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PEBP2-β/CBF-β-dependent phosphorylation of RUNX1 and p300 by HIPK2: implications for leukemogenesis
Wee, Hee-Jun,Voon, Dominic Chih-Cheng,Bae, Suk-Chul,Ito, Yoshiaki American Society of Hematology 2008 Blood Vol.112 No.9
<P>The heterodimeric transcription factor RUNX1/PEBP2-β (also known as AML1/CBF-β) is essential for definitive hematopoiesis. Here, we show that interaction with PEBP2-β leads to the phosphorylation of RUNX1, which in turn induces p300 phosphorylation. This is mediated by homeodomain interacting kinase 2 (HIPK2), targeting Ser249, Ser273, and Thr276 in RUNX1, in a manner that is also dependent on the RUNX1 PY motif. Importantly, we observed the in vitro disruption of this phosphorylation cascade by multiple leukemogenic genetic defects targeting RUNX1/CBFB. In particular, the oncogenic protein PEBP2-β-SMMHC prevents RUNX1/p300 phosphorylation by sequestering HIPK2 to mislocalized RUNX1/β-SMMHC complexes. Therefore, phosphorylation of RUNX1 appears a critical step in its association with and phosphorylation of p300, and its disruption may be a common theme in RUNX1-associated leukemogenesis.</P>
Mutant p53-Notch1 Signaling Axis Is Involved in Curcumin-Induced Apoptosis of Breast Cancer Cells
Yun-Hee Bae,Jong Hyo Ryu,Hyun-Joo Park,Kwang Rok Kim,Hee-Jun Wee,Ok-Hee Lee,Hye-Ock Jang,Moon-Kyoung Bae,Kyu-Won Kim,Soo-Kyung Bae 대한생리학회-대한약리학회 2013 The Korean Journal of Physiology & Pharmacology Vol.17 No.4
Notch1 has been reported to be highly expressed in triple-negative and other subtypes of breast cancer. Mutant p53 (R280K) is overexpressed in MDA-MB-231 triple-negative human breast cancer cells. The present study aimed to determine whether the mutant p53 can be a potent transcriptional activator of the Notch1 in MDA-MB-231 cells, and explore the role of this mutant p53-Notch1 axis in curcumin-induced apoptosis. We found that curcumin treatment resulted in an induction of apoptosis in MDA-MB-231 cells, together with downregulation of Notch1 and its downstream target, Hes1. This reduction in Notch1 expression was determined to be due to the decreased activity of endogenous mutant p53. We confirmed the suppressive effect of curcumin on Notch1 transcription by performing a Notch1 promoter-driven reporter assay and identified a putative p53-binding site in the Notch1 promoter by EMSA and chromatin immunoprecipitation analysis. Overexpression of mutant p53 increased Notch1 promoter activity, whereas knockdown of mutant p53 by small interfering RNA suppressed Notch1 expression, leading to the induction of cellular apoptosis. Moreover, curcumin-induced apoptosis was further enhanced by the knockdown of Notch1 or mutant p53, but it was decreased by the overexpression of active Notch1. Taken together, our results demonstrate, for the first time, that Notch1 is a transcriptional target of mutant p53 in breast cancer cells and suggest that the targeting of mutant p53 and/or Notch1 may be combined with a chemotherapeutic strategy to improve the response of breast cancer cells to curcumin.
Mutant p53-Notch1 Signaling Axis Is Involved in Curcumin-Induced Apoptosis of Breast Cancer Cells
Bae, Yun-Hee,Ryu, Jong Hyo,Park, Hyun-Joo,Kim, Kwang Rok,Wee, Hee-Jun,Lee, Ok-Hee,Jang, Hye-Ock,Bae, Moon-Kyoung,Kim, Kyu-Won,Bae, Soo-Kyung The Korean Society of Pharmacology 2013 The Korean Journal of Physiology & Pharmacology Vol.17 No.4
Notch1 has been reported to be highly expressed in triple-negative and other subtypes of breast cancer. Mutant p53 (R280K) is overexpressed in MDA-MB-231 triple-negative human breast cancer cells. The present study aimed to determine whether the mutant p53 can be a potent transcriptional activator of the Notch1 in MDA-MB-231 cells, and explore the role of this mutant p53-Notch1 axis in curcumin-induced apoptosis. We found that curcumin treatment resulted in an induction of apoptosis in MDA-MB-231 cells, together with downregulation of Notch1 and its downstream target, Hes1. This reduction in Notch1 expression was determined to be due to the decreased activity of endogenous mutant p53. We confirmed the suppressive effect of curcumin on Notch1 transcription by performing a Notch1 promoter-driven reporter assay and identified a putative p53-binding site in the Notch1 promoter by EMSA and chromatin immunoprecipitation analysis. Overexpression of mutant p53 increased Notch1 promoter activity, whereas knockdown of mutant p53 by small interfering RNA suppressed Notch1 expression, leading to the induction of cellular apoptosis. Moreover, curcumin-induced apoptosis was further enhanced by the knockdown of Notch1 or mutant p53, but it was decreased by the overexpression of active Notch1. Taken together, our results demonstrate, for the first time, that Notch1 is a transcriptional target of mutant p53 in breast cancer cells and suggest that the targeting of mutant p53 and/or Notch1 may be combined with a chemotherapeutic strategy to improve the response of breast cancer cells to curcumin.
