• Journal of Gastric Cancer
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• v.20 no.3
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• pp.300-312
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• 2020

Purpose: Circular RNAs (circRNAs) are a new class of RNA molecules whose function is largely unknown. There is a growing evidence that circRNAs play an important regulatory role in the progression of a variety of human cancers. However, the exact roles and the mechanisms of circRNAs in gastric cancer are not clear. In this study, we aimed to elucidate the mechanism of hsa_circ_0005556. Materials and Methods: Real-time quantitative polymerase chain reaction was used to detect the expression of hsa_circ_0005556, miR-4270, and matrix metalloproteinase-19 (MMP19) in gastric cancer tissues and cell lines. The expression of hsa_circ_0005556 in gastric cancer cells was silenced by lentivirus, and cell proliferation, invasion, migration, and tumorigenesis in nude mice were assessed to evaluate the function of hsa_circ_0005556 in gastric cancer. Results: The expression of hsa_circ_0005556 in gastric cancer tissues and gastric cancer cell lines was higher compared to normal controls. In vitro, the downregulation of hsa_ circ_0005556 significantly inhibited proliferation, migration, and invasion of gastric cancer cells. In vivo, the downregulation of hsa_circ_0005556 suppressed tumor growth in nude mice. Conclusions: Our study shows that the hsa_circ_0005556/miR-4270/MMP19 axis is involved in proliferation, migration, and invasion of gastric cancer cells through the competing endogenous RNA (ceRNA) mechanism.

• The Korean Journal of Pharmacology
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• v.30 no.2
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• pp.205-215
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• 1994

It is well known that chronic stimulation with CCK gives rise to growth of exocrine pancreas and to increased content of enzyme proteins in pancreas. However, littls Is known about changes of the secretory function of exocrine pancreas which has been chronically stimulated with CCK, especially about the responsiveness to secretagogues such as CCK, caerulein and carbachol. The present study was performed to investigate the effect of camostat on secretory profiles and the responsiveness to secretagogues of exocrine pancreas by observing in vitro amylase release stimulated by cholecystokinin-octapeptide(CCK-8) and carbachol in dispersed isolated pancreatic acini from camostat-treated rats for 4 or 10 days. The results summarized as follows : 1) The maximal effective concentration of CCK-8 in amylase release in the camostat treated group was greater than control group, but that of carbachol was not different between groups. 2) Analysis of the stimulated amylase release as the percentage of the maximal response revealed that camostat treatment caused right-shift of the dose-response curve of CCK-8. Camostat did not cause significant changes in the dose-response curve of carbachol. 3) There were considerable increases in the amylase release in the camostat-treated group, compared to the control when acini were stimulated with CCK-8 $10^{-9}\;M$ and carbaochol $10^{-6}\;M$, and higher concentrations. 4) There was a reverse correlation between the tissue content and the maximal release(percent of the total content) of amylase. These results suggest that chronic exposure of exocrine pancreas to increased endogenous CCK can enhance the responsiveness of exocrine enzyme secretion to secretagogues, especially at higher concentrations of CCK and carbachol.

• Journal of Environmental Science International
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• v.16 no.2
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• pp.219-225
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• 2007

Endocrine disrupting compounds (EDC's) are chemicals that either mimic endogenous hormones interfering with pharmacokinetics or act by other mechanisms. Some endocrine disrupters were reported to be chemical substances that cause apoptosis in cells. A number of reports have indicated that 1,3-DCP, one of the EDC's may act as an endocrine disrupter and also has possible carcinogenic effects. 1,3-DCP, present in commercial protein hydrolysates used for human nutrition, are genotoxic and 1,3-dichloro-2-propanol induced tumors in rats. In the present study, it was investigated whether 1,3-DCP induces ROS generation and apotosis in A549 adenocarcinoma cells. Here we show that 1,3-DCP inhibits the growth of lung cancer cell lines and generates reactive oxygen species (ROS), a major cause of DNA damage and genetic instability, It was investigated that 1,3-DCP increases G1 phase cells after 12 hours, thereafter abruptly draws A549 cells to G0 state after 24 hours by flow cytometric analysis. 1,3-DCP induces p53 and $p21^{Cip1/WAF1}$ activation time- and dose-dependently by 24 hours, while the level $p21^{Cip1/WAF1}$ was decreased after 48 hours. These results suggest that 1,3-DCP, an EDC's generates ROS and regulates genes involved with cell cycle and apoptosis.

