http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
임은선 ( Eun Seon Im ),주창우 ( Chang Woo Choo ),김상욱 ( Sang Wook Kim ),성중엽 ( Jung Yeob Sung ),박정우 ( Jeong Woo Park ),김혜령 ( Hae Ryoung Kim ),지병철 ( Byung Chul Jee ) 대한산부인과학회 2009 Obstetrics & Gynecology Science Vol.52 No.6
A 17-year-old girl presented with primary amenorrhea, short stature, and clitomegaly. Her karyotype showed Turner mosaicism of 45,X/46,XY,idic(Y)(q11.23)del(Y)(q11.23). Laparoscopic bilateral gonadectomy was performed and there was testicular tissue in left ovary.
위암에서 에스트로젠 수용체 알파의 소실과 프로모터 과메틸레이션
우인숙,문도호,김성훈,임소희,이명아,강진형,홍영선,이경식,최명규,정인식,박경신 대한내과학회 2004 대한내과학회지 Vol.66 No.5
목적 : 위암에서 에스트로겐 수용체 알파의 프로모터 부위의 메틸레이션으로 인한 위암 조직 내 발현소실이나 불활성화에 대해서는 아직 보고된 바가 없다. 본 연구에서는 위암 세포주와 위암으로 진단 받은 환자들의 조직에서 에스트로젠 수용체 알파의 발현을 평가한 후 위암에서 에스트로젠 수용체 알파의 소실이 5' 프로모터 부위의 메틸레이션과 관련이 있는지를 알고자 하였다. 방법 : 위암 세포주에 대하여 에스트로젠 수용체 알파의 발현을 보기 위하여 웨스턴블롯(12개 세포주)과 RT-PCR(13개 세포주)을 시행하였다. DNA에 대하여 bisulfite modification을 하여 메틸레이션 특이적 중합효소 연쇄반응과 TA 클로닝 후에 염기서열 분석을 시행하였다. 위내시경 조직검사에서 위암으로 진단 받은 42명의 위암 환자의 조직에 대하여 에스트로젠 수용체 알파에 대한 면역조직 화학검사를 시행하였다. 결과 : 위스턴블롯과 RT-PCR결과 KatoⅢ 세포주의 mRNA만 약하게 발현되었으며 모두 음성 반응을 보였다. 메틸레이션 특이적 중합효소 연쇄반응에서 모두 양성이었다. 염기서열 분석에서 ATG 시작 코돈 주변의 CpG island의 methylation을 확인할 수 있었다. 결론 : 위암에서 에스트로젠 수용체 알파의 ATG 시작 코돈주변의 프로모터 부위의 CpG 부위에서 관찰된 메틸레이션은 ER-α유전자의 소실을 일으킬 수 있는 원인의 하나가 될 수 있을 것으로 생각된다. Background : The significance of ER expression and hormone manipulation in gastric cancer is not established. There have been several reports supporting the role of the ER gene as tumor suppressor gene in carcinogenesis. The ER-α gene is located on chromosome 6q25.1. Deletions of the long arm of chromosome 6 are common in gastric carcinoma, suggesting the pressence of tumor suppressor genes in this region. The proportion of ER-positive gastric cancers ranges between 0% and 67% depending on the method of detection. Epigenetic inactivation might explain the loss of ER-α gene expression in gastric cancer. There is no information available regarding the methylation status of the ER-α gene promotor region in gastric cancer so far. The aim of this study was to assess the expression of ER-α in gastric cancer cell lines and determine whether methylation of the 5' promotor region is associated with loss of ER-α expression in gastric cancer. Methods : We investigated such methylation in 13 gastric cancer cell lines. Western blot analysis, reverse transcription-polymerase chain reaction (PCR), methylation-specific PCR (MS-PCR) and bisulfite sequencing analyses were used. Immunohistochemical staining for the ER-α gene was dome for forty-two paraffin embedded tissues from gastric cancer patients. Results : ER-α protein was not detected in any cell line, ER-α mRNA was expressed in only Kato Ⅲline. MS-PCR and bisulfite sequencing showed all thirteen gastric cancer cell lines had methylated CpG regions in their ER-α gene promoters. Immunohistochemical staining of ER-α showed no positivity in any of examined samples. Conclusion : Inactivation of ER-α gene expression in gastric cancer cell lines appears associated with CpG island methylation near the TGA initiation codon of the ER-α gene.
Im Joo-Young,Kim Soo Jin,Park Jong-Lyul,Han Tae-Hee,Kim Woo-il,Kim Inhyub,Ko Bomin,Chun So-Young,Kang Mi-Jung,Kim Bo-Kyung,Jeon Sol A.,Kim Seon-Kyu,Ryu Incheol,Kim Seon-Young,Nam Ki-Hoan,Hwang Inah,Ba 생화학분자생물학회 2024 Experimental and molecular medicine Vol.56 No.-
Cytochrome b5 reductase 3 (CYB5R3) is involved in various cellular metabolic processes, including fatty acid synthesis and drug metabolism. However, the role of CYB5R3 in cancer development remains poorly understood. Here, we show that CYB5R3 expression is downregulated in human lung cancer cell lines and tissues. Adenoviral overexpression of CYB5R3 suppresses lung cancer cell growth in vitro and in vivo. However, CYB5R3 deficiency promotes tumorigenesis and metastasis in mouse models. Transcriptome analysis revealed that apoptosis- and endoplasmic reticulum (ER) stress-related genes are upregulated in CYB5R3-overexpressing lung cancer cells. Metabolomic analysis revealed that CYB5R3 overexpression increased the production of nicotinamide adenine dinucleotide (NAD+) and oxidized glutathione (GSSG). Ectopic CYB5R3 is mainly localized in the ER, where CYB5R3-dependent ER stress signaling is induced via activation of protein kinase RNA-like ER kinase (PERK) and inositol-requiring enzyme 1 alpha (IRE1α). Moreover, NAD+ activates poly (ADP-ribose) polymerase16 (PARP16), an ER-resident protein, to promote ADP-ribosylation of PERK and IRE1α and induce ER stress. In addition, CYB5R3 induces the generation of reactive oxygen species and caspase-9-dependent intrinsic cell death. Our findings highlight the importance of CYB5R3 as a tumor suppressor for the development of CYB5R3-based therapeutics for lung cancer.
