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Cho, Hana,Kim, Yeon A,Ho, Won-Kyung Korean Society for Molecular Biology 2006 Molecules and cells Vol.22 No.1
<P>Phosphoinositides are critical regulators of ion channel and transporter activity. There are multiple isomers of biologically active phosphoinositides in the plasma membrane and the different lipid species are non-randomly distributed. However, the mechanism by which cells impose selectivity and directionality on lipid movements and so generate a non-random lipid distribution remains unclear. In the present study we investigated which structural elements of phosphoinositides are responsible for their subcellular location and movement. We incubated phosphatidylinositol (PI), phosphatidylinositol 4-monophosphate (PI(4)P) and phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) with short or long acyl chains in CHO and HEK cells. We show that phosphate number and acyl chain length determine cellular location and translocation movement. In CHO cells, PI(4,5)P2 with a long acyl chain was released into the cytosol easily because of a low partition coefficient whereas long chain PI was released more slowly because of a high partition coefficient. In HEK cells, the cellular location and translocation movement of PI were similar to those of PI in CHO cells, whereas those of PI(4,5)P2 were different; some mechanism restricted the translocation movement of PI(4,5)P2, and this is in good agreement with the extremely low lateral diffusion of PI(4,5)P2. In contrast to the dependence on the number of phosphates of the phospholipid head group of long acyl chain analogs, short acyl chain phospholipids easily undergo translocation movement regardless of cell type and number of phosphates in the lipid headgroup.</P>
Nucleotides as Nontoxic Endogenous Endosomolytic Agents in Drug Delivery
Cho, Hana,Cho, Yong-Yeon,Bae, You Han,Kang, Han Chang Wiley (John WileySons) 2014 Advanced Healthcare Materials Vol.3 No.7
<P>Nontoxic endogenous nucleotides such as adenosine triphosphate and guanosine triphosphate have secondary phosphate groups, causing proton-buffering capacity and/or hemolytic activity in endolysosomal pH ranges. Nucleotides co-delivered in single polymeric pDNA nanocarrier induce highly enhanced transfection efficiency with negligible cytotoxicity due to their endosomolytic functions.</P>
Cho, Hana,Park, Ok Hyun,Park, Joori,Ryu, Incheol,Kim, Jeonghan,Ko, Jesang,Kim, Yoon Ki National Academy of Sciences 2015 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.112 No.13
<P><B>Significance</B></P><P>Glucocorticoid receptor (GR) belongs to the nuclear receptor superfamily and functions as a transcription factor. GR regulates various physiological processes, including cell proliferation, energy homeostasis, and inflammation. In this study, we provide molecular evidence for the role of GR in the regulation of mRNA stability, which we term GR-mediated mRNA decay (GMD). Efficient GMD requires a ligand, a GR loaded onto target mRNA, upstream frameshift 1 (UPF1), and proline-rich nuclear receptor coregulatory protein 2. GMD functions in the chemotaxis of human monocytes by targeting <I>chemokine (C-C motif) ligand 2</I> mRNA. Thus, we unravel a previously unappreciated role of GR, which is traditionally considered a transcription factor, in posttranscriptional regulation.</P><P>Glucocorticoid receptor (GR), which was originally known to function as a nuclear receptor, plays a role in rapid mRNA degradation by acting as an RNA-binding protein. The mechanism by which this process occurs remains unknown. Here, we demonstrate that GR, preloaded onto the 5′UTR of a target mRNA, recruits UPF1 through proline-rich nuclear receptor coregulatory protein 2 (PNRC2) in a ligand-dependent manner, so as to elicit rapid mRNA degradation. We call this process GR-mediated mRNA decay (GMD). Although GMD, nonsense-mediated mRNA decay (NMD), and staufen-mediated mRNA decay (SMD) share upstream frameshift 1 (UPF1) and PNRC2, we find that GMD is mechanistically distinct from NMD and SMD. We also identify de novo cellular GMD substrates using microarray analysis. Intriguingly, GMD functions in the chemotaxis of human monocytes by targeting chemokine (C-C motif) ligand 2 (<I>CCL2</I>) mRNA. Thus, our data provide molecular evidence of a posttranscriptional role of the well-studied nuclear hormone receptor, GR, which is traditionally considered a transcription factor.</P>
( Hana Cho ),( Joo-hyuk Son ),( Tae-wook Kong ),( Jiheum Paek ),( Suk-joon Chang ),( Hee-sug Ryu ) 대한산부인과학회 2018 대한산부인과학회 학술대회 Vol.104 No.-
Objective: The aim of this study was to analyze risk factors for septic complications during adjuvant chemotherapy and their impact on survival in patients with advanced epithelial ovarian cancer treated with neoadjuvant chemotherapy (NACT) followed by interval debulking surgery (IDS). Methods: We retrospectively reviewed the medical records of 69 patients with advanced epithelial ovarian cancer from 2004 to 2017. All patients underwent three cycles of NACT followed by IDS and adjuvant chemotherapy. We identified grade 3 or 4 hematologic complications and severe adverse events accompanied by neutropenia, including sepsis or septic shock, that occurred during treatment. Clinicopathologic data including demographic factors, preoperative medical conditions, surgical procedures, and survival times were evaluated. Results: Of 69 patients, 27 (39.1%), 6 (8.8%), and 2 (2.9%) patients experienced grade 3 or 4 neutropenia, anemia, and thrombocytopenia, respectively, during NACT. Thirteen patients (18.8%) had a neutropenic fever with sepsis and 2 patients (2.9%) died of septic shock during adjuvant chemotherapy. Concurrent medical disease, splenectomy during IDS, and anemia or thrombocytopenia during NACT were significant risk factors for septic adverse events. In multivariate analysis, anemia (hemoglobin < 8 g/dL, p = 0.004) during NACT was the only significant factor associated with septic adverse events during adjuvant chemotherapy. Although there was no significant difference in progression-free survival, overall survival was significantly shorter in patients with septic adverse events (median, 82.3 vs. 17.3 months, p = 0.007). Conclusion: Grade 3 anemia during NACT may be an early indicator for septic adverse events during adjuvant chemotherapy. Considering the adverse impact on survival, the interval between IDS and adjuvant chemotherapy should be tailored, and careful follow-up evaluation should be ensured in this patient group.
