• Korean Journal of Microbiology
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• v.36 no.4
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• pp.312-315
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• 2000

Paecilomyces tenuipes DGUM 32001, an entomopathogenic fungus, was examined to evaluate in vitro cytotoxicity against several human cancer cells. The fruiting bodies of P. tenuipes were extracted with methanol and fractioned with some organic solvents i.e. chloroform, ethyl acetate, and butanol. The methanol extracts of P. tenuipes showed significant cytotoxicity against human cancer cell lines; HeLa, HeLa S3, and A-431. Among the fractions tested, the ethyl acetate fraction had the highest cytotoxicity against three cancer cell lines. The $IC_{50}$ values of ethyl acetate fraction against HeLa, HeLa S3, and A-431 were 13, 35, and 30 $\mu$g/ml, respectively. However, cytotoxicity might not be due to apoptosis. The methanol extract of cultured mycelia showed high cytotoxicity against HeLa cell lines.

• The Journal of Korean Obstetrics and Gynecology
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• v.18 no.4
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• pp.10-23
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• 2005

Purpose : This study is to examine the ability of Rhizoma Scirpi (RS) to induce HeLa cell viability. Methods : We culture HeLa cell which is human metrocarcinoma cell in D-MEM included 10% fetal bovine serum(Hyclone Laboratories) below $37^{\circ}C$, 5% CO2. Then we observed apoptosis of log phage cell which is changed cultivation liquid 24 Hours periodically. Results : 1. RS induces mitochondria membrane potential collapse. 2. P38 MAPK is involved in RS-induced death in HeLa cells. 3. P38 MAPK is involved in RS-induced apoptosis in HeLa cells. 4. P38 MAPK reguates RS-induced caspase-3, -8 and -9 activation in HeLa cells. 5. The inhibition of caspase regulates RS-induced cell death in HeLa cells. 6. RS induces mitochondria membrane potential collapse in HeLa cells. 7. P38 MPK is involved in the regulation of Bcl-2 and Bfu in HeLa cells.8. RS regulates the expression of Bcl-2 and Bax in HeLa cells. 9. SR induces p38 MAPK activation in HeLa cells. Conclusion : RS induces apoptosis in HeLa cells via p38 MAPK activation.

• Biomedical Science Letters
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• v.17 no.4
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• pp.291-295
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• 2011

PD98059 is the specific inhibitor of extracellular signaling-regulated kinase (ERK) kinase (MEK). ERK is involved in a mitogen-activated protein kinase (MAPK) cascade controlling cell growth and differentiation. Although the inhibition of ERK is known to induce cell death in various cell lines, this effect is still controversial and the role of PD98059 on the death of HeLa $S_3$ cells, a subclone of the cervical cancer cell line, is not well understood. The apoptosis of HeLa $S_3$ cells increased after the treatment of 50 ${\mu}M$ PD98059. The induction of apoptosis by PD98059 was occurred in a time- and a dose-dependent manners. The expression of Bcl-2 was reduced in accordance with decrease of ERK2 expression. Taken together, these results indicate that PD98059 has a cytotoxicity in HeLa $S_3$ cells and it may be used as a potential target for the treatment of cervical cancer.

• The Journal of Korean Obstetrics and Gynecology
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• v.19 no.4
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• pp.47-60
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• 2006

Purpose : This study was conducted to investigate the inhibitory effects of Scutellaria barbata D. D on on the cell proliferation of HeLa Cells. Methods : Human uterine cervical carcinoma HeLa cells were cultured in the 1%, 5% and 10% concentration of Scutellaria barbata D. D on solution for 24, 48 and 72 hours for the direct inhibitory effects of Scutellaria barbata D. D on. Then we examined the effect of Scutellaria barbata D. D on solution on the cell proliferation inhibition by XTT assay. DNA fragmentation, MAP kinase activity and caspase activity by FACS analysis in HeLa cells. Results : We found that the proliferation of HeLa cells was significantly decreased in Scutellaria barbata D. D on solution containing groups comparing with a control group in a concentration-dependant manner. When HeLa cells were cultivated for 24 hours with 5% Scutellaria barbata D. D on solution containing group, the percentage of HeLa cells with activated caspase was the highest. Scutellaria barbata D. D on solution reduced the MAP kinase activity of HeLa cells comparing with the control group. By the XTT assay, the cell's activity was decreased in 5% and 10% Scutellaria barbata D. D on solution containing groups in 24 and 72 hours cultivation and 10% group in 48 hours. DNA fragmentation and caspase-3 activity of HeLa cells, however, were changed insignificantly. Conclusion : From this study we could suggest that Scutellaria barbata D. D on is available to the inhibition and apoptosis of human cervical carcinoma cell line, HeLa cells in vitro.

