Young‐Ah Suh

ORCID: 0000-0002-4694-714X
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About
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Research Areas
  • Cancer, Hypoxia, and Metabolism
  • Cancer-related Molecular Pathways
  • Fibroblast Growth Factor Research
  • Cancer, Lipids, and Metabolism
  • RNA modifications and cancer
  • Cancer Research and Treatments
  • Pancreatic and Hepatic Oncology Research
  • Hepatocellular Carcinoma Treatment and Prognosis
  • Epigenetics and DNA Methylation
  • RNA and protein synthesis mechanisms
  • Cancer Genomics and Diagnostics
  • Cancer Cells and Metastasis
  • Wnt/β-catenin signaling in development and cancer
  • Kruppel-like factors research
  • Metabolism, Diabetes, and Cancer
  • Lung Cancer Treatments and Mutations
  • Monoclonal and Polyclonal Antibodies Research
  • Cell death mechanisms and regulation
  • Autophagy in Disease and Therapy
  • Ferroptosis and cancer prognosis
  • PI3K/AKT/mTOR signaling in cancer
  • Hepatitis C virus research
  • Cancer, Stress, Anesthesia, and Immune Response
  • Ubiquitin and proteasome pathways
  • Advanced biosensing and bioanalysis techniques

Seoul National University
2020-2024

Asan Medical Center
2013-2023

University of Ulsan
2013-2023

Ulsan College
2012-2023

New Generation University College
2023

Seoul National University Hospital
2022

Seoul Medical Center
2016

The University of Texas MD Anderson Cancer Center
2000-2011

Baylor Genetics
2011

University of Colorado Denver
2011

Abstract —Reactive oxygen species have been implicated in the pathogenesis of atherosclerosis, hypertension, and restenosis, part by promoting vascular smooth muscle cell (VSMC) growth. Many VSMC growth factors are secreted act an autocrine manner. Here we demonstrate that cyclophilin A (CyPA), a member immunophilin family, is VSMCs response to oxidative stress mediates extracellular signal–regulated kinase (ERK1/2) activation reactive species. Human recombinant CyPA can mimic effects...

10.1161/01.res.87.9.789 article EN Circulation Research 2000-10-27

We screened a chemical library in MCF-7 cells stably expressing green fluorescent protein (GFP)-conjugated microtubule-associated 1 light chain 3 (LC3) (GFP-LC3-MCF-7) using cell-based assay, and identified BIX-01294 (BIX), selective inhibitor of euchromatic histone-lysine N-methyltransferase 2 (EHMT2), as strong autophagy inducer. BIX enhanced formation GFP-LC3 puncta, LC3-II, free GFP, signifying autophagic activation. Inhibition these phenomena with chloroquine increasement punctate...

10.4161/auto.26308 article EN Autophagy 2013-12-05

Many anticancer agents as well ionizing radiation have been shown to induce autophagy which is originally described a protein recycling process and recently reported play crucial role in various disorders. In HCT116 human colon cancer cells, we found that curcumin, polyphenolic phytochemical extracted from the plant Curcuma longa, markedly induced conversion of microtubule-associated 1 light chain 3 (LC3)-I LC3-II degradation sequestome-1 (SQSTM1) marker autophagosome degradation. Moreover,...

10.4196/kjpp.2011.15.1.1 article EN cc-by-nc Korean Journal of Physiology and Pharmacology 2011-01-01

The transcription factor p53 is a tumor suppressor. As such, the P53 gene frequently altered in human cancers. However, over 80% of mutations found cancers are missense that lead to expression mutant proteins not only lack transcriptional activity but exhibit new functions as well. Recent studies show restoration leads regression mice carrying deletions. therapeutic efficacy restoring tumors containing has been evaluated. Here we demonstrate wild-type halted growth inheriting p53R172H...

10.1172/jci44504 article EN Journal of Clinical Investigation 2011-02-01

p53 levels are tightly regulated in normal cells, and thus, the wild-type protein is nearly undetectable until stimulated through a variety of stresses. In response to stress, released from its negative regulators, mainly murine double minute 2 (Mdm2), allowing be stabilized activate cell-cycle arrest, senescence, apoptosis programs. Many upstream signals that regulate known; however, limited information for regulation mutant exists. Previously, we showed p53R172H similar manner absence Mdm2...

10.1158/0008-5472.can-11-0459 article EN Cancer Research 2011-10-08

Ovarian cancer is the number one cause of death from gynaecological malignancy. Platinum-based and taxol-based chemotherapy has been used as a standard therapy, but intrinsic acquired resistance to major obstacle treat disease. In present study, we found that in chemoresistant ovarian SKOV3/TR cells, interleukin-6 (IL-6), IL-6 receptor signal transducers activators transcription 3 (STAT3) expression well STAT3 phosphorylation were upregulated compared those parental cells. Silencing using...

10.3892/ijo.2014.2808 article EN International Journal of Oncology 2014-12-23

Significance Mutations of p53 occur in approximately 50% human cancer. missense mutations exhibit gain-of-function activities. In this study, we discovered a previously unidentified mechanism mutant osteosarcoma and mammary tumors. Our data indicate that binds to E26 transformation-specific motifs the Pla2g16 phospholipase promoter induce its expression, which leads more aggressive metastatic phenotypes. Thus, study implicates regulation lipid metabolism cancer cells confer gain-of-function....