Cho, Hana,Hong, Kiryong,Strader, Matthew L.,Lee, Jae Hyuk,Schoenlein, Robert W.,Huse, Nils,Kim, Tae Kyu American Chemical Society 2016 Inorganic Chemistry Vol.55 No.12
<P>We present a time-resolved X-ray spectroscopic study of the structural and electronic rearrangements of the photocatalyst Mn-2(CO)(10) upon photodeavage of the metal-metal bond. Our study of the manganese K-edge fine structure reveals details of both the molecular structure and valence charge distribution of the photodissociated radical product. Transient X-ray absorption spectra of the formation of the Mn(CO)(5) radical demonstrate surprisingly small structural modifications between the parent molecule and the resulting two identical manganese monomers. Small modifications of the local valence charge distribution are decisive for the catalytic activity of the radical product. The spectral changes reflect altered hybridization of metal-3d, metal-4p, and ligand-2p orbitals, particularly loss of interligand interaction, accompanied by the necessary spin transition due to radical formation. The spectral changes in the manganese pre- and main-edge region are well-reproduced by time-dependent density functional theory and ab initio multiple scattering calculations.</P>
Hana Cho,Jae-Rin Lee,Jong-Yoon Lee,김현지,Myong-Joon Hahn,Jong-Sun Kang 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-
Chloride intracellular channel 1 (CLIC1) is a promising therapeutic target in cancer due to its intrinsic characteristics; it is overexpressed in specific tumor types and its localization changes from cytosolic to surface membrane depending on activities and cell cycle progression. Ca2+ and reactive oxygen species (ROS) are critical signaling molecules that modulate diverse cellular functions, including cell death. In this study, we investigated the function of CLIC1 in Ca2+ and ROS signaling in A549 human lung cancer cells. Depletion of CLIC1 via shRNAs in A549 cells increased DNA double-strand breaks both under control conditions and under treatment with the putative anticancer agent chelerythrine, accompanied by a concomitant increase in the p-JNK level. CLIC1 knockdown greatly increased basal ROS levels, an effect prevented by BAPTA-AM, an intracellular calcium chelator. Intracellular Ca2+ measurements clearly showed that CLIC1 knockdown significantly increased chelerythrine-induced Ca2+ signaling as well as the basal Ca2+ level in A549 cells compared to these levels in control cells. Suppression of extracellular Ca2+ restored the basal Ca2+ level in CLIC1-knockdown A549 cells relative to that in control cells, implying that CLIC1 regulates [Ca2+]i through Ca2+ entry across the plasma membrane. Consistent with this finding, the L-type Ca2+ channel (LTCC) blocker nifedipine reduced the basal Ca2+ level in CLIC1 knockdown cells to that in control cells. Taken together, our results demonstrate that CLIC1 knockdown induces an increase in the intracellular Ca2+ level via LTCC, which then triggers excessive ROS production and consequent JNK activation. Thus, CLIC1 is a key regulator of Ca2+ signaling in the control of cancer cell survival.
Cho, Hana,Kim, Kyoung Mi,Kim, Yoon Ki Elsevier 2009 Molecular cell Vol.33 No.1
<P><B>Summary</B></P><P>Nonsense-mediated mRNA decay (NMD) is the best-characterized mRNA surveillance mechanism by which aberrant mRNAs harboring premature termination codons are degraded before translation. However, to date, how NMD machinery recruits the general decay complex to faulty mRNAs and degrades those mRNAs remains unclear. Here we identify human proline-rich nuclear receptor coregulatory protein 2 (PNRC2) as a Upf1- and Dcp1a-interacting protein. Downregulation of PNRC2 abrogates NMD, and artificially tethering PNRC2 downstream of a normal termination codon reduces mRNA abundance. Accordingly, PNRC2 preferentially interacts with hyperphosphorylated Upf1 compared with wild-type Upf1 and triggers movement of hyperphosphorylated Upf1 into processing bodies (P bodies). Our observations suggest that PNRC2 plays an essential role in mammalian NMD, mediating the interaction between the NMD machinery and the decapping complex, so as to target the aberrant mRNA-containing RNPs into P bodies.</P>