• Development and Reproduction
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• v.21 no.2
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• pp.193-204
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• 2017

The influence of triploidization on histological characteristics of retina, trunk kidney, liver and midgut tissue, and cell cycle of tail fin and gill tissue in far eastern catfish, Silurus asotus were analyzed. In the infertile triploid fish, the nucleus and/or cell size of secondary proximal tubule cells of trunk kidney, hepatocyte and midgut epithelium are much larger than those of the corresponding cells in the diploid fish (P<0.05). However, triploid tissue showed fewer number of outer nuclear layer in retina and nuclei in secondary proximal tubule of trunk kidney than those for diploid tissue. The mean percentages of the $G_l-$, the S- and the $G_2+M-phase$ fractions were 92.5%, 3.2% and 4.3% in tail fin tissue of diploid, and 93.4%, 2.6% and 4.0% in those of triploid, respectively. There were no significant differences in the percentages of each cell cycle fraction between diploid and triploid. The mean percentages of each phase fractions were 75.1%, 11.1% and 13.8% in gill tissue of diploid and 85.2%, 8.9% and 5.9% in those of triploid, respectively. The differences of cell cycle between tail fin tissue and gill tissue were statistically significant in diploid and triploid (P<0.05). Also, the differences between diploid and triploid were statistically significant in tail fin tissue and gill tissue (P<0.05). Cyclin D1 and cyclin E expressions were not significantly difference between gill tissue and tail fin tissue, and protein expressions of induced triploid were higher than those of diploid. Results from this study suggest that some characteristics in the triploid exhibiting larger cell and nucleus size with fewer number of cell than diploid can be used as an indicator in the identification of triploidization and ploidy level in far eastern catfish.

• Reproductive and Developmental Biology
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• v.33 no.4
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• pp.243-248
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• 2009

To examine the differential expression of proteins during the cycling (70~80% confluences) and G0/G1 (full confluences) phases in porcine fetal fibroblast cells, we used a global proteomics approach by 2-D gel electrophoresis (2-DE) and MALDI-TOF-MS. Cycling cell were harvested at approximately 70% to 80% confluent state while cells in G0/G1 phase were recovered after maintenance of a confluent state for 48 hr. Cellular proteins with isoelectric points ranging between 3.0~10.0, were analyzed by 2-DE with 2 replicates of each sample. A total of approximately 700 spots were detected by 2.D gels stained with Coomassie brilliant blue. On comparing the cell samples obtained from the cycling and G0/G1 phases, a total of 13 spots were identified as differentially expressed proteins, of which 8 spots were up-regulated in the cycling cell and 5 were up-regulated in the G0/G1 phase. Differentially expressed proteins included K3 keratin, similar to serine protease 23 precursor, protein disulfide-isomerase A3, microsomal protease ER-60, alpha-actinin-2, and heat-shock protein 90 beta. The identified proteins were grouped on the basis of their basic functions such as molecular binding, catabolic, cell growth, and transcription regulatory proteins. Our results show expression profiles of key proteins in porcine fetal fibroblast cells during different cell cycle status.

• Biomolecules & Therapeutics
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• v.28 no.6
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• pp.561-568
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• 2020

We examined the anticancer effects of a novel sirtuin inhibitor, MHY2256, on HCT116 human colorectal cancer cells to investigate its underlying molecular mechanisms. MHY2256 significantly suppressed the activity of sirtuin 1 and expression levels of sirtuin 1/2 and stimulated acetylation of forkhead box O1, which is a target protein of sirtuin 1. Treatment with MHY2256 inhibited the growth of the HCT116 (TP53 wild-type), HT-29 (TP53 mutant), and DLD-1 (TP53 mutant) human colorectal cancer cell lines. In addition, MHY2256 induced G0/G1 phase arrest of the cell cycle progression, which was accompanied by the reduction of cyclin D1 and cyclin E and the decrease of cyclin-dependent kinase 2, cyclin-dependent kinase 4, cyclin-dependent kinase 6, phosphorylated retinoblastoma protein, and E2F transcription factor 1. Apoptosis induction was shown by DNA fragmentation and increase in late apoptosis, which were detected using flow cytometric analysis. MHY2256 downregulated expression levels of procaspase-8, -9, and -3 and led to subsequent poly(ADP-ribose) polymerase cleavage. MHY2256-induced apoptosis was involved in the activation of caspase-8, -9, and -3 and was prevented by pretreatment with Z-VAD-FMK, a pan-caspase inhibitor. Furthermore, the autophagic effects of MHY2256 were observed as cytoplasmic vacuolation, green fluorescent protein-light-chain 3 punctate dots, accumulation of acidic vesicular organelles, and upregulated expression level of light-chain 3-II. Taken together, these results suggest that MHY2256 could be a potential novel sirtuin inhibitor for the chemoprevention or treatment of colorectal cancer or both.

• Mycobiology
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• v.48 no.3
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• pp.219-227
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• 2020

Androgen-independent prostate cancer accounts for mortality in the world. In this study, various extracts of a medical fungus dubbed Ganoderma formosanum were screened for inhibition of DU145 cells, an androgen-independent prostate cancer cell line. Results demonstrated that both hexane (GF-EH) and butanol (GF-EB) fraction of G. formosanum ethanol extract inhibited DU145 cell viability in a dose-dependent manner. GF-EH induced cell-cycle arrest in G1 phase of DU145 cells via downregulation of cyclin E2 protein expression. In addition, GF-EB triggered extrinsic apoptosis of DU145 cells by activating caspase 3 gene expression resulting in programed cell death. Above all, both GF-EH and GF-EB show lower toxicity to normal human fibroblast cell line compared to DU145 cell, implying that they possess specific drug action on cancer cells. This study provides a molecular basis of G. formosanum extract as a potential ingredient for treatment of androgen-independent prostate cancer.

