• Molecules and Cells
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• v.37 no.12
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• pp.881-887
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• 2014

Cell proliferation is tightly controlled by the cell-cycle regulatory proteins, primarily by cyclins and cyclin-dependent kinases (CDKs) in the $G_1$ phase. The ankyrin repeat-rich membrane spanning (ARMS) scaffold protein, also known as kinase D-interacting substrate of 220 kDa (Kidins 220), has been previously identified as a prominent downstream target of neurotrophin and ephrin receptors. Many studies have reported that ARMS/Kidins220 acts as a major signaling platform in organizing the signaling complex to regulate various cellular responses in the nervous and vascular systems. However, the role of ARMS/Kidins220 in cell proliferation and cell-cycle progression has never been investigated. Here we report that knockdown of ARMS/Kidins220 inhibits mouse neuroblastoma cell proliferation by inducing slowdown of cell cycle in the $G_1$ phase. This effect is mediated by the upregulation of a CDK inhibitor p21, which causes the decrease in cyclin D1 and CDK4 protein levels and subsequent reduction of pRb hyperphosphorylation. Our results suggest a new role of ARMS/Kidins220 as a signaling platform to regulate tumor cell proliferation in response to the extracellular stimuli.

• Archives of Plastic Surgery
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• v.32 no.3
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• pp.363-368
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• 2005

It was assumed that the effect of estrogen on wound healing would be variable according to patient's gender and age since estrogen is a sex steroid. This study was designed to determine the variability of the effect of estrogen on proliferation of human dermal fibroblasts and collagen synthesis which are most important in wound healing considering patient's gender and age. Fibroblasts were isolated from the dermis of female patients in premenstrual, menstrual, or postmenopausal age group and that of male patients. The isolated fibroblasts were cultivated in the presence of estrogen($1.0{\mu}g/ml$). The cells were seeded at $5.0{\times}10^3cell/well$ in Dulbecco's Modified Eagle's Medium/Ham's F-12 nutrient including 5% fetal bovine serum in 96-well plates. The cells were incubated for 3 days. For fibroblast proliferation MTT assay method was used. To measure the production of collagen, the collagen type I carboxy- terminal propeptide enzyme immunoassay was carried out. Estrogen stimulated the proliferation of fibroblasts in female patients, but not in male patients. The greatest cell proliferation and collagen synthesis was seen at women in menstrual and postmenopausal age. These results demonstrated that effects of estrogen on dermal fibroblast proliferation and collagen synthesis were variable with gender and age.

• The Plant Pathology Journal
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• v.23 no.3
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• pp.151-154
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• 2007

Phytoplasma was identified from leaf lettuce (Lactuca sativa) cultivated in commercial green-house in Korea. Diseased leaf lettuce revealed proliferation of shoots, and yellowing and shrinking of leaves (lettuce proliferation-K). Polymerase chain reaction (PCR) with universal primer pair P1/P6, and aster yellows (AY) specific primer pair R16F1/R1 amplified 1.5kb and 1.1kb length of DNA fragments, respectively. Nucleotide sequences of 16S rRNA gene were determined (Gen Bank accession no EF489024). Phylogenetic analysis of 16S rDNA showed the closest relationship with AY phytoplasma (GenBank accession no. AY389822 and AY389826), indicating that lettuce proliferation-K is a member of AY. Phytoplasma bodies were detected in phloem sieve tubes of diseased lettuce by transmission electron microscopy. The structures had round or pleomorphic shapes with a diameter of 130-300nm. Phylogenetic analysis of 16S rRNA gene, microscopic observation of phytoplasma bodies and symptomatology indicated that lettuce proliferation-K is caused by phytoplasma in the AY group. This is the first report of phytoplasma disease in lettuce in Korea.

• Korean Journal of Plant Tissue Culture
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• v.25 no.6
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• pp.515-518
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• 1998

The effect of ethylene on the proliferation of rhizomes and plant regeneration were investigated from rhizome segment culture of Cymbidium niveo-marginatum. Ethylene levels in the rhizome culture vessels were reached a maximum after 8 days of culture; total amount of ethylene evolution was much on the initiation of shoot induction than of rhizome proliferation. The treatment with ethephon on rhizomes was inhibited in the proliferation of rhizome and the growth of shoot length; however, the treatment was effective on shoot induction from rhizomes. Aminoethoxyvinylglycine(AVG) 1mg/L was effective on the proliferation of rhizomes and shoot induction from them; however, the proliferation of them was inhibited, and the growth of shoot length was significantly promoted at the concentration of 10mg/L AVG. The presence of $\textrm{AgNO}_{3}$ inhibited in the proliferation of rhizomes and shoot induction from them.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.15
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• pp.6349-6352
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• 2014

The present study was undertaken to determine the roles of insulin in the growth of transplanted breast cancer in nude mice, and the proliferation and migration of MCF-7 human breast cancer cells and assess its influence on downstream signaling pathways. In a xenograft mouse model with injection of MCF-7 human breast cancer cells, tumor size was measured every other day. The insulin level and insulin receptor (IR) were increased in the breast cancer patient tissues. Insulin injected subcutaneously around the tumor site in mice caused increase in the size and weight of tumor masses, and promoted proliferation and migration of MCF-7 cells. The effects of insulin on the increase in the proliferation and migration of MCF-7 human breast cancer cells were abolished by pretreatment with the extracellular regulated kinase (ERK) inhibitor PD98059. Insulin increased the phosphorylation of ERK in the MCF-7 cells. These results indicate that insulin promotes the growth of breast cancer in nude mice, and increases the proliferation and migration of MCF-7 human breast cancer cells via the ERK pathway.

