Jung-jin Park
Korea University · 生化学・遺伝学・分子生物学
研究室紹介
Professor Jung-jin Park's research lab focuses on the molecular mechanisms underlying cancer progression and metabolic regulation, with a particular emphasis on post-translational modifications such as glycosylation and their roles in tumor metastasis and therapy resistance. The lab investigates the functional roles of glycosyltransferases—especially ST6Gal I—in modulating cell adhesion, radioresistance, and signaling pathways in colorectal and other cancers. Additionally, the lab explores mitochondrial metabolism and insulin signaling in skeletal myogenesis and insulin resistance, identifying key regulators such as NDUFV1 and MG53-IRS-1 interactions. These studies integrate glycobiology, cancer biology, and metabolic regulation to uncover novel therapeutic targets.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
11Abnormal glycosylation due to dysregulated glycosyltransferases and glycosidases is a key phenomenon of many malignancies, including colorectal cancer (CRC). In particular, increased ST6 Gal I (β-galactoside α 2, 6 sialyltransferase) and subsequently elevated levels of cell-surface α 2, 6-linked sialic acids have been associated with metastasis and therapeutic failure in CRC. As many CRC patients experience metastasis to the liver or lung and fail to respond to curative therapies, intensive rese
We have recently demonstrated that ionizing radiation (IR) of cells increased the expression of beta-galactoside alpha-(2,6)-sialyltransferase (ST6Gal I) and the level of glycoprotein sialylation, especially for the key adhesion molecule integrin beta1. In addition, ST6Gal I-mediated sialylation of integrin beta1 contributed to cell adhesion-mediated radioresistance in colon cancer cells. In this study, we examined IR-induced cell adhesion to the extracellular matrix and evaluated the role of in
To address whether mitochondrial biogenesis is essential for skeletal myogenesis, C2C12 myogenesis was investigated after knockdown of NADH dehydrogenase (ubiquintone) flavoprotein 1 (NDUFV1), which is an oxidative phosphorylation complex I subunit that is the first subunit to accept electrons from NADH. The NDUFVI knockdown enhanced C2C12 myogenesis by decreasing the NAD(+)/NADH ratio and subsequently inactivating SIRT1 and SIRT1 activators (pyruvate, SRT1720, and resveratrol) abolished the NDU
Our results suggest that soluble ST6Gal I, possibly in cooperation with the Golgi-bound form, may participate in cancer progression and metastasis prior to being secreted from cancer cells.
Mitsugumin 53 (MG53) is an E3 ligase that interacts with and ubiquitinates insulin receptor substrate-1 (IRS-1) in skeletal muscle; thus, an MG53-IRS-1 interaction disruptor (MID), which potentially sensitizes insulin signaling with an elevated level of IRS-1 in skeletal muscle, is an excellent candidate for treating insulin resistance. To screen for an MID, we developed a bimolecular luminescence complementation system using an N-terminal luciferase fragment fused with IRS-1 and a C-terminal lu
Objective: Although some sporadic reports reveal the link between the homeobox (HOX) genes and ovarian carcinoma, there is no comprehensive analysis of the expression pattern of the class I homeobox genes in ovarian carcinoma that determines the candidate genes involved in ovarian carcinogenesis. Methods: The different patterns of expression of 36 HOX genes were analyzed, including 4 ovarian cancer cell lines and 4 normal ovarian tissues. Using a reverse transcription-polymerase chain reaction (
Gene-manipulated mice were discovered for the first time about a quarter century ago. Since then, numerous sophisticated technologies have been developed and applied to answer key questions about the fundamental roles of the genes of interest. Functional genomics can be characterized into gain-of-function and loss-of-function, which are called transgenic and knock-out studies, respectively. To make transgenic mice, the most widely used technique is the microinjection of transgene-containing vect