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Ja Lok Ku,Jae Gahb Park 대한암학회 2005 Cancer Research and Treatment Vol.37 No.1
SNU (Seoul National University) cell lines have been established from Korean cancer patients since 1982. Of these 109 cell lines have been characterized and reported, i.e., 17 colorectal carcinoma, 12 hepatocellular carcinoma, 11 gastric carcinoma, 12 uterine cervical carcinoma, 17 B-lymphoblastoid cell lines derived from cancer patients, 5 ovarian carcinoma, 3 malignant mixed Mllerian tumor, 6 laryngeal squamous cell carcinoma, 7 renal cell carcinoma, 9 brain tumor, 6 biliary tract, and 4 pancreatic carcinoma cell lines. These SNU cell lines have been distributed to biomedical researchers domestic and worldwide through the KCLB (Korean Cell Line Bank), and have proven to be of value in various scientific research fields. The characteristics of these cell lines have been reported in over 180 international journals by our laboratory and by many other researchers from 1987. In this paper, the cellular and molecular characteristics of SNU human cancer cell lines are summarized according to their genetic and epigenetic alterations and functional analysis.
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A Long Non-Coding RNA snaR Contributes to 5-Fluorouracil Resistance in Human Colon Cancer Cells
Lee, Heejin,Kim, Chongtae,Ku, Ja-Lok,Kim, Wook,Kim Yoon, Sungjoo,Kuh, Hyo-Jeong,Lee, Jeong-Hwa,Nam, Suk Woo,Lee, Eun Kyung Korean Society for Molecular and Cellular Biology 2014 Molecules and cells Vol.37 No.7
Several types of genetic and epigenetic regulation have been implicated in the development of drug resistance, one significant challenge for cancer therapy. Although changes in the expression of non-coding RNA are also responsible for drug resistance, the specific identities and roles of them remain to be elucidated. Long non-coding RNAs (lncRNAs) are a type of ncRNA (> 200 nt) that influence the regulation of gene expression in various ways. In this study, we aimed to identify differentially expressed lncRNAs in 5-fluorouracil-resistant colon cancer cells. Using two pairs of 5-FU-resistant cells derived from the human colon cancer cell lines SNU-C4 and SNU-C5, we analyzed the expression of 90 lncRNAs by qPCR-based profiling and found that 19 and 23 lncRNAs were differentially expressed in SNU-C4R and SNU-C5R cells, respectively. We confirmed that snaR and BACE1AS were down-regulated in resistant cells. To further investigate the effects of snaR on cell growth, cell viability and cell cycle were analyzed after transfection of siRNAs targeting snaR. Down-regulation of snaR decreased cell death after 5-FU treatment, which indicates that snaR loss decreases in vitro sensitivity to 5-FU. Our results provide an important insight into the involvement of lncRNAs in 5-FU resistance in colon cancer cells.
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Hereditary nonpolyposis colorectal cancer in endometrial cancer patients
Yoon, Sang Nam,Ku, Ja-Lok,Shin, Young-Kyoung,Kim, Kyung-Hee,Choi, Jin-Sung,Jang, Eun-Ja,Park, Hyoung-Chul,Kim, Duck-Woo,Kim, Min A.,Kim, Woo Ho,Lee, Taek Sang,Kim, Jae Weon,Park, Noh-Hyun,Song, Yong-S Wiley Subscription Services, Inc., A Wiley Company 2008 International journal of cancer: Journal internati Vol.122 No.5
<P>Endometrial cancer is the second most common cancer in hereditary nonpolyposis colorectal cancer (HNPCC). It has often been overlooked to explore the possibility of HNPCC in endometrial cancer patients. Our study was to investigate how many HNPCC patients existed among endometrial cancer patients. Among patients who underwent hysterectomy for endometrial cancer at Seoul National University Hospital from 1996 to 2004, 113 patients were included, whose family history and clinical data could be obtained and tumor specimens were available for microsatellite instability (MSI) testing and immunohistochemical (IHC) staining of MLH1, MSH2 and MSH6 proteins. There were 4 (3.5%) clinical HNPCC patients fulfilling the Amsterdam criteria II, and 2 (2/4, 50%) of them carried MSH2 germline mutations. There were also 8 (7.1%) suspected HNPCC (s-HNPCC) patients fulfilling the revised criteria for s-HNPCC, and one (1/8, 12.5%) of them revealed MLH1 germline mutation. In 101 patients, who were not clinical HNPCC or s-HNPCC, 11 patients showed both MSI-high and loss of expression of MLH1, MSH2 or MSH6 proteins, and 2 (2/11, 18.2%) of them showed MSH6 germline mutations. In 113 patients with endometrial cancer, we could find 5 (4.4%) HNPCC patients with MMR germline mutation and 2 (1.8%) clinical HNPCC patients without identified MMR gene mutation. Family history was critical in detecting 3 HNPCC patients with MMR germline mutation, and MSI testing with IHC staining for MLH1, MSH2 and MSH6 proteins was needed in the diagnosis of 2 HNPCC patients who were not clinical HNPCC or s-HNPCC, especially for MSH6 germline mutation. © 2007 Wiley-Liss, Inc.</P>
