Author Description

This dissertation, "Role of MiR-338-5p in Targeting Id-1 and Modulating Esophageal Cancer Cell Invasion and Chemoresistance" by Liang, Han, , was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author.<br> Abstract:<br> Esophageal cancer is the eighth most frequent cancer and the sixth leading cause of cancer mortality in the world. Esophageal squamous cell carcinoma (ESCC) is the predominant histologic subtype of esophageal cancer in Asia. Late diagnosis, metastasis and resistance to chemoradiotherapy all contribute to the low survival rate. Inhibitor of differentiation or DNA binding (Id-1) is overexpressed in esophageal cancer and activates the phosphatidylinositol-3-kinase (PI3K)/Akt signaling pathway, which plays important roles in regulating a wide range of cellular functions including cell proliferation, survival and angiogenesis. In this study, tumor suppressive microRNAs (miRNAs) targeting Id-1 in esophageal cancer were identified. Ten miRNAs containing seed sequences complementary to the 3''UTR of Id-1 were identified using bioinformatics software. Amongst these miRNAs, western blot analysis and dual luciferase assay showed that miR-29b, miR-29c and miR-338-5p could suppress Id-1 by direct binding to its 3''UTR. MTT cell proliferation, colony formation, wound healing and invasion chamber assays were used to show that miR-29b and miR-29c exerted suppressive effects on ESCC cell proliferation, migration and invasion in vitro.<br> Importantly, qRT-PCR and western blot analyses showed that miR-338-5p, which became the focus of this study, was downregulated whereas Id-1 was upregulated in 5-fluorouracil (5-FU) resistant (FR) esoph