• KOREAN JOURNAL OF CROP SCIENCE
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• v.50 no.5
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• pp.325-331
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• 2005

Seedlings of two rice genotyopes, cvs. Ilpumbyeo and Gancheokbyeo, were exposed to 0, 50 and 100 mM NaCl in nutrient solution for nine days. Plants were collected at the interval of 3 days and organic and inorganic solutes in leaves and roots and antioxidative enzyme activity in leaves were determined. Under salinity, the accumulation of soluble sugars occurred considerably in the older leaves of stressed seedlings compared to younger leaves and roots. The endogenous Na+ contents markedly increased at higher NaCl concentration in leaves and roots of seedlings, though it was higher accumulated in roots. Salinity resulted in an excessive proline accumulation in the stressed plants. A more pronounced increase was observed in Gancheokbyeo leaves. SOD activity in Impumbyeo cannot found any remarkable change, whereas, in Gancheokbyeo, its activity was rapidly decreased. CAT and POD activities increased with an increase in NaCl concentration in both genotypes. In sum­mary, the high capacity of rice seedlings to overcome an unfavorable growth condition such salt stress appears to be related to an adequate partition of organic solutes between shoots and roots and to changes in absorption, transport and re-translocation of salts.

• The Journal of Internal Korean Medicine
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• v.30 no.2
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• pp.375-387
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• 2009

Objective : Gyehyuldeung (GHD) has been widely used in oriental medicine for the treatments of cardiovascular and neurological disorders. Thus, its potential facilitatory activity on axonal regeneration was investigated in the rats. Methods: Sprague-Dawley rats were given crush injury at the sciatic nerve and the changes of axon growth after nerve injury on each nerve injury model were investigated with anti-NF-200 antibody, DiI, GAP-43 protein and Cdc2 protein Results : GHD-mediated enhancement of axonal regeneration after crush injury was measured in both qualitative and quantitative ways by immunofluorescence staining with anti-NF-200 antibody and retrograde tracing of fluorescence dye DiI. GAP-43 protein levels were elevated by GHD treatments in the distal injured sciatic nerve and DRG sensory neurons. The neurite outgrowth of DRG sensory neurons was facilitated by GHD treatment when co-cultured with Schwann cells and astrocytes prepared from injured sciatic nerves and injured spinal cord tissues, respectively. It was observed that Cdc2 protein was up-regulated in co-cultured Schwann cells or astrocytes and Cdc2 protein signals were co-localized to a certain extent with those of phospho-vimentin protein. Conclusions : These results suggest that GHD may play a facilitatory role in axonal regeneration by acting on the injured axons and adjacent non-neuronal cells. The current findings may be useful for the development of therapeutic targets through more specific explorations on molecular interactions between herbal components and endogenous factors.

• Korean Journal of Medicinal Crop Science
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• v.14 no.5
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• pp.303-306
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• 2006

Seed of Codonopsis lanceolata exhibits low germination due to impermeable seed coat. Prolonged seed dormancy can be overcome by the application of gibberellins, as it promotes growth of the embryo and weakens the structures surrounding of embryo. The effects of photoperiod, sugar and gibberellin concentration were investigated at constant temperature for 12 days and 22 days in vitro and invivo conditions respectively. The rate of germination of seeds of Codonopsis lanceolata in wet filter paper in both complete dark and light treatments was significantly lower than that of seed treated with $GA_3$. It clearly indicates that there is significant coat imposed dormancy in the seed of Codonopsis lanceolata. The rate of germination in vivo condition was lower than that of the in vitro condition supplemented with $GA_3$ Thus, the physical dormancy due to impermeable seed coat and low level of endogenous gibberellins in the seed was the cause of poor germination rate in Codonopsis lanceolata.

• BMB Reports
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• v.45 no.11
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• pp.629-634
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• 2012

The human glycoprotein, stanniocalcin 2 (STC2) plays multiple roles in several tumor types, however, its function and clinical significance in hepatocellular carcinoma (HCC) remain unclear. In this study, we detected STC2 expression by quantitative real-time PCR and found STC2 was upregulated in HCC tissues, correlated with tumor size and multiplicity of HCC. Ectopic expression of STC2 markedly promoted HCC cell proliferation and colony formation, while silencing of endogenous STC2 resulted in a reduced cell growth by cell cycle delay in G0/G1 phase. Western blot analysis demonstrated that STC2 could regulate the expression of cyclin D1 and activate extracellular signal-regulated kinase 1/2 (ERK1/2) in a dominant-positive manner. Transwell chamber assay also indicated altered patterns of STC2 expression had an important effect on cell migration. Our findings suggest that STC2 functions as a potential oncoprotein in the development and progression of HCC as well as a promising molecular target for HCC therapy.

