• Development and Reproduction
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• v.16 no.4
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• pp.329-338
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• 2012

The proliferation of embryonic cells or adult stem cells in tissue is critically regulated during development and repair. How limited the proliferation of cells, so far, is not much explored. Cell-cell contact proliferation inhibition is known as a crucial mechanism regulating cell proliferation in vitro and in vivo. In this study we examined the characters of mouse subcutaneous adipose derived stem cells (msADSC) whether they lost or get contact inhibition during in vitro culture. The characters of msADSC growth after confluence were analyzed using confocal microscope and the expression profiles of contact inhibition related genes were analyzed according to the morphological changes using real-time PCR method. msADSC showed overlapping growth between them but not after passage 14. The cell shapes were also changed after passage 14. The expression profiles of genes which are involved in contact inhibition were modified in the msADSC after passage 14. The differentiation ability of msADSCs to adipocyte, chondrocyte and osteocyte was not changed by such changes of gene expression profiles. Based on these results, it is revealed that smADSC were characterized by getting of strong cell-cell contact inhibition after passage 14 but the proliferation and developmental ability were not blocked by the change of cell-cell contact proliferation inhibition. These finding will help to understand the growth of adipose tissue, although further studies are needed to evaluate the physiological meaning of the cell-cell contact proliferation inhibition during in vitro culture of msADSC.

• Journal of the Korea Convergence Society
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• v.12 no.9
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• pp.179-183
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• 2021

This study was carried out examine the effect of Celeriac Extract, which contains various anticancer ingredients, on the proliferation inhibition of human-derived cancer cells and the degree of inhibition. The five cell lines used in the experiment were lung cancer cells A549, prostate cancer cells DU-145, uterine cancer cells HeLa, breast cancer cells MCF-7, and liver cancer cells SNU-182. All cancer cells derived from the human body were used, and the inhibition of cancer cell proliferation with Celeriac Extract 10ug/mL, 100ug/mL, and 1000ug/mL was measured using the CCK-8 method. As a result of examining the inhibition of cancer cell proliferation, Celeriac Extract 1000ug/mL showed significant proliferation inhibition in lung cancer cells A549, prostate cancer cells DU-145, uterine cancer cells HeLa, and liver cancer cells SNU-182, and showed a concentration dependence. However, only a concentration-dependent decrease was observed in breast cancer cells MCF-7.In conclusion, it can be seen that the cell proliferation inhibition mechanisms of Celeriac Extract using various human-derived cancer cell lines provide the potential for cancer prevention and therapeutic development.

• Journal of Digital Policy
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• v.2 no.1
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• pp.31-35
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• 2023

This study was conducted to examine the effect of Broccoli Extract on the proliferation inhibition of human-derived cancer cells and the degree of inhibition. The three cell lines used in the experiment were respiratory system lung cancer cells A549, digestive system liver cancer cells SNU-182 and biliary tract cancer SNU-1196. All cancer cells were derived from the human body, and the CCK-8 method was used to measure the degree of inhibition of cancer cell proliferation. As a result of examining the effect on Broccoli Extract 10ug/mL, 100ug/mL, 1000ug/mL, Broccoli Extract inhibited proliferation in a concentration-dependent manner in most cancer cells, In particular, lung cancer cell A549 and liver cancer cell SNU-182 showed significant proliferation inhibition at 1000ug/mL.As a result, it can be seen that broccoli extract provides potential as a cancer preventive and therapeutic agent for tumor suppression mechanisms proven through cell experiments.

• Journal of Ginseng Research
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• v.20 no.3
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• pp.219-225
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• 1996

This study was performed to investigate the inhibition mechanism of cancer cell proof iferation caused by the petroleum-ether extract of ginseng against human rectum (HRT-18), colon (HT-29), llepatoma (Hep G2) and prostate (LNCaP) cancer cells and monkey kidney cells (Vero 76). Cells were treated with the petroleum-ether extract of ginseng (50 to 200 $\mu\textrm{g}$/ml) in G1 or S phase of the cell cycle, and proliferation and protein kinase C activity were measured. The petroleum-eth or extract of ginseng inhibited proliferation of HRT-18, HT-29, Hep G2 and LNCaP when treated in Gl phase, but not in S phase. This result shows that the ginseng extract arrests the cell cycle in G1 phase, resulting in the inhibition of cell proliferation. At the same concentrations, treatment of the ginseng extract in G1 phase decreased protein kinase C activity, while the treatment in S phase had no effect. This reault suggests that protein kinase C might be involved in the inhibition of the cell cycle and proliferation of cancer cells caused by the petroleum-ether extract of ginseng.