• Journal of Biomedical Engineering Research
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• v.16 no.3
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• pp.331-336
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• 1995

A composite material was produced as an artificial bone substitute which is gradually degrAded and replaced by the regenerated natural bones after implantation. To detect the effect of the material on the cell's activity, the composite specimens were placed in MEMs and incubated at $37^{\circ}C$ for one week. Human uterus cervical cancer origin HeLa 3 cells and mouse subcutaneous origin L929 cells were cul- tured in the specimen dissolved MEMs for 5 days to investigate cytotoxicity via cell growth rates. ${Na_2}^{51}CrO_4$ solution was added to the media, to label the HeLa 53 cells, and the released amount of $^{51}Cr$ was measured by a $\gamma$-counter. On the cell growth investigation, no significant cytotoxic phenomena were revealed in both HeLa S3 and L929 cell cultures. On the released 51CR from the incubated HeLa 53 cells, no significant cell degeneration was observed from the composite embedded MEMs.

• Biomedical Science Letters
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• v.12 no.2
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• pp.57-63
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• 2006

Deazaadenosine analogs such as 3-deazaadenosine (DZA), 3-deazaaristeromycin (DZAri) and ara-3-deazaadenine (DZAra-A) were developed as inhibitors of S-adenosylhomocysteine (Ado-Hcy) hydrolase (EC 3.3.1.1). These analogs were reported to induce apoptosis in human and murine leukemic cells. But, the mechanism involved in this apoptosis was not clarified yet. In the present study, we analyze the apoptosis induced by deazaadenosine analogs in human cervival cancer cell line, HeLa and the effect of Bcl-2 on this apoptosis. Whereas neither DZAri nor DZAra-A showed inhibitory effect on HeLa cell growth, DZA induced apoptosis in HeLa cells accompanied by cytochrome c release and activation of various caspases such as caspase-2,-8,-9 and -3. In HeLa-bcl-2 cell line, a stable transfectant of HeLa cell to overexpress Bcl-2, cytochrome c release, activation of all these caspases and the resulted apoptosis by DZA were completely prevented. By in vitro assay of cytochrome c release, in addition, DZA induced cytochrome c release from purified mitochondria of HeLa-pcDNA3 cells, but not HeLa-bcl-2 cells, even in the absence of cytosolic fraction. Therefore, it can be suggested that DZA might damage directly mitochondria leading to activate intrinsic pathway of caspase and thus induce apoptosis. DZA-induced apoptosis in HeLa cells may be in a bcl-2-inhibitable manner and irrelative of Ado-Hcy hydrolase.

• The Journal of Korean Obstetrics and Gynecology
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• v.19 no.3
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• pp.25-40
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• 2006

Purpose : This study was undertaken to evaluate the inhibitory effects of Arisaematis rhizoma on the cell proliferation in HeLa cells. Methods : The cultured cell after treatment in the different duration in 24, 48, 72 hours with solution of 1%. 5%, 10% Arisaematis rhizoma was quantified by trypan blue exclusin method. The control group was treated with 2% FBS in the different duration in 24, 48, 72 hours. We examined DNA of activated caspase by FACS analysis, caspase-3 activity, DNA fragmentation by DNA laddering, activity of HeLa Cells by the XTT assay, activity of MAP kinase by RT-PCR analysis. Results : After 72 hours culture, the growth activities of 1%, 5%, 10% Arisaematis rhizoma-treated Hela cell were significantly reduced with control group, respectively. After 24 hours culture, the ratio of cells showing caspase activity by FACS analysis were increased in 1%, 5%, 10% Arisaematis rhizoma-treated Hela cell. It were also increased in 48 hours culture of 10% and 72 hours culture of 5%, 10% Arisaematis rhizoma-treated Hela cell. In 24, 48 and 72 hours culture, DNA fragmentations of 5%, 10% Arisaematis rhizoma-treated Hela cell were obviously observed. These results meaned that Arisaematis rhizoma induces apoptosis of HeLa cells. It was supported by increased caspase-3 activity and decreased MAP kinase activity according to time periods and concentrations of Arisaematis rhizoma solution. Conclusion : The study shows that Arisaematis rhizoma has inhibitory effect on cell proliferation and induction capacity of apoptosis of human cevical carcinoma cell line, HeLa cells, in vitro. These results suggest that Arisaematis rhizoma should be useful for treatment of human cevical carcinoma.