• BMB Reports
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• v.40 no.6
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• pp.1009-1015
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• 2007

In this communication, we report the efficacy of $\beta$-carotene towards differentiation and apoptosis of leukemia cells. Dose ($20{\mu}M$) and time dependence (12 h) tests of $\beta$-carotene showed a higher magnitude of decrease (significance p < 0.05) in cell numbers and cell viability in HL-60 cells than U937 cells but not normal cell like Peripheral blood mononuclear cell (PBMC). Microscopical observation of $\beta$-carotene treated cells showed a distinct pattern of morphological abnormalities with inclusion of apoptotic bodies in both leukemia cell lines. When cells were treated with $20{\mu}M$ of $\beta$-carotene, total genomic DNA showed a fragmentation pattern and this pattern was clear in HL-60 than U937 cells. Both the cell lines, on treatment with $\beta$-carotene, showed a clear shift in $G_1$ phase of the cell cycle. In addition the study also revealed anti-oxidant properties of $\beta$-carotene since there was reduction in relative fluorescent when treated than the control at lower concentration. Collectively this study shows the dual phenomenon of apoptosis and differentiation of leukemia cells on treatment with $\beta$-carotene.

• Archives of Pharmacal Research
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• v.26 no.12
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• pp.1055-1060
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• 2003

Lysophosphatidic acid (LPA) is a well-known mitogen in various cell types. However, we found that LPA inhibits melanocyte proliferation. Thus, we further investigated the possible signaling pathways involved in melanocyte growth inhibition. We first examined the regulation of the three major subfamilies of mitogen-activated protein (MAP) kinases and of the Akt pathway by LPA. The activations of extracellular signal-regulated protein kinase (ERK) and c-Jun N-terminal kinase (JNK) were observed in concert with the inhibition of melanocyte proliferation by LPA, whereas p38 MAP kinase and Akt were not influenced by LPA. However, the specific inhibition of the ERK or JNK pathways by PD98059 or D-JNKI1, respectively, did not restore the antiproliferative effect. We next examined changes in the expression of cell cycle related proteins. LPA decreased cyclin $D_1 and cyclin D_2$ levels but increased $p21^{WAF1/CIP1}$ (p21) and $p27^{KIP1}$ (p27) levels, which are known inhibitors of cyclin-dependent kinase. Flow cytometric analysis showed the inhibition of DNA synthesis by a reduction in the S phase and an increase in the $G_0/G_1$ phase of the cell cycle. Our results suggest that LPA induces cell cycle arrest by regulating the expressions of cell cycle related proteins.

• The Korea Genome Conference
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• 2005.09a
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• pp.60-60
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• 2005

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.15
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• pp.6513-6519
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• 2015

Background: Recent attention on chemotherapeutic intervention against cancer has been focused on discovering and developing phytochemicals as anticancer agents with improved efficacy, low drug resistance and toxicity, low cost and limited adverse side effects. In this study, we investigated the effects of Curcuma C20-dialdehyde on growth, apoptosis and cell cycle arrest in colon and cervical cancer cell lines. Materials and Methods: Antiproliferative, apoptosis induction, and cell cycle arrest activities of Curcuma C20-dialdehyde were determined by WST cell proliferation assay, flow cytometric Alexa fluor 488-annexin V/propidium iodide (PI) staining and PI staining, respectively. Results: Curcuma C20 dialdehyde suppressed the proliferation of HCT116, HT29 and HeLa cells, with IC50 values of $65.4{\pm}1.74{\mu}g/ml$, $58.4{\pm}5.20{\mu}g/ml$ and $72.0{\pm}0.03{\mu}g/ml$, respectively, with 72 h exposure. Flow cytometric analysis revealed that percentages of early apoptotic cells increased in a dose-dependent manner upon exposure to Curcuma C20-dialdehyde. Furthermore, exposure to lower concentrations of this compound significantly induced cell cycle arrest at G1 phase for both HCT116 and HT29 cells, while higher concentrations increased sub-G1 populations. However, the concentrations used in this study could not induce cell cycle arrest but rather induced apoptotic cell death in HeLa cells. Conclusions: Our findings suggest that the phytochemical Curcuma C20-dialdehyde may be a potential antineoplastic agent for colon and cervical cancer chemotherapy and/or chemoprevention. Further studies are needed to characterize the drug target or mode of action of the Curcuma C20-dialdehyde as an anticancer agent.

• Proceedings of the Zoological Society Korea Conference
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• 1998.10b
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• pp.322.1-322
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• 1998

No Abstract, See Full Text

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.91.2-91.2
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• 2003

Cyclin-dependent kinases (CDKs) regulate the cell division cycle, apoptosis, transcription and differentiation. Inhibition of CDK is a promising target in development of anti-cancer agents. An indirubin analog (AGM01l), a CDK inhibitor, is a synthetic compound that inhibits human cancer cell growth in vitro. AGM01l showed a potent cytotoxicity in cultured human cancer cell lines (IC$\sub$50/ = 5.43 ${\mu}$M for A549, human colon cancer cell; IC$\sub$50/ = 1.21 ${\mu}$M for SNU-638, human stomach cancer cell; IC$\sub$50/ 9.23 ${\mu}$M for HL-60, human leukemia cell). (omitted)