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Kim, Yong-Eun,Kim, Jong Ok,Park, Ki-Sun,Won, Minho,Kim, Kyoon Eon,Kim, Kee K. Korean Society for Molecular and Cellular Biology 2016 Molecules and cells Vol.39 No.8
The RNA-binding protein Rbfox3 is a well-known splicing regulator that is used as a marker for post-mitotic neurons in various vertebrate species. Although recent studies indicate a variable expression of Rbfox3 in non-neuronal tissues, including lung tissue, its cellular function in lung cancer remains largely unknown. Here, we report that the number of RBFOX3-positive cells in tumorous lung tissue is lower than that in normal lung tissue. As the transforming growth factor-${\beta}$ (TGF-${\beta}$) signaling pathway is important in cancer progression, we investigated its role in RBFOX3 expression in A549 lung adenocarcinoma cells. TGF-${\beta}1$ treatment inhibited RBFOX3 expression at the transcriptional level. Further, RBFOX3 depletion led to a change in the expression levels of a subset of proteins related to epithelial-mesenchymal transition (EMT), such as E-cadherin and Claudin-1, during TGF-${\beta}1$-induced EMT. In immunofluorescence microscopic analysis, mesenchymal morphology was more prominent in RBFOX3-depleted cells than in control cells. These findings show that TGF-${\beta}$-induced RBFOX3 inhibition plays an important role in EMT and propose a novel role for RBFOX3 in cancer progression.
Kim, Yong-Eun,Park, Chungoo,Kim, Kyoon Eon,Kim, Kee K. Elsevier 2018 Biochemical and biophysical research communication Vol.499 No.1
<P><B>Abstract</B></P> <P>Alternative splicing is an essential process in eukaryotes, as it increases the complexity of gene expression by generating multiple proteins from a single pre-mRNA. However, information on the regulatory mechanisms for alternative splicing is lacking, because splicing occurs over a short period via the transient interactions of proteins within functional complexes of the spliceosome. Here, we investigated in detail the molecular mechanisms connecting alternative splicing with epigenetic mechanisms. We identified interactions between histone proteins and splicing factors such as Rbfox2, Rbfox3, and splicing factor proline and glutamine rich protein (SFPQ) by <I>in vivo</I> crosslinking and immunoprecipitation. Furthermore, we confirmed that splicing factors were bound to specific modified residues of histone proteins. Additionally, changes in histone methylation due to histone methyltransferase inhibitor treatment notably affected alternative splicing in selected genes. Therefore, we suggested that there may be crosstalk mechanisms connecting histone modifications and RNA-binding proteins that increase the local concentration of RNA-binding proteins in alternative exon loci of nucleosomes by binding specific modified histone proteins, leading to alternative splicing. This crosstalk mechanism may play a major role in epigenetic processes such as histone modification and the regulation of alternative splicing.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Rbfox proteins interact with distinctive histone proteins. </LI> <LI> Modified histone proteins bind directly to RNA-binding proteins. </LI> <LI> Methylation of histone proteins regulates AS. </LI> </UL> </P>
( Dong Hyun Kim ),( Hye-min Kim ),( Pham Thi Thu Huong ),( Ho-jin Han ),( Joonsung Hwang ),( Hyunjoo Cha-molstad ),( Kyung Ho Lee ),( In-ja Ryoo ),( Kyoon Eon Kim ),( Yang Hoon Huh ),( Jong Seog Ahn ) 생화학분자생물학회(구 한국생화학분자생물학회) 2019 BMB Reports Vol.52 No.5
Methylation is a primary epigenetic mechanism regulating gene expression. 5-aza-2’-deoxycytidine is an FDA-approved drug prescribed for treatment of cancer by inhibiting DNA-Methyl-Transferase 1 (DNMT1). Results of this study suggest that prolonged treatment with 5-aza-2’-deoxycytidine could induce centrosome abnormalities in cancer cells and that CEP131, a centrosome protein, is regulated by DNMT1. Interestingly, cancer cell growth was attenuated in vitro and in vivo by inhibiting the expression of Cep131. Finally, Cep131-deficient cells were more sensitive to treatment with DNMT1 inhibitors. These findings suggest that Cep131 is a potential novel anti-cancer target. Agents that can inhibit this protein may be useful alone or in combination with DNMT1 inhibitors to treat cancer. [BMB Reports 2019; 52(5): 342-347]
Kee K. Kim,Yong-Eun Kim,Jong Ok Kim,Ki-Sun Park,원민호,Kyoon Eon Kim 한국분자세포생물학회 2016 Molecules and cells Vol.39 No.8
The RNA-binding protein Rbfox3 is a well-known splicing regulator that is used as a marker for post-mitotic neurons in various vertebrate species. Although recent studies indicate a variable expression of Rbfox3 in non-neuronal tissues, including lung tissue, its cellular function in lung cancer remains largely unknown. Here, we report that the number of RBFOX3-positive cells in tumorous lung tissue is lower than that in normal lung tissue. As the transforming growth factor- (TGF-) signaling pathway is important in cancer progression, we investigated its role in RBFOX3 expression in A549 lung adenocarcinoma cells. TGF-1 treatment inhibited RBFOX3 expression at the transcriptional level. Further, RBFOX3 depletion led to a change in the expression levels of a subset of proteins related to epithelial-mesenchymal transition (EMT), such as E-cadherin and Claudin-1, during TGF-1-induced EMT. In immunofluorescence microscopic analysis, mesenchymal morphology was more prominent in RBFOX3-depleted cells than in control cells. These findings show that TGF--induced RBFOX3 inhibition plays an important role in EMT and propose a novel role for RBFOX3 in cancer progression.