10.1073/pnas.1404139111 article EN Proceedings of the National Academy of Sciences 2014-07-14

Lupeol, a dietary triterpene, was shown to decrease serum prostate-specific antigen levels and inhibit the tumorigenicity of prostate cancer (CaP) cells in vivo . Here, we show that Lupeol inhibits proliferative potential CaP delineated its mechanism action. Employing focused microarray human CaP-associated genes, found significantly modulates expression level genes such as ERBB2, tissue inhibitor metalloproteinases-3, cyclin D1 matrix metalloproteinase (MMP)-2 are known be associated with...

10.1093/carcin/bgp044 article EN Carcinogenesis 2009-02-20

High levels of the critical p53 inhibitor Mdm4 is common in tumors that retain a wild-type allele, suggesting overexpression an important mechanism for inactivation during tumorigenesis. To test this hypothesis vivo, we generated transgenic mice with widespread expression Mdm4. Two independent lines mice, Mdm4(Tg1) and Mdm4(Tg15), developed spontaneous tumors, most prevalent which were sarcomas. determine whether also cooperated heterozygosity to induce tumorigenesis, p53(+/-) mice. These...

10.1158/0008-5472.can-10-1457 article EN Cancer Research 2010-08-25

Cellular stresses inhibit retinoid signaling, but the molecular basis for this phenomenon has not been revealed. Here, we present evidence that X receptor (RXR) is a substrate both mitogen-activated protein kinase kinase-4 (MKK4/SEK1) and its downstream mediator c-Jun N-terminal (JNK). MKK4/SEK1 JNK recognized distinct features on RXR in DE AB regions, respectively. Phosphorylation by had profound effects biochemical properties of RXR, inhibiting expression genes activated RXR-retinoic acid...

10.1074/jbc.m005490200 article EN cc-by Journal of Biological Chemistry 2000-10-01

Abstract Purpose: Dysregulated expression of PLD1 has emerged as a hallmark feature colorectal cancer, which remains major cause mortality worldwide. Aberrant activation Wnt/β-catenin signaling is critical event in the development cancer. Here, we investigated molecular crosstalk between and PI3K/Akt pathways via inhibitor β-catenin T-cell factor (ICAT), negative regulator signaling. We also explored effect inhibition on growth cancer hyperactivated by Experimental Design: Expression ICAT...

10.1158/1078-0432.ccr-17-0749 article EN Clinical Cancer Research 2017-09-23

To identify the divalent metal Ions that can support self-cleavage activity of genomic ribozyme human hepatitis delta virus (HDV), we tested various ions In reactions catalyzed by HDV88 (683–770 nt) and 88D13 (HDV88 with sequence from 740–752 nt deleted). Among tested, Mg2+, Mn2+, Ca2+ Sr2+ efficiently supported ribozymes. in case 88DI3 ribozyme, other ions, such as Cd2+, Ba2+ Co2+ Pb2+ Zn2+ were also able to reaction some extent (≤10%). presence spermidlne (0.5 mM), cleavage was promoted at...

10.1093/nar/21.14.3277 article EN Nucleic Acids Research 1993-01-01

Aberrant Wnt/β-catenin signalling is implicated in the progression of several human cancers, including non-small cell lung cancer (NSCLC). However, mutations pathway components are uncommon NSCLC, and their epigenetic control remains unclear. Here, we show that KIF3A, a member kinesin-2 family, plays role suppressing NSCLC cells. KIF3A knockdown increases both β-catenin levels transcriptional activity with concomitant promotion malignant potential, such as increased proliferation migration...

10.1038/srep32770 article EN cc-by Scientific Reports 2016-09-06

// Yoon Kyung Jo 1 , Na Yeon Park So Jung Byung-Gyu Kim 2 Ji Hyun Shin Doo Sin Dong-Jun Bae 3 Young-Ah Suh Jeong Ho Chang 4 Eun Lee 5 Sang-Yeob Jin Cheon 3, 6 Dong-Hyung Cho Department of Gerontology, Graduate School East-West Medical Science, Hee University, Yongin, South Korea Leading-edge Research Center for Drug Discovery and Development Diabetes Metabolic Disease, Medicine, Kyungpook National University Hospital, Daegu, Asan Institute Life Sciences, Center, Seoul, Biology Education,...

10.18632/oncotarget.11083 article EN Oncotarget 2016-08-05

Quiescent cancer cells are believed to cause progression after chemotherapy through unknown mechanisms. We show here that human non-small cell lung (NSCLC) line-derived, quiescent-like, slow-cycling (SCC) and residual patient-derived xenograft (PDX) tumors experience activating transcription factor 6 (ATF6)-mediated upregulation of various cytokines, which acts in a paracrine manner recruit fibroblasts. Cancer-associated fibroblasts (CAF) underwent transcriptional COX2 type I collagen...

10.1158/0008-5472.can-19-0631 article EN Cancer Research 2020-03-19

Abstract The increased expression of cyclooxygenase (COX)-2 significantly enhances carcinogenesis and inflammatory reactions, its regulation may be a reasonable target for cancer chemoprevention. We demonstrated previously that deguelin inhibits proliferation premalignant human bronchial epithelial (HBE) cells, such as 1799 cells squamous HBE by regulating phosphatidylinositol-3-kinase Akt activity, which is involved in COX-2 expression. sought to determine the effect on cells. Deguelin...

10.1158/1078-0432.ccr-0833-3 article EN Clinical Cancer Research 2004-02-01
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