| Summary: | 碩士 === 中國醫藥大學 === 生物科技學系碩士班 === 97 === Section I：Chemical proteomic characterization of the LYF-17 inhibits the proliferation in human breast cancer MDA-MB-435
LYF-17 is a kind of 2-PN to spread out extends the thing. Many beneficial properties have been attributed to 2-PN, including inhibition of tubulin polymerization etc.
A fundamental goal of chemical proteomics is to identify target proteins for bioactive small molecules and then apply them to drug discovery and development as valid and drugable targets. Here, we introduce integrated technologies for the rapid identification of target proteins, methodologies for validating them as drugable targets, and applications of chemical proteomics in drug discovery and development. Protein interaction with LYF-17 is a critical step in the effects of LYF-17 on the regulation of various key proteins involved in signal transduction. We have identified a novel molecular target of LYF-17 using affinity chromatography, two-dimensional electrophoresis, and mass spectrometry for protein identification. We found the spots of interest were identified as the Protein disulfide isomerase family A, member 3(PDIA3)；zinc finger protein；beta-site APP-cleaving enzyme 2(BACE2)；T cell receptor alpha(TCRA)；CD44；dysferlin；Ribosomal protein and Microtubule-associated protein 1B (MAP1B).
Section II：LYF-17 Inhibits EMT via the Induction of miR-200c and miR-141 in Human Breast Cancer Cells
MicroRNAs (miRNAs) have been reported that they play important roles in mRNA transcription and protein expression. Recently, miRNAs function as either tumor suppressor genes or oncogenes in many cancer cells. Evidence is emerging rapidly that specific miRNAs might play a role in human cancer pathogenesis. In the current study, we test whether LYF-17 could alter the miRNA expression profiles. We found that LYF-17 induced the expression of miR-200c and miR-141 that regulated epithelial to mesenchymal transition (EMT) by targeting ZEB1. EMT facilitates tissue remodelling during embryonic development and is viewed as an essential early step in tumour metastasis. E-cadherin and Vimentine are target protein for EMT. After treatment of LYF-17, we could show that overexpression of miR-200c and miR-141 led to reduce expression of ZEB1 and Vimentin However, overexpression of miR-200c and miR-141 led to induce expression of E-cadherin, and the other candidate genes in undifferentiated cancer cells.
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