• The Journal of Korean Medicine
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• v.22 no.4
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• pp.37-44
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• 2001

Objectives : Cellular death by apoptosis is an active process, depending on gene transcription and protein synthesis. It was reported that nitric oxide can induce apoptosis in several cancer cell-lines. We have previously observed that proliferation of Ll210 cells was inhibited by the administration of Gleditsiae Spina water extract (GE). In this present study, the mechanism of inhibitory action on the proliferation of L l210 cells was examined. Methods : The cell proliferation was determined by MTT assay and DNA fragmentation was determined by a flow cytometry. Results : The administration of GE decreased proliferation of L1210 cells and enhanced DNA fragmentation in vivo system. DNA fragmentation of L1210 cells was enhanced by co-culture of peritoneal macrophages obtained from GE-administered mice in vitro and it was partly inhibited by L-NMMA, nitric oxide synthetase inhibitor. In addition, GE increased nitric oxide production from peritoneal macrophages of L1210-transplanted mice. Conclusions : These results suggest that the inhibitory action of GE on proliferation of transplanted-L1210 cells is partly caused by an induction of apoptosis via production of nitric oxide in macrophages.

• Journal of Nutrition and Health
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• v.32 no.4
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• pp.394-400
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• 1999

Since it has generally been considered that high-hat diets promote carcinogenesis, fat intake of less than 30% of total calories has been recommended to reduce the risk of cancer. Specific dietary guidelines for fat intake to reduce the risk of colon cancer have not yet been established. In order to determine the level of dietary fat needed the risk of colon cancer, rats were fed one of four experimental fat diets, very low(7% of total calories from corn oil, VLC), low(15% LC), medium (30%, MC), and high fat(45%, HC). Cell proliferation as an intermediate biomarker of color carcinogenesis was measured by the in vivo incorporation of bromodeoxyuridine into DNA. Fecal lipid excretion was measured by gravimetric method. As fat levels in the diet increased, fecal lipid concentrations also increased (VLC

• Journal of Nutrition and Health
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• v.27 no.6
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• pp.552-562
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• 1994

The study was designed to observe the effect of different dietary fats on the incidence of colorectal tumor and in vivo cell proliferation in colon carcinogenesis. Male Sprague Dawley rats were intrarectally infused with chemical carcinogen(methylnitrosourea, MNU) and fed 16%(w/w) fat diet containing one of dietary fats(beef tallow, corn oil, perilla oil) for 30 weeks. To measure in vivo cell proliferation, the incorporation of 5-bromo-2-deoxyuridine(BrdU) into DNA was localized using the monoclonal anti-BrdU antibody. Large number of tumors were found in the distal colon and tumor incidence was increased in the order of perilla oil(57.7%)$\alpha$-linolenic acid rich in perilla oil could have a protective effect against colon cancer compared to saturated fatty acid or n-6 linoleic acid.

• Clinical and Experimental Reproductive Medicine
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• v.29 no.4
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• pp.295-302
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• 2002

Uterine cells carry out proliferation and differentiation for preparation the embryonic implantation during pregnancy. Therefore regulation of the cell proliferation is an essential step for uterine preparation, but there is not much information about the proliferation related genes in pregnant uterus. To identify these implantation specific genes, a PCR-select cDNA subtraction method was employed and got a few genes. One of the identified genes is a novel gene encoding oral tumor suppressor doc-1. To detect the doc-1 expression on the pregnant uterus, dot blotting, RT-PCR, and in situ hybridization were employed. Dot blotting revealed that doc-1 mRNA expression increase after implantation. During normal pregnancy, doc-1 mRNA expression was detected as early as day 1 of pregnancy with RT-PCR. Its expression was increased about 15 times after embryonic implantation. doc-1 transcript was localized in luminal epithelial cells but it was very faint during preimplantation. After starting the implantation, it localized in the stromal cells; heightened expression of doc-1 correlates with intense stromal cell proliferation surrounding the implanting blastocyst on day 6 morning. However in the decidualized cells, the intensity of localized doc-1 mRNA was weak. From those results, it is revealed that doc-1 express at pregnant uterus of the mouse. In addition it is suggested that doc-1 is the gene regulating the proliferation of the luminal epithelial cells and stromal cells during early implantation and decidualization.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.12 no.1
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• pp.79-98
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• 1999

The purpose of this Study was to investigate effect of TakliSodokSan(TSS) on the anti-tumor, immunocytes and nitric oxide(NO) production from mice peritoneal macrophages. This Study estimated the proliferation of L1210 cell lines, A431 cell lines, Hep-G2 cell lines, K562 cell lines, 3T3 cell lines, mouse thymocytes and mouse splenocytes and NO production from pcritoneal macrophages in vitro, and estimated the proliferation of L1210 cells, thymocytes and splenocytcs, NO production from peritoneal macrophages and body weight in L1210 cells-transplanted mice in vivo. The results were obtained as follows; 1. TSS inhibited significantly the proliferation of L1210, A431, Hep-G2, K562 cell lines in vitro. 2. TSS accelerated the proliferation of mice thymocytes and splenocytes in vitro. 3. TSS was not increased the nitric oxide production from mice peritoneal macrophages in vitro. 4. TSS inhibited significantly the proliferation of L1210 cells in Ll210 cells∼transplanted mice. 5. TSS accelerated the proliferation of mice thymocytes and splenocytes In L1210 cells-transplanted mice. 6. TSS was increased significantly the nitric oxide production from mice peritoneal macrophages in L1210 cells-transplanted mice. 7. TSS was increased the body weight as comparing with control group in Ll210 cells-transplanted mice.