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Shin, Han-Na,Moon, Hyun-Hye,Ku, Ja-Lok UNKNOWN 2012 INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE Vol.30 No.6
<P>Metastasis of cancer cells is a major cause of death in cancer patients. The process of cancer metastasis includes the proliferation of primary cancer cells, local invasion, intravasation and cancer cell survival in blood flow, extravasation and attachment to secondary organs and metastatic growth in a new environment. In these mechanisms of cancer metastasis, CXC chemokine receptor 4 (CXCR4) and its ligand play an important role. Stromal cell-derived factor-1α (SDF-1α, also known as CXCL12) is well known as a ligand of CXCR4, and macrophage migration-inhibitory factor (MIF) has recently become known as a ligand of CXCR4. In many types of cancers including breast, pancreatic and colorectal cancer (CRC), CXCR4/SDF-1α has been investigated in metastasis-related cancer behavior, which include cell proliferation, adhesion, migration and invasion. However, CXCR4/MIF has rarely been investigated in the metastatic behavior of colon cancer cells. In this report, the effect of SDF-1α or MIF was studied on cell cycle, cell proliferation, adhesion and migration of the CXCR4-expressing colon cancer cell line SW480. SDF-1α or MIF caused a decrease in the number of cells in G0/G1 phase and an increase in the numbers of cells in S and G2/M phases. In addition, SDF-1α or MIF caused an increase in cell proliferation, cell adhesion to fibronectin and migration. AMD3100, a CXCR4 antagonist, attenuated these effects, which included increased cell proliferation, adhesion and migration due to treatment of CXCR4-expressing colon cancer cells with SDF-1α or MIF. In conclusion, SDF-1α or MIF affects the metastasis-related behaviors of CXCR4-expressing colon cancer cells.</P>
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MOON, HYUN-HYE,KIM, SUNG-HEE,KU, JA-LOK Spandidos Publications 2016 ONCOLOGY REPORTS Vol.35 No.1
<P>Resistance to chemotherapeutic agents has been considered as a major reason for the high incidence rate of recurrence and metastasis suffered by colorectal cancer (CRC) patients. ATP-binding cassette sub-family G member 2 (ABCG2) is involved in drug resistance. DNA methylation of the ABCG2 promoter site has a significant influence on the regulation of epigenetic gene expression. In the present study, we investigated whether the methylation status of the ABCG2 promoter is related to drug sensitivity in CRC cell lines. In order to examine the ABCG2 expression level and identify the methylation status, RT-PCR, qRT-PCR analysis, MS-PCR and bisulfite sequencing were conducted on 32 CRC cell lines. SNU-C4, LS174T and NCI-H716 were selected as low ABCG2-expressing and high promoter methylated cell lines. The cell proliferation assay for 5-fluorouracil, oxaliplatin and irinotecan was performed after 5-aza-2'-deoxycytidine (5-aza) treatment in these cell lines. In the 32 CRC cell lines, 25% of the cell lines expressed low or no ABCG2 expression. Of these cell lines, SNU-C4, LS174T and NCI-H716 were hypermethylated at the promoter region, similar to 20%. Demethylation of ABCG2 was induced by 5-aza, which enhanced the ABCG2 expression level and influenced the cell proliferation similar to treatment with the anticancer agents. Our data suggest that the ABCG2 expression level regulated by methylation is related to anticancer drug sensitivity. Based on these results, it can be applied to predict the anticancer drug response.</P>
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Lee Jee Hyung,Kim Haeryoung,이상협,Ku Ja-Lok,Chun Jung Won,Seo Ha Young,Kim Soon Chan,Paik Woo Hyun,Ryu Ji Kon,Lee Sang Kook,Lowy Andrew M.,Kim Yong-Tae 거트앤리버 소화기연관학회협의회 2022 Gut and Liver Vol.16 No.4