Isolation of hyperthermal stress responsive genes in soft coral (Scleronephthya gracillimum)
Woo, Seon-Ock,Jeon, Hye-Young,Lee, Jong-Rak,Song, Jun-Im,Park, Hong-Seog,Yum, Seung-Shic The Korean Society of Toxicogenomics and Toxicopro 2010 Molecular & cellular toxicology Vol.6 No.4
The extensive isolation of genes responsive to hyperthermal stress conditions in soft coral (Scleronephthya gracillimum) is described. Soft coral colonies were exposed to high seawater temperature conditions. Gene candidates whose transcript levels changed in response to hyperthermal conditions were identified by differential display polymerase chain reaction (DD-PCR). Twenty-four types of candidate genes were identified, 18 of which were upregulated in expression and 6 of which were downregulated. The genes were found to function in post-translational modification, protein turnover and chaperones (O); translation, ribosomal structure and biogenesis (J); signal transduction mechanisms (T); defense mechanisms (V); inorganic ion transport and metabolism (P); energy production and conversion (C); cytoskeleton (Z); cell cycle control, cell division and chromosome partitioning (D); lipid transport and metabolism (I); chromatin structure and dynamics (B); transcription (K); replication, recombination and repair (L); secondary metabolites biosynthesis, transport and catabolism (Q); extracellular structures (W); general function prediction (R); and finally, unknown function (S) based on KOG classification. Among these candidates, their expressional changes were confirmed by real-time quantitative PCR (qRT-PCR). These 24 isolated gene candidates were differentially expressed and therefore have great potential as molecular biomarkers for the identification of environmental stressors.
Woo, Seon Min,Seo, Seung Un,Min, Kyoung-jin,Im, Seung-Soon,Nam, Ju-Ock,Chang, Jong-Soo,Kim, Shin,Park, Jong-Wook,Kwon, Taeg Kyu MDPI 2018 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.19 No.5
<P>Corosolic acid is one of the pentacyclic triterpenoids isolated from <I>Lagerstroemia speciose</I> and has been reported to exhibit anti-cancer and anti-proliferative activities in various cancer cells. In the present study, we investigated the molecular mechanisms of corosolic acid in cancer cell death. Corosolic acid induces a decrease of cell viability and an increase of cell cytotoxicity in human renal carcinoma Caki cells. Corosolic acid-induced cell death is not inhibited by apoptosis inhibitor (z-VAD-fmk, a pan-caspase inhibitor), necroptosis inhibitor (necrostatin-1), or ferroptosis inhibitors (ferrostatin-1 and deferoxamine (DFO)). Furthermore, corosolic acid significantly induces reactive oxygen species (ROS) levels, but antioxidants (<I>N</I>-acetyl-<SMALL>L</SMALL>-cysteine (NAC) and trolox) do not inhibit corosolic acid-induced cell death. Interestingly, corosolic acid induces lipid oxidation, and α-tocopherol markedly prevents corosolic acid-induced lipid peroxidation and cell death. Anti-chemotherapeutic effects of α-tocopherol are dependent on inhibition of lipid oxidation rather than inhibition of ROS production. In addition, corosolic acid induces non-apoptotic cell death in other renal cancer (ACHN and A498), breast cancer (MDA-MB231), and hepatocellular carcinoma (SK-Hep1 and Huh7) cells, and α-tocopherol markedly inhibits corosolic acid-induced cell death. Therefore, our results suggest that corosolic acid induces non-apoptotic cell death in cancer cells through the increase of lipid peroxidation.</P>
Jee-Woo Kim,Yeo-Seon Kwon,Yoon-Young Chang,Sung-Ho Hong,Jung-Won Shin,Jung-Im Na,허창훈 대한의학레이저학회 2020 MEDICAL LASERS Vol.9 No.2
Background and Objectives Low-level laser therapy (LLLT) is used widely to promote hair growth in androgenetic alopecia (AGA). This study examined the clinical efficacy and safety of a home-use LLLT device with a newly designed array of light sources and software optimized for individual types of AGA. Materials and Methods The study was a randomized, double-blind, sham device-controlled trial. Forty-eight subjects (39 men and nine women) were assigned randomly in a 2:1 ratio to use either the test device (LG Pra’L HGN1, LG electronics, Korea) or sham device. The subjects used the LLLT device three times a week for 16 weeks. Phototrichogram was used to measure the hair density and hair thickness at 0, 8, and 16-weeks. Adverse events were closely monitored. Results After 16 weeks of using the device, the test group showed a significant increase in hair density and hair thickness compared to the control. In the test group, the hair density increased 6.96 counts/cm2 at eight weeks and 13.67 counts/cm2 at 16 weeks from the baseline. The hair thickness increased 7.21 μm at eight weeks and 11.80 μm at 16 weeks compared to the baseline. Conclusion The home-use LLLT device with a novel array of light sources and an individualized program according to the types of hair loss appears to be an effective and safe treatment modality for both male and female AGA patients.