• 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.

• The Journal of Korean Obstetrics and Gynecology
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• v.24 no.3
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• pp.14-27
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• 2011

Objectives: This study was designed to investigate the effects of Acanthopanacis Cortex Radicis extract(ACRE) on the apoptosis in HeLa cell and MCF-7 cell. Methods: After treatment with various concentration of ACRE, cell growth was evaluated in HeLa cell and MCF-7 cell. Hoechst 33342 staining was performed to estimate DNA fragment effect of ACRE on the apoptosis in HeLa cell and MCF-7 cell. Annexin V/PI apoptosis assay was used to estimate the effects of ACRE on the early apoptosis in HeLa cell and MCF-7 cell. RT-PCR was used to estimate the apoptosis gene expression effect of ACRE on Hela cell MCF-7 cell. Results: Under $0.1mg/m\ell$ of ACRE, cytotoxic effect was not found per NIH3T3 cell. The viability of HeLa cell and MCF-7 cells was significantly decreased ACRE ($100{\mu}g/m\ell$) in HeLa cell and MCF-7 cell, ACRE ($50{\mu}g/m\ell$) in HeLa cell 3 days after treatment, in MCF-7 cell 1&3 days after treatment (p<0.01). DNA fragmentation was observed 3 days after treatment of cl of ACRE on HeLa cell and MCF-7 cell. In Annexin V/PI apoptosis assay, after treatment of $100{\mu}g/m\ell$ of ACRE, the early apoptotic cell increased both in HeLa cell and MCF-7 cell. In RT-PCR analysis, after treatment of $100{\mu}g/m\ell$ of ACRE, bcl-2 were decreased and bax, caspase-3 were increased both in HeLa cell and MCF-7 cell. Conclusions: ACRE appears to have considerable activity on the apoptosis in HeLa cell and MCF-7 cell.

• 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.

• 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 Korean Journal of Zoology
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• v.19 no.3
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• pp.113-122
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• 1976

The rate of $^{3}H$-thymidine uptake induced by MMS in asynchronous HeLa $S_3$ suspension cells was decreased in direct proprotion to dose increase. The combined treatment of BUdR or IUdR with MMS was more effective in reducing the rate of $^{3}H$-thymidine uptake. MMS-stimulated $^{3}H$-thymidine uptake was detected in synchronized $G_2$ stage cells of HeLa $S_3$ suspension cultures following treatment with thymidine double shock. BUdR and IUdR greatly enhanced MMS-stimulated $^{3}H$-thymidine uptake. IUdR was found to be a more effective sensitizer than BUdR in this respect.

• BMB Reports
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• v.42 no.5
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• pp.310-314
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• 2009

Globotriaosylceramide (Gb3) and globotetraosylceramide (Gb4) are the proposed functional receptors for Shiga toxin (Stx). To elucidate the effect of Gb3 content on Stx-induced cytotoxicity in HeLa cells, we cloned HeLa cells and determined the correlation between glycolipids content and Stx-induced cytotoxicity. The 29 HeLa cell clone (HLCC) lines used showed a wide range of sensitivity to Stx, compared to Gb3-rich cells which were more sensitive, showing as little as 20% viability to 100 pg/ml Stx. In contrast, Gb3-deficient cells proved resistant as they were more than 80% viable to 100 ng/ml Stx. Gb3 content in the HLCC lines corresponded with Stxs-induced cytotoxicity as well as Gb3 synthase expression, but no correlation with Gb4 content was noted. These data show that Gb3 content, which is regulated by the expression of Gb3 synthase, determines the sensitivity of HeLa cells toward Stx.

• 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.

• Biomedical Science Letters
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• v.19 no.1
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• pp.1-8
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• 2013

Parkin is known to be a tumor suppressor protein. Previously, we determined that parkin expression restores susceptibility to TNF-${\alpha}$-induced death of HeLa cells, a human cervical cancer cell line resistant to TNF-${\alpha}$-induced cell death. MMP-3 is a zinc-dependent protease recently reported to activate intracellular apoptotic signaling. In this study we examined the regulation of MMP-3 expression by parkin in TNF-${\alpha}$-treated HeLa cells. Furthermore, we investigated the signaling pathway involved in parkin-induced expression of MMP-3. We found that HeLa cells exhibit low levels of MMP-3 but is induced after introduction of the parkin gene into HeLa cells. Furthermore, MMP-3 expression increased further when parkin expressing cells were treated with TNF-${\alpha}$. Using chemical inhibitors of cell signaling pathways, we found that MEK-1 (PD98059), PI3K (LY294002), p38 MAPK (SB203580), and JNK inhibitors alleviated parkin-induced up-regulation of MMP-3. Finally, we show that TNF-