Benzoic Acid Enhances Embryo Implantation through LIF-Dependent Expression of Integrin αVβ3 and αVβ5
( Hee-jung Choi ),( Tae-wook Chung ),( Mi-ju Park ),( Hyung Sik Kim ),( Sooseong You ),( Myeong Soo Lee ),( Bo Sun Joo ),( Kyu Sup Lee ),( Keuk-jun Kim ),( Gabbine Wee ),( Choong-yong Kim ),( Cheorl-h 한국미생물 · 생명공학회 2017 Journal of microbiology and biotechnology Vol.27 No.4
Embryo implantation is the crucial step for a successful pregnancy. Diverse factors, including adhesion molecules, growth factors, and cytokines are important for embryo implantation through improving endometrial receptivity. Benzoic acid (BA), a component of various plants, has been shown to have antifungal and antioxidant effects. However, the effect of BA on embryo implantation remains unknown. Here, we showed the contribution of BA for the enhancement of endometrial receptivity through the leukemia inhibitory factor (LIF)-dependent increase of integrin αV, β3, and β5 expression. Furthermore, in vivo study using a mifepristone-induced implantation failure model showed that BA definitely improves the numbers of implantation embryos. Taken together, we suggest that BA has a novel function for embryo implantation through the up-regulation of LIF-mediated integrins, and may be a candidate for therapeutic medicine to increase the pregnancy rate.
박의현,천병렬,전재은,조용근,채성철,이영숙,손재희 경북대학교 병원 2002 경북대학교병원의학연구소논문집 Vol.6 No.1
Objectives: This study was conducted to examine the 30-day survial rate and prognostic factors of acute myocardial infarction(MI). Methods: Two hundred patients with acute MI were recruited from the Kyungpook university hospital in Daegu city from 1 july 1997 to 30 june 1998.Data were collected by interviewing with a questionnaire and their medical chats were reviewed by cardiologists.The survial status of patients were followes by telephone interview. Results: The 30-dat case fatality rate(CFR) of acute MI was 9%.Prognostic factor significantly associated with CFR were age, smoking, total cholesterol, anythmia, aspirin treatment, and beta-blocker treatment by simple analysis(p<0.05); Above age 70(21.6%) versus below age 70(4.7%), non-smoker(22.0%) vs.smoker(4.7%), above cholesterol 200㎎/㎗(2.2%) vs.below (14.5%), arrhythmia(29.0%) vs.no arrhythmia(5.3%), no aspirin(46.7%) vs.aspirin (6.0%), and no beta-blocker(22.6%) vs. beta-blocker(4.1%).In multiple logistic regression analysis, the significant prognostic factors were smoking,arrtythmia, and aspirin treatment(p<0.05).The relavite risk of smoking(yes/no)was 0.43(95% CI;0.31∼0.69),arrtythmia(yes/no)3.63(95% CI; 1.25∼6.91) aspirin(yes/no)0.33(95% CI;0.11∼0.65),respectively. COnclusion: The 30day case fatality rate of acute MI was 9% and the significant prognostic factor were smoking, arrtythmia, and aspirin treatment.
The rate of ischemia-driven target lesion revascularization of paclitaxel-eluting stents (초)
( Sun Hee Park ),( Hun Sik Park ),( Jang Hoon Lee ),( Hyeon Min Ryu ),( Myung Hwan Bae ),( Yong Seop Kwon ),( Dong Heon Yang ),( Yong Keun Cho ),( Shung Chull Chae ),( Jae Eun Jun ),( Wee Hyun Park ) 대한내과학회 2008 대한내과학회 추계학술대회 Vol.2008 No.-