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Furthermore, we demonstrated that ADSC-derived MIVs promoted the cell migration and invasion of the HUVEC endothelial cells. The PKH26-labeled ADSC-derived MIVs were effectively uptaken into the cytoplasm of HUVEC cells. Collectively, our results demonstrate that the ADSC-derived MIVs can promote migration and invasion abilities of endothelial cells, suggesting pro-angiogenetic potential. Future studies should focus on investigating the roles and mechanisms through which ADSC-derived MIVs regulate angiogenesis. © 2019 Chongqing Medical University. Production and hosting by Elsevier B.V.Prostate cancer (PCa) metastasis is considered the leading cause of cancer death in males. Therapeutic strategies and diagnosis for stage-specific PCa have not been well understood. Rho guanine nucleotide exchange factor 38 (ARHGEF38) is related to tumor cell polarization and is frequently expressed in PCa. Microarray data of PCa were downloaded from GEO and TCGA databases. A total of 243 DEGs were screened, of which, 32 genes were upregulated. The results of enrichment analysis showed the participation of these DEGs in the tumor cell metastasis pathway. ARHGEF38 was significantly up-regulated in the four most prevalent cancers worldwide (p  less then  0.05), and its expression was higher in the tumor samples with higher Gleason score (GS). IHC, qRT-PCR, and western-blot analyses showed the higher expression of ARHGEF38 in PCa than benign prostatic hyperplasia (BPH). In addition, IHC results demonstrated a higher expression of ARHGEF38 in high-grade PCa than the low-grade PCa. © 2019 Chongqing Medical University. Production and hosting by Elsevier B.V.The breast cancer is one of the most common cancer affecting millions of lives worldwide. Though the prevalence of breast cancer is worldwide; however, the developing nations are having a comparatively higher percentage of breast cancer cases and associated complications. The molecular etiology behind breast cancer is complex and involves several regulatory molecules and their downstream signaling. Studies have demonstrated that the CD44 remains one of the major molecule associated not only in breast cancer but also several other kinds of tumors. The complex structure and functioning of CD44 posed a challenge to develop and deliver precise anti-cancerous drugs against targeted tissue. There are more than 20 isoforms of CD44 reported till date associated with several kinds of tumor in the using breast cancer. The success of any anti-cancerous therapy largely depends on the precise drug delivery system, and in modern days nanotechnology-based drug delivery vehicles are the first choice not only for cancer but several other chronic diseases as well. The Carbon nanotubes (CNTs) have shown tremendous scope in delivering the drug by targeting a particular receptor and molecules. Functionalized CNTs including both SWCNTs and MWCNTs are a pioneer in drug delivery with higher efficacy. The present work emphasized mainly on the potential of CNTs including both SWCNTs and MWCNTs in drug delivery for anti-cancerous therapy. The review provides a comprehensive overview of the development of various CNTs and their validation for effective drug delivery. The work focus on drug delivery approaches for breast cancer, precisely targeting CD44 molecule. © 2019 Chongqing Medical University. Production and hosting by Elsevier B.V.RNA-induced silencing complex (RISC) is one of the basic eukaryotic cellular machinery which plays a pivotal role in post-transcriptional gene regulation. Discovery of miRNAs and their role in gene regulation have changed the course of modern biology. The method of gene silencing using small interfering RNAs and miRNAs has become major tool in molecular biology and genetic engineering. Hepatocellular Carcinoma (HCC) is a very common malignancy of liver in developing countries and due to various risk factors; the prevalence of this disease is rapidly increasing throughout the globe. There exists an imbalance in interplay between oncogenes and tumor suppressor genes and their regulation plays a major role in HCC growth, development and metastasis. The regulatory function of RISC and miRNAs make them a very important mediators of cancer signaling in HCC. A939572 in vitro Therefore, targeting the RISC complex for HCC therapy is the need of the time. © 2019 Chongqing Medical University. Production and hosting by Elsevier B.V.The genetic alterations associated with cell transformation are in large measure expressed in the metabolic phenotype as cancer cells proliferate and change their local environment, and prepare for metastasis. Qualitatively, the fundamental biochemistry of cancer cells is generally the same as in the untransformed cells, but the cancer cells produce a local environment, the TME, that is hostile to the stromal cells, and compete for nutrients. In order to proliferate, cells need sufficient nutrients, either those that cannot be made by the cells themselves, or must be made from simpler precursors. However, in solid tumors, the nutrient supply is often limiting given the potential for rapid proliferation, and the poor quality of the vasculature. Thus, cancer cells may employ a variety of strategies to obtain nutrients for survival, growth and metastasis. Although much has been learned using established cell lines in standard culture conditions, it is becoming clear from in vivo metabolic studies that this can also be misleading, and which nutrients are used for energy production versus building blocks for synthesis of macromolecules can vary greatly from tumor to tumor, and even within the same tumor. Here we review the operation of metabolic networks, and how recent understanding of nutrient supply in the TME and utilization are being revealed using stable isotope tracers in vivo as well as in vitro. © 2019 Chongqing Medical University. Production and hosting by Elsevier B.V.Epithelial-mesenchymal Transition (EMT) is a de-differentiation program that imparts tumor cells with the phenotypic and cellular plasticity required for drug resistance, metastasis, and recurrence. This dynamic and reversible events is governed by a network of EMT-transcription factors (EMT-TFs) through epigenetic regulation. Many chromatin modifying-enzymes utilize metabolic intermediates as cofactors or substrates; this suggests that EMT is subjected to the metabolic regulation. Conversely, EMT rewires metabolic program to accommodate cellular changes during EMT. Here we summarize the latest findings regarding the epigenetic regulation of EMT, and discuss the mutual interactions among metabolism, epigenetic regulation, and EMT. Finally, we provide perspectives of how this interplay contributes to cellular plasticity, which may result in the clinical manifestation of tumor heterogeneity. © 2019 Chongqing Medical University. Production and hosting by Elsevier B.V.