PAS1-modified optical SIS sensor for highly sensitive and specific detection of toluene
Dung, Tran Thi,Lee, Ui Jin,Kim, Myung Hee,Kim, Kyoon Eon,Cho, Hyun Mo,Fermin, Cesar D.,Kim, Dong Hyung,Kim, Moonil Elsevier 2019 Biosensors & bioelectronics Vol.141 No.-
<P><B>Abstract</B></P> <P>We report on a novel solution immersed silicon (SIS) sensor modified with bio-receptor to detect toluene. To perform this approach, bio-receptor PAS1 which specifically interacts with toluene was chosen as a capture agent for SIS ellipsometric sensing. We constructed wild PAS1 and mutant PAS1 (F46A and F79Y) which are toluene binding-defective. Especially, we utilized an easily accessible capturing approach based on silica binding peptide (SBP) for direct immobilization of PAS1 on the SiO<SUB>2</SUB> surfaces. After the immobilization of SBP-tagged PAS1 to the sensing layers, PAS1-based SIS sensor was evaluated for its ability to recognize toluene. As a result, a significant up-shift in Psi (Ψ) was clearly observed with a low limit of detection (LOD) of 0.1 μM, when treated with toluene on wild PAS1-surface, but not on mutant PAS1-sensing layers, indicating the selective interactions between PAS1 and toluene molecule. The PAS1-SIS sensor showed no changes in Psi (Ψ), if any, negligible, when exposed to benzene, phenol, xylene and 4-nitrophenol as negative controls, thereby demonstrating the specificity of interaction between PAS1 and toluene. Taken together, our results strongly indicate that PAS1-modified ellipsometry sensor can provide a high fidelity system for the accurate and selective detection of toluene.</P> <P><B>Highlights</B></P> <P> <UL> <LI> SIS sensor modified with bio-receptor (PAS1) was developed for highly sensitive and specific detection of toluene. </LI> <LI> PAS1 receptor was tagged with silica binding peptide (SBP) to immobilize directly on the biosensing layers. </LI> <LI> The biosensing performance of SIS coupled with PAS1 represented a low detection limit of 0.1 μM to toluene. </LI> <LI> The PAS1-based SIS sensor showed an analytical specificity to toluene without cross-reactions by other toxic molecules. </LI> </UL> </P>
<i>Pseudomonas aeruginosa</i> Eliminates Natural Killer Cells via Phagocytosis-Induced Apoptosis
Chung, Jin Woong,Piao, Zheng-Hao,Yoon, Suk Ran,Kim, Mi Sun,Jeong, Mira,Lee, Suk Hyung,Min, Jeong Ki,Kim, Jae Wha,Cho, You-Hee,Kim, Jin Chul,Ahn, Jeong Keun,Kim, Kyoon Eon,Choi, Inpyo Public Library of Science 2009 PLoS pathogens Vol.5 No.8
<▼1><P><I>Pseudomonas aeruginosa</I> (PA) is an opportunistic pathogen that causes the relapse of illness in immunocompromised patients, leading to prolonged hospitalization, increased medical expense, and death. In this report, we show that PA invades natural killer (NK) cells and induces phagocytosis-induced cell death (PICD) of lymphocytes. <I>In vivo</I> tumor metastasis was augmented by PA infection, with a significant reduction in NK cell number. Adoptive transfer of NK cells mitigated PA-induced metastasis. Internalization of PA into NK cells was observed by transmission electron microscopy. In addition, PA invaded NK cells via phosphoinositide 3-kinase (PI3K) activation, and the phagocytic event led to caspase 9-dependent apoptosis of NK cells. PA-mediated NK cell apoptosis was dependent on activation of mitogen-activated protein (MAP) kinase and the generation of reactive oxygen species (ROS). These data suggest that the phagocytosis of PA by NK cells is a critical event that affects the relapse of diseases in immunocompromised patients, such as those with cancer, and provides important insights into the interactions between PA and NK cells.</P></▼1><▼2><P><B>Author Summary</B></P><P>Phagocytic leukocytes, including neutrophils and macrophages, are critical for innate immunity against invading bacteria. Binding and internalization of bacteria by these immune cells stimulates a variety of anti-microbial activities. Although the immune cells are specialized for elimination of bacteria, cellular apoptosis by bacterial phagocytosis has emerged as an important mechanism of pathogenesis. NK cells are non-phagocytic lymphocytes that are responsible for innate immunity via elimination of virus or bacteria-infected cells, as well as transformed cells. We found that PA invades NK cells and that this phagocytic event results in the generation of ROS within the NK cells, leading to apoptosis. The elimination of NK cells, at least in part, may be responsible for the relapse in PA-infected cancer patients. Based on these findings, studies on the interactions between bacterial determinants and host receptors should provide further insight into the mechanisms of bacterial pathogenesis.</P></▼2>