• Biomolecules & Therapeutics
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• v.11 no.2
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• pp.151-156
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• 2003

Cornis fructus have various biological effects and major chemical components have been tannins, saponins, ursolic acids, gallic acids, linoleic acids, morronisides, cornins and loganins. The main aim of the present study is measurment the effect of chloroform extract from Cornis fructus on proliferation inhibition and Cell death. Cells were cultured in the presence of chloroform extracts from Cornis fructus for 48 h. after 48h treatment of B16/F10 melanoma cells with chloroform extracts, the cells were observed a dose-dependent inhibitions of cell viability with cell death in their proliferation. the cells were estimated cell viability, cell number, total DNA fragmentation and chromatin condensation in a dose-dependent manner. It also caused cell death as measured by cell morphology, DNA fragmentation and nucleus chromatin condensation. therefore, these results suggest that chloroform extracts from C. fructus is inhibitory proliferation and is related to cell death in this cells.

• The Korean Journal of Physiology and Pharmacology
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• v.14 no.5
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• pp.299-304
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• 2010

Losartan is a selective angiotensin II (Ang II) type 1 ($AT_1$) receptor antagonist which inhibits vascular smooth muscle cells (VSMCs) contraction and proliferation. We hypothesized that losartan may prevent cell proliferation by activating AMP-activated protein kinase (AMPK) in VSMCs. VSMCs were treated with various concentrations of losartan. AMPK activation was measured by Western blot analysis and cell proliferation was measured by MTT assay and flowcytometry. Losartan dose- and time-dependently increased the phosphorylation of AMPK and its downstream target, acetyl-CoA carboxylase (ACC) in VSMCs. Losartan also significantly decreased the Ang II- or 15% FBS-induced VSMC proliferation by inhibiting the expression of cell cycle associated proteins, such as p-Rb, cyclin D, and cyclin E. Compound C, a specific inhibitor of AMPK, or AMPK siRNA blocked the losartan-induced inhibition of cell proliferation and the $G_0/G_1$ cell cycle arrest. These data suggest that losartan-induced AMPK activation might attenuate Ang II-induced VSMC proliferation through the inhibition of cell cycle progression.

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.2
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• pp.103-109
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• 2003

The cellular mechanisms that contribute to the acceleration of atherosclerosis in diabetes are poorly understood. Therefore, the potential mechanisms involved in the diabetes-dependent increase in vascular smooth muscle cell (VSMC) proliferation was investigated. Using primary culture of VSMC from streptozotocin-induced diabetic rat aorta, cell proliferation assay showed two-fold increase in cell number accompanied with enhanced superoxide generation compared to normal VSMC, 2 days after plating. Both the increased superoxide production and cell proliferation in diabetic VSMC were significantly attenuated by not only tiron (1 mM), a superoxide scavenger, but also by diphenyleneiodonium (DPI; $10{\mu}M$), an NAD(P)H oxidase inhibitor. NAD(P)H oxidase activity in diabetic VSMC was significantly higher than that in control cell, accompanied with increased mRNA expression of p22phox, a membrane subunit of oxidase. Furthermore, inhibition of p22phox expression by transfection of antisense p22phox oligonucleotides into diabetic VSMC resulted in a decrease in superoxide production, which was accompanied by a significant inhibition of cell proliferation. Based on these results, it is suggested that diabetes-associated increase in NAD(P)H oxidase activity via enhanced expression of p22phox contributes to augmented VSMC proliferation in diabetic rats.

