Binbin Fang

RNA interference (RNAi) is an endogenous post-transcriptional gene regulatory mechanism, where non-coding, double-stranded RNA molecules interfere with the expression of certain genes in order to silence it. Since its discovery, this phenomenon has evolved as powerful technology to diagnose and treat diseases at cellular and molecular levels. With a lot of attention, short interfering RNA (siRNA) therapeutics has brought a great hope for treatment of various undruggable diseases, including genetic diseases, cancer, and resistant viral infections. However, the challenge of their systemic delivery and on how they are integrated to exhibit the desired properties and functions remains a key bottleneck for realizing its full potential. Nanoparticles are currently well known to exhibit a number of unique properties that could be strategically tailored into new advanced siRNA delivery systems. This review summarizes the various nanoparticulate systems developed so far in the literature for systemic delivery of siRNA, which include silica and silicon-based nanoparticles, metal and metal oxides nanoparticles, carbon nanotubes, graphene, dendrimers, polymers, cyclodextrins, lipids, hydrogels, and semiconductor nanocrystals. Challenges and barriers to the delivery of siRNA and the role of different nanoparticles to surmount these challenges are also included in the review.

ADVERTISEMENT RETURN TO ISSUEPREVViewpointNEXTChina's Soil Pollution Control: Choices and ChallengesChangsheng Qu‡, Wei Shi*†, Jing Guo†, Binbin Fang‡, Shui Wang‡, John P. Giesy§∥†, and Peter E. Holm⊥View Author Information† State Key Laboratory of Pollution Control and Resource Reuse, School of the Environment, Nanjing University, Nanjing, China‡ Institute of Soil Environment and Key Laboratory of Environmental Engineering, Jiangsu Academy of Environmental Sciences, Nanjing, China§ Department of Biomedical and Veterinary Biosciences and Toxicology Centre, University of Saskatchewan, Saskatoon, Saskatchewan, Canada∥ State Key Laboratory of Environment Criteria and Risk Assessment, Chinese Research Academy of Environmental Sciences, Beijing, China⊥ Department of Plant and Environmental Sciences, University of Copenhagen and Sino-Danish Centre for Education and Research (SDC), Copenhagen, Denmark*E-mail: [email protected]Cite this: Environ. Sci. Technol. 2016, 50, 24, 13181–13183Publication Date (Web):December 8, 2016Publication History Received6 October 2016Published online8 December 2016Published inissue 20 December 2016https://pubs.acs.org/doi/10.1021/acs.est.6b05068https://doi.org/10.1021/acs.est.6b05068newsACS PublicationsCopyright © 2016 American Chemical Society. This publication is available under these Terms of Use. Request reuse permissions This publication is free to access through this site. Learn MoreArticle Views8505Altmetric-Citations92LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail PDF (771 KB) Get e-AlertscloseSUBJECTS:Environmental pollution,Quality management,Remediation,Soil pollution,Soils Get e-Alerts

// Jia Ma 1, 2 , Binbin Fang 3 , Fanpeng Zeng 3 , Cong Ma 3 , Haijie Pang 3 , Long Cheng 4 , Ying Shi 2 , Hui Wang 3 , Bin Yin 1 , Jun Xia 2 , Zhiwei Wang 1 1 The Cyrus Tang Hematology Center and Collaborative Innovation Center of Hematology, Jiangsu Institute of Hematology, The First Affiliated Hospital, Soochow University, Suzhou 215123, China 2 Department of Biochemistry and Molecular Biology, Bengbu Medical College, Anhui 233030, China 3 Research Center of Clinical Laboratory Science, Bengbu Medical College, Anhui 233030, China 4 Department of Clinical Laboratory, Yijishan Hospital, Wannan Medical College, Wuhu 241000, Anhui, China Correspondence to: Zhiwei Wang, e-mail: zwang6@bidmc.harvard.edu Jun Xia, e-mail: xiajunbbmc@126.com Bin Yin, e-mail: yinbin@suda.edu.cn Keywords: Gemcitabine, miR-223, EMT, invasion, pancreatic cancer Received: October 01, 2014      Accepted: November 08, 2014      Published: December 31, 2014 ABSTRACT Recent studies have demonstrated that acquisition of epithelial-to-mesenchymal transition (EMT) is associated with drug resistance in pancreatic cancer cells; however, the underlying mechanisms are not fully elucidated. Emerging evidence suggests that microRNAs play a crucial role in controlling EMT. The aims of this study were to explore the potential role of miR-223 in governing EMT in gemcitabine-resistant (GR) pancreatic cancer cells. To achieve this goal, real-time reverse transcription-PCR and western blot analysis were used to validate whether GR cells acquired EMT in AsPC-1 and PANC-1 cells. Invasion, migration, and detachment assays were performed to further identify the EMT characteristics in GR cells. The miR-223 inhibitor was used to determine its role in GR-induced EMT. We found that GR cells acquired EMT features, which obtained elongated fibroblastoid morphology, decreased expression of epithelial marker E-cadherin, and up-regulation of mesenchymal markers. Furthermore, we observed that GR cells are associated with high expression of miR-223. Notably, inhibition of miR-223 led to the reversal of EMT phenotype. More importantly, miR-223 governs GR-induced EMT in part due to down-regulation of its target Fbw7 and subsequent upregulation of Notch-1 in pancreatic cancer. Our study implied that down-regulation of miR-223 could be a novel therapy for pancreatic cancer.

Although mitochondrial dysfunction has been observed in various types of human cancer cells, the molecular mechanism underlying mitochondrial dysfunction mediated tumorigenesis remains largely elusive. To further explore the function of mitochondria and their involvement in the pathogenic mechanisms of cancer development, mitochondrial dysfunction clones of breast cancer cells were generated by rotenone treatment, a specific inhibitor of mitochondrial electron transport complex I. These clones were verified by mitochondrial respiratory defect measurement. Moreover, those clones exhibited increased reactive oxygen species (ROS), and showed higher migration and invasive behaviors compared with their parental cells. Furthermore, antioxidant N-acetyl cysteine, PEG-catalase, and mito-TEMPO effectively inhibited cell migration and invasion in these clones. Notably, ROS regulated malignant cellular behavior was in part mediated through upregulation of hypoxia-inducible factor-1 α and vascular endothelial growth factor. Our results suggest that mitochondrial dysfunction promotes cancer cell motility partly through HIF1α accumulation mediated via increased production of reactive oxygen species.