• Journal of Life Science
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• v.17 no.8 s.88
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• pp.1027-1033
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• 2007

Although paclitaxel induces apoptosis of cancer cells, its exact mechanism of action is not yet known. The present study has been performed to determine whether influence of paclitaxel in HeLa $S_{3}$ uterine cancer cells. Three assays were employed in this study: cell cytotoxicity, morphological assessments of apoptotic cells (DAPI staining assay), and western blot analysis. The results indicated that paclitaxel has cytotoxic effects in HeLa $S_{3}$ cells. Especially, the $IC_{50}$ value of paclitaxel was about 1 ${\mu}M$. And morphological changes (fragmentation) of cells were observed by paclitaxel in HeLa $S_{3}$ cells. The flow cytometric analysis of paclitaxel-treated cells indicated a block of G2/M phase. The results that pacli-taxel regulates the cell cycle, especially Sub-$G_{1}$ phase. Paclitaxel induces apoptosis of HeLa $S_{3}$ cells via PARP-dependent fashion, and this apoptosis is related to disappearance of Bcl-2 proteins.

• KSBB Journal
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• v.11 no.4
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• pp.438-444
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• 1996

Using recombinant Vaccinia virus(vSC8) that express ${\beta}$-galactosidase, a model heterologous protein, conditions for virus and protein production were investigated in tissue culture flask. As host animal cells HeLa and HeLa S3 were used. It was demonstrated that cells infected during the exponential growth phase gave higher protein yield than those infected during the stationary growth phase and calf serum concentration after virus infection did not significantly alter protein yield. Pretreatment of cell layer with hypotonic solution enhanced the virus infectivity. Optimum cell growth and recombinant protein production was achieved at $37^{\circ}C$. But, during 2 hours of virus infection period incubation temperature must be lowered to 20∼$30^{\circ}C$ for maximum recombinant protein yield. To enhance virus replication, the effects of adrenal glucocorticoid hormone (Dexamethasone) and silkworm hemolymph were evaluated. Only dexamethasone increased about 20% of ${\beta}$-galactosidase yield in HeLa S3 cells when added with 10-7∼10-5M concentration 24 hours before infection.

• The Journal of Korean Medicine
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• v.38 no.2
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• pp.7-14
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• 2017

Objectives: This study evaluated the effect of aqueous extract from roots of Siberian ginseng on mTORC1 pathway. Methods: mTORC1 activity was measured by the phosphorylation status of p70 S6 kinase (S6K) in HeLa cells as well as the brain, liver and muscle tissues in diabetic db/db mice. Autophagy induction after the treatment of Siberian ginseng extract was evaluated by monitoring the conversion of cytoplasmic LC3I into lipidated LC3II in cultured human HeLa GFP-LC3 cells. Cell cycle analysis was performed in HeLa cells treated with Siberian ginseng using flow cytometry. Results: Among >2,800 plant products used for oriental medicine, Siberian ginseng was found to inhibit mTORC1 to phosphorylate S6 kinsase (S6K) in HeLa cells as well as the brain, liver and muscle tissues in diabetic db/db mice. Siberian ginseng-mediated mTORC1 activity was reversible unlike the prolonged suppression of mTORC1 by rapamycin when HeLa cells were grown in fresh media after the removal of the inhibitors. Siberian ginseng extract at concentrations to inhibit mTORC1 was not overly cytotoxic in cultured HeLa cells whereas rapamycin was obviously cytotoxic. The conversion of cytoplasmic LCI into lipidated LCII was increased by fivefold in HeLa GFP-LC3 cells treated with Siberian ginseng extract. Progression of cell cycle was attenuated at G2/M phase by the treatment of Siberian ginseng extract. Conclusions: These results suggest that the aqueous extract of Siberian ginseng possibly plays a good therapeutic role in various diseases involving mTORC1 signaling.