Nanjing Medical University

About: Nanjing Medical University is a education organization based out in Nanjing, China. It is known for research contribution in the topics: Cancer & Cell growth. The organization has 52221 authors who have published 37904 publications receiving 635831 citations. The organization is also known as: National Jiangsu Medical College & Nanjing Medical College.

Tailoring the component of protein corona via simple chemistry.

Abstract: Control over the protein corona of nanomaterials allows them to function better. Here, by taking graphene/gold as examples, we comprehensively assessed the association of surface properties with the protein corona. As revealed by in vitro measurements and computations, the interaction between graphene/gold and HSA/IgE was inversely correlated with the hydroxyl group availability, whereas the interaction between that and ApoE was comparatively less relevant. Molecular simulations revealed that the number and the distribution of surface hydroxyl groups could regulate the manner in which nanomaterials interact with proteins. Moreover, we validated that ApoE pre-adsorption before injection enhances the blood circulation of nanomaterials relative to their pristine and IgE-coated counterparts. This benefit can be attributed to the invulnerability of the complementary system provided by ApoE, whose encasement does not increase cytotoxicity. Overall, this study offers a robust yet simple way to create protein corona enriched in dysopsonins to realize better delivery efficacy.

MiR-143 acts as a tumor suppressor by targeting N-RAS and enhances temozolomide-induced apoptosis in glioma

Abstract: // Lin Wang 1,* , Zhu-mei Shi 1,2,* , Cheng-fei Jiang 1,* , Xue Liu 1 , Qiu-dan Chen 1 , Xu Qian 1 , Dong-mei Li 1 , Xin Ge 1 , Xie-feng Wang 2 , Ling-Zhi Liu 3 , Yong-ping You 2 , Ning Liu 2 and Bing-Hua Jiang 1,3 1 State Key Lab of Reproductive Medicine, Department of Pathology, Nanjing Medical University, Nanjing, China 2 Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China 3 Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, USA * These authors contributed equally to this work Correspondence: Bing-Hua Jiang, email: // Ning Liu, email: // Keywords : miR-143, N-RAS, tumor growth, Glioma Received : April 18, 2014 Accepted : June 17, 2014 Published : June 18, 2014 Abstract Therapeutic applications of microRNAs (miRNAs) in RAS-driven glioma were valuable, but their specific roles and functions have yet to be fully elucidated. Here, we firstly report that miR-143 directly targets the neuroblastoma RAS viral oncogene homolog (N-RAS) and functions as a tumor-suppressor in glioma. Overexpression of miR-143 decreased the expression of N-RAS, inhibited PI3K/AKT, MAPK/ERK signaling, and attenuated the accumulation of p65 in nucleus of glioma cells. In human clinical specimens, miR-143 was downregulated where an adverse with N-RAS expression was observed. Furthermore, overexpression of miR-143 decreased glioma cell migration, invasion, tube formation and slowed tumor growth and angiogenesis in a manner associated with N-RAS downregulation in vitro and in vivo . Finally, miR-143 also sensitizes glioma cells to temozolomide (TMZ),the first-line drug for glioma treatment. Taken together, for the first time, our results demonstrate that miR-143 plays a significant role in inactivating the RAS signaling pathway through the inhibition of N-RAS, which may provide a novel therapeutic strategy for treatment of glioma and other RAS-driven cancers.

Diagnostic value of a plasma microRNA signature in gastric cancer: a microRNA expression analysis.

Abstract: The differential expression of microRNAs (miRNAs) in plasma of gastric cancer (GC) patients may serve as a diagnostic biomarker A total of 33 miRNAs were identified through the initial screening phase (3 GC pools vs 1 normal control (NC) pool) using quantitative reverse transcription polymerase chain reaction (qRT-PCR) based Exiqon panel (miRCURY-Ready-to-Use-PCR-Human-panel-I + II-V1M) By qRT-PCR, these miRNAs were further assessed in training (30 GC VS 30 NCs) and testing stages (71 GC VS 61 NCs) We discovered a plasma miRNA signature including five up-regulated miRNAs (miR-185, miR-20a, miR-210, miR-25 and miR-92b), and this signature was evaluated to be a potential diagnostic marker of GC The areas under the receiver operating characteristic curve of the signature were 086, 074 and 087 for the training, testing and the external validation stages (32 GC VS 18 NCs), respectively The five miRNAs were consistently dysregulated in GC tissues (n = 30) Moreover, miR-185 was decreased while miR-20a, miR-210 and miR-92b were increased in arterial plasma (n = 38) However, none of the miRNAs in the exosomes showed different expression between 10 GC patients and 10 NCs In conclusion, we identified a five-miRNA signature in the peripheral plasma which could serve as a non-invasive biomarker in detection of GC

Exosomal circRNA_100284 from arsenite-transformed cells, via microRNA-217 regulation of EZH2, is involved in the malignant transformation of human hepatic cells by accelerating the cell cycle and promoting cell proliferation.

Abstract: Intercellular communication between malignant cells and neighboring nonmalignant cells is involved in carcinogenesis. In the progression of carcinogenesis, exosomes are messengers for intercellular communication. Circular RNAs (circRNAs) are noncoding RNAs with functions that include regulation of the cell cycle and proliferation. However, the functions of exosomal circRNAs are not clear. The present research aimed to determine whether circRNAs secreted from arsenite-transformed human hepatic epithelial (L-02) cells are transferred into normal L-02 cells and become functionally active in the normal cells. The results showed that circRNA_100284 is involved in the malignant transformation of L-02 cells induced by arsenite. The medium from transformed L-02 cells induced upregulation of circRNA_100284, accelerated the cell cycle, and promoted proliferation of normal L-02 cells. Transformed cells transferred circRNA_100284 into normal L-02 cells via exosomes and led to the malignant transformation of the non-transformed cells. Knockdown of circRNA_100284, which reduced circRNA_100284 levels in exosomes derived from transformed L-02 cells, blocked the accelerated cell cycle and reduced proliferation and malignancy. In addition, in normal L-02 cells, exosomal circRNA_100284 derived from arsenite-transformed L-02 cells induced acceleration of the cell cycle and promoted proliferation via acting as a sponge of microRNA-217. Further, exosomal circRNA_100284 was upregulated in the sera of people exposed to arsenite. Thus, exosomes derived from transformed L-02 cells transferred circRNA_100284 to surrounding cells, which induced an accelerated cell cycle and promoted proliferation of normal liver cells and led to the malignant transformation of the non-transformed cells. The findings support the concept that exosomal circRNAs are involved in cell–cell communication during carcinogenesis induced by arsenite.