who die from breast cancer each year. 1 The principal reason for mortality in breast cancer is invasion and metastasis rather than the primary cancer itself; therefore, there is an urgent need to understand the molecular mechanism and pathways that participate in the invasion and metastasis of breast cancer for better and improved treatment of women diagnosed with breast cancer. 2 Epithelial-mesenchymal transition (EMT) is a key step toward cancer metastasis, and E-cadherin is regarded as a main indicator of the epithelial-mesenchymal phenotype switching. 3 E-cadherin loss is suggestive of EMT, and tumor cell invasion and metastasis are associated with EMT. [4][5] EMT is triggered by many signaling pathways-for example, transforming growth factor-b (TGF-b), 6 fibroblast growth factor, 7 epidermal growth factor, 8 hepatocyte growth factor, 9 plateletderived growth factors 10 as well as different isoforms of Wnt proteins, 11 matrix metalloproteinases, 12 bone morphogenic proteins 13 and many others. Among these signaling pathways, TGF-b has been claimed to be critical for induction of the EMT phenotype, and TGF-b as a potent induc...

Purpose Long‐chain noncoding RNAs (lncRNAs) are involved in regulating the sensitivity of cancer cells to chemotherapeutic drugs, but the specific mechanism of action is not well understood. The aim of this study was to investigate the effect of lncRNA growth‐stasis specific transcript 5 (GAS5) on triple‐negative breast cancer (TNBC). Methods Quantitative real‐time polymerase chain reaction and flow cytometry were used to screen lncRNA associated with tumor resistance. Double luciferase reporter gene assay, flow cytometry, and Western blot assay were used to determine whether miRNA 378a‐5p and SUFU were involved in tumor cell apoptosis induced by lncRNA GAS5. A mouse model of subcutaneous xenografts was established to investigate the relationship between lncRNA GAS5 and tumor resistance in vivo. Results In this study, the expression of lncRNA GAS5 was significantly downregulated in cells treated with paclitaxel (PTX) or cisplatin (CIS). Furthermore, TNBC cells with low expression of lncRNA GAS5 had a lower percentage of apoptosis under stress conditions, especially in serum‐free medium. More interestingly, the expression level of lncRNA GAS5 in TNBC patients was associated with tumor resistance to PTX and CIS. In addition, RNA immunoprecipitation experiments confirmed that lncRNA GAS5 and miR‐378 could directly bind to each other. Moreover, the miR‐378a‐5p target of SUFU could promote lncRNA GAS5‐induced apoptosis of TNBC cells. Finally, lncRNA GAS5 overexpressed MDA‐231R could enhance the sensitivity of TNBC to PTX. Conclusion The above results confirmed that lncRNA GAS5 could induce apoptosis in TNBC cells by targeting miR‐378a‐5p/SUFU signaling.

We have identified a set of biomarkers that could discriminate breast cancer from non-cancer controls. An efficient strategy, including SELDI-TOF-MS analysis, HPLC purification, MALDI-TOF-MS trace and LC-MS/MS identification, has been proved very successful.

Introduction: Long non-coding RNAs (lncRNAs) are key regulators in multiple cancers. lncRNA, SNHG1, was shown to be associated with tumorigenesis. However, little is known about the role SNHG1 plays in breast cancer. The aim of the study was to study the role and underlying mechanism of SNHG1 regulation in breast cancer. Methods: Quantitative real-time PCR was used to measure the levels of SNHG1, miR-382 and ZEB1 levels in breast cancer tissue or cells. The proliferation, colony formation, migration and invasion of breast cancer cells, under SNHG1 knockdown achieved by transfection of SNHG1-specific siRNAs, were assessed by Cell Counting Kit-8, colony forming, scratch wound and transwell assays. Bioinformatical analysis and luciferase assay were used to explore the interaction between SNHG1 and its potential miRNA target. Western blot was used to evaluate the expression of epithelial-to-mesenchymal transition (EMT) markers. MDA-MB-231 cells with or without SNHG1 knockdown were used to initiate tumor xenografts in vivo. Tumor growth and expression of SNHG1, miR-382-5p and EMT markers were evaluated. Results: SNHG1 upregulation was observed in breast cancer tissues and cells. Knockdown of SNHG1 attenuated breast cancer proliferation, colony formation, migration and invasion. A miRNA, miR-382-5p, was identified as the target of SNHG1. A reciprocal negative regulation was found between SNHG1 and miR-382-5p. SNHG1 knockdown attenuated EMT both in vitro and in vivo. miR-382-5p transfection reversed the tumor-promoting role by SNHG1. In vivo, SNHG1 knockdown decreased breast tumor growth. Conclusion: SNHG1 promotes breast cancer through the regulation of miR-382-5p and EMT markers. Our results report SNHG1 as a novel miRNA that govern the progression of breast cancer, providing a potential new therapeutic target in breast cancer.

In this paper, we for the first time utilize the microring resonators (MRs) in optical networks-on-chip (ONoCs) to implement thermal sensing without requiring additional hardware or chip area. The challenges in accuracy and reliability that arise from fabrication-induced process variations (PVs) and device-level wavelength tuning mechanism are resolved. We quantitatively model the intrinsic thermal sensitivity of MRs with finegrained consideration of wavelength tuning mechanism. Based on it, a novel PV-tolerant thermal sensor design is proposed. By exploiting the hidden 'redundancy' in wavelength division multiplexing (WDM) technique, our sensor achieves accurate and efficient temperature measurement with the capability of PV tolerance. Evaluation results based on professional photonic component and circuit simulations show an average of 86.49% improvement in measurement accuracy compared to the state-ofthe-art on-chip thermal sensing approach using MRs. Our thermal sensor achieves stable performance in the ONoCs employing dense WDM with an inaccuracy of only 0.8650 K.