• Journal of Chest Surgery
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• v.50 no.3
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• pp.153-162
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• 2017

Background: The mesenchymal-epithelial transition factor (MET) receptor can be overexpressed in solid tumors, including small cell lung cancer (SCLC). However, the molecular mechanism regulating MET stability and turnover in SCLC remains undefined. One potential mechanism of MET regulation involves the C-terminus of Hsp70-interacting protein (CHIP), which targets heat shock protein 90-interacting proteins for ubiquitination and proteasomal degradation. In the present study, we investigated the functional effects of CHIP expression on MET regulation and the control of SCLC cell apoptosis and invasion. Methods: To evaluate the expression of CHIP and c-Met, which is a protein that in humans is encoded by the MET gene (the MET proto-oncogene), we examined the expression pattern of c-Met and CHIP in SCLC cell lines by western blotting. To investigate whether CHIP overexpression reduced cell proliferation and invasive activity in SCLC cell lines, we transfected cells with CHIP and performed a cell viability assay and cellular apoptosis assays. Results: We found an inverse relationship between the expression of CHIP and MET in SCLC cell lines (n=5). CHIP destabilized the endogenous MET receptor in SCLC cell lines, indicating an essential role for CHIP in the regulation of MET degradation. In addition, CHIP inhibited MET-dependent pathways, and invasion, cell growth, and apoptosis were reduced by CHIP overexpression in SCLC cell lines. Conclusion: C HIP is capable of regulating SCLC cell apoptosis and invasion by inhibiting MET-mediated cytoskeletal and cell survival pathways in NCI-H69 cells. CHIP suppresses MET-dependent signaling, and regulates MET-mediated SCLC motility.

• Asian-Australasian Journal of Animal Sciences
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• v.13 no.11
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• pp.1568-1575
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• 2000

Growing pigs (N=25; 18 kg) were used to study effects of L-carnitine and protein intake on plasma carnitine, energy and carnitine balance, and carnitine biosynthesis. Corn-soybean meal basal diets containing low or high protein (13.6% or 18%) were formulated so that protein accretion would be limited by metabolizable energy (ME). Each basal diet was supplemented with 0 or 500 mg/kg L-carnitine and limit fed to pigs for 10 d in a balance trial. Final carnitine concentration was compared with weight/age matched pigs measured on d 0 to calculate carnitine retention rates. Supplementation of carnitine increased (p<0.01) plasma free carnitine (by 250%), short-chain (by 160%) and long-chain acyl-carnitine concentrations (by 80%) irrespective of blood sampling time (p<0.01). The proportion of long-chain carnitine esters decreased by 40% (p<0.01) by carnitine supplementation; whereas, the proportion of short-chain acyl-carnitine concentration was not changed (p>0.10). All criteria of energy balance were unaffected by L-carnitine (p>0.10). Total body carnitine retention was increased by 450% over unsupplemented controls (p<0.01). Carnitine biosynthesis rates in pigs fed diets without L-carnitine were estimated at 6.71 and $10.63{\mu}mol{\cdot}kg^{-1}{\cdot}d^{-1}$ in low protein and high protein groups, respectively. In supplemented pigs, L-carnitine absorption and degradation in the intestinal tract was estimated at 30-40% and 60-70% of L-carnitine intake, respectively. High protein feeding effect did not affected plasma carnitine concentrations, carnitine biosynthesis or carnitine retention (p>0.10). We conclude that endogenous carnitine biosynthesis may be adequate to maintain sufficient tissue levels during growth, but that supplemental dietary carnitine (at 500 ppm) sufficiently increased plasma acyl-carnitine and total body carnitine.

• Molecules and Cells
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• v.28 no.6
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• pp.575-581
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• 2009

Ornithine decarboxylase (ODC) is a rate-limiting enzyme in the biosynthesis of polyamines, which are essential for cell growth, differentiation, and proliferation. This report presents the characterization of an ODC-encoding cDNA (SlitODC) isolated from a moth species, the tobacco cutworm, Spodoptera litura (Lepidoptera); its expression in a polyamine-deficient strain of yeast, S. cerevisiae; and the recovery in polyamine levels and proliferation rate with the introduction of the insect enzyme. SlitODC encodes 448 amino acid residues, 4 amino acids longer than B. mori ODC that has 71% identity, and has a longer C-terminus, consistent with B. mori ODC, than the reported dipteran enzymes. The null mutant yeast strain in the ODC gene, SPE1, showed remarkably depleted polyamine levels; in putrescine, spermidine, and spermine, the levels were > 7, > 1, and > 4%, respectively, of the levels in the wild-type strain. This consequently caused a significant arrest in cell proliferation of > 4% of the wild-type strain in polyamine-free media. The transformed strain, with the substituted SlitODC for the deleted endogenous ODC, grew and proliferated rapidly at even a higher rate than the wild-type strain. Furthermore, its polyamine content was significantly higher than even that in the wild-type strain as well as the spe1-null mutant, particularly with a very continuously enhanced putrescine level, reflecting no inhibition mechanism operating in the putrescine synthesis step by any corresponding insect ODC antizymes to SlitODC in this yeast system.