• BMB Reports
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• v.55 no.5
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• pp.244-249
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• 2022

Characterized by abnormal proliferation and migration of vascular smooth muscle cells (VSMCs), neointima hyperplasia is a hallmark of vascular restenosis after percutaneous vascular interventions. Vaccinia-related kinase 1 (VRK1) is a stress adaption-associated ser/thr protein kinase that can induce the proliferation of various types of cells. However, the role of VRK1 in the proliferation and migration of VSMCs and neointima hyperplasia after vascular injury remains unknown. We observed increased expression of VRK1 in VSMCs subjected to platelet-derived growth factor (PDGF)-BB by western blotting. Silencing VRK1 by shVrk1 reduced the number of Ki-67-positive VSMCs and attenuated the migration of VSMCs. Mechanistically, we found that relative expression levels of β-catenin and effectors of mTOR complex 1 (mTORC1) such as phospho (p)-mammalian target of rapamycin (mTOR), p-S6, and p-4EBP1 were decreased after silencing VRK1. Restoration of β-catenin expression by SKL2001 and re-activation of mTORC1 by Tuberous sclerosis 1 siRNA (siTsc1) both abolished shVrk1-mediated inhibitory effect on VSMC proliferation and migration. siTsc1 also rescued the reduced expression of β-catenin caused by VRK1 inhibition. Furthermore, mTORC1 re-activation failed to recover the attenuated proliferation and migration of VSMC resulting from shVrk1 after silencing β-catenin. We also found that the vascular expression of VRK1 was increased after injury. VRK1 inactivation in vivo inhibited vascular injury-induced neointima hyperplasia in a β-catenin-dependent manner. These results demonstrate that inhibition of VRK1 can suppress the proliferation and migration of VSMC and neointima hyperplasia after vascular injury via mTORC1/β-catenin pathway.

• Journal of Physiology & Pathology in Korean Medicine
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• v.26 no.4
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• pp.527-531
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• 2012

The flowers and leaves buds of Buddleja officinalis are used to treat eye troubles, hernia, gonorrhea and liver troubles in Asia. The present study investigated the effect of aqueous extract of Buddleja officinalis (ABO) on indoxyl sulfate (IS)-induced inhibition of cell proliferation in HK-2 cells. The HK-2 cells were incubated with 5 mM IS 5 mM in the absence or presence of ABO (2, 5, 10, 20 ${\mu}g/ml$) for 24 hr. The effect of ABO on IS-treated HK-2 cells was investigated by using MTT assay, flow cytometric analysis and Western blot. IS-induced proliferation inhibition was recovered dose-dependently by treatment with ABO. ABO reduced S and G2/M phase cell cycle arrest induced by IS. Recovery effect of ABO on inhibition of cell proliferation by IS is related to the decrease of p21 expression. Taken together, these results suggest that recovery effect of ABO on proliferation of IS-treated HK-2 cells be associated with cell cycle progression through down-regulation of p21 levels.

• Archives of Pharmacal Research
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• v.20 no.6
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• pp.572-578
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• 1997

To gain further insight into how antiestrogens modulate cell function, the effects of antiestrogen on cell proliferation were studied in human breast cancer cells. We examined the effects of trans-tamoxifen on the proliferation of three human breast cancer cell lines that differed in their estrogen receptor contents. Trans-tamoxifen $(1{\mu}M)$ markedly inhibited the estrogen stimulated proliferation of MCF-7 human breast cancer cells that contained high levels of estrogen receptor $(1.15{\pm}0.03 pmole/mg protein)$ over that of control. In T47D cells that contained low levels of estrogen receptor $(0.23{\pm}0.05 pmole/mg protein)$, trans-tamoxifen $(1{\mu}M)$ showed minimal inhibition of estrogen stimulated cell proliferation over that of control. MDA-MB-231 cells, that contained no detectable levels of estrogen receptors, had their growth unaffected by trans-tamoxifen treatment. These results showed their sensitivity to growth inhibition by antiestrogen conrrelated well with their estrogen receptor content. Also we examined the effect of antiestrogen on cellular progestrone receptor level as well as plasminogen activator activity in MCF-7 cells. Trans-tamoxifen $(1{\mu}M)$ showed maximal inhibition of estrogen stimulated progestrone receptor level as well as plasminogen activator activity in MCF-7 cells that were stimulated by estrogen. It is not clear whether these inhibitions of progestrone receptor and plasminogen activator activity by estrogen are related to the antiestrogen inhibition of cell proliferation of MCF-7 cells. From the results of this study, it is clearly demonstrated that trans-tamoxifen is an antiestrogen in MCF-7 human breast cancer cells. Our data suggest that the biological effectiveness of trans-tamoxifen appear to result from its affinity of interaction with the estrogen receptor.