Background/Aims: Three-dimensional cultures of human pancreatic cancer tissue also known as “organoids” have largely been developed from surgical specimens. Given that most patients present with locally advanced and/or metastatic disease, such organoids are not representative of the majority of patients. Therefore, we used endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) to collect pancreatic cancer tissues from patients with advanced pancreatic cancer to create organoids, and evaluated their utility in pancreatic cancer research. Methods: Single-pass EUS-FNA samplings were employed to obtain the tissue for organoid generation. After establishment of the organoid, we compared the core biopsy tissues with organoids using hematoxylin and eosin staining, and performed whole exome sequencing (WES) to detect mutational variants. Furthermore, we compared patient outcome with the organoid drug response to determine the potential utility of the clinical application of such organoid-based assays. Results: Organoids were successfully generated in 14 of 20 tumors (70%) and were able to be passaged greater than 5 times in 12 of 20 tumors (60%). Among them, we selected eight pairs of organoid and core biopsy tissues for detailed analyses. They showed similar patterns in hematoxylin and eosin staining. WES revealed mutations in KRAS, TP53, CDKN2A, SMAD4, BRCA1, and BRCA2 which were 93% homologous, and the mean nonreference discordance rate was 5.47%. We observed moderate drug response correlations between the organoids and clinical outcomes in patients who underwent FOLFIRINOX chemotherapy. Conclusions: The established organoids from EUS-FNA core biopsies can be used for a suitable model system for pancreatic cancer research.
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Kim, Sujin,Cho, Yoon Hee,Won, Sungho,Ku, Ja-Lok,Moon, Hyo-Bang,Park, Jeongim,Choi, Gyuyeon,Kim, Sungkyoon,Choi, Kyungho Elsevier 2019 Environment international Vol.130 No.-
<P><B>Abstract</B></P> <P>Exposure to persistent organic pollutants (POPs) during pregnancy is associated with a disruption in thyroid hormone balance. The placenta serves as an important environment for fetal development and also regulates thyroid hormone supply to the fetus. However, epigenetic changes of thyroid regulating genes in placenta have rarely been studied. This study was conducted to evaluate the association between several POP concentrations in maternal serum and DNA methylation of thyroid hormone-related genes in the placenta. The placenta samples were collected from 106 Korean mother at delivery, and the promoter methylation of the placental genes was measured by a bisulfite pyrosequencing. The <I>deiodinase type 3</I> (<I>DIO3</I>), <I>monocarboxylate transporter 8</I> (<I>MCT8</I>), and <I>transthyretin</I> (<I>TTR</I>) genes were selected as the target genes as they play an important role in the regulation of fetal thyroid balance. Because people are exposed to multiple chemicals at the same time, a multiple-POP model using principal component analysis (PCA) was applied to evaluate the association between the multiple POPs exposure and the epigenetic change in placenta. In addition, a single-POP model which includes one chemical each in the statistical model for association was conducted.</P> <P>Based on the single-POP models, serum concentrations of <I>p,p</I>′-dichlorodiphenyldichloroethylene (<I>p,p</I>′-DDE) and brominated diphenyl ether-47 (BDE-47) were significantly associated with an increase in placental <I>DIO3</I> methylation, but only among female infants. Among male infants, a positive association between serum <I>p,p</I>′-DDT and <I>MCT8</I> methylation level was found. According to the multiple-POP models, serum DDTs were positively associated with <I>DIO3</I> methylation in the placenta of female infants, while a positive association with <I>MCT8</I> methylation was observed in those of the male infants. Our observation showed that in utero exposure to DDTs may influence the DNA methylation of <I>DIO3</I> and <I>MCT8</I> genes in the placenta, in a sexually dimorphic manner. These alterations in placental epigenetic regulation may in part explain the thyroid hormone disruption observed among the newborns or infants followed by in utero exposure to POPs.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Promoter DNA methylation of placental genes related to thyroid hormone was measured. </LI> <LI> Some maternal serum POPs were associated with methylation of these placental genes. </LI> <LI> DNA methylation of <I>DIO3</I> and <I>MCT8</I> genes by maternal POP was differed by infant sex. </LI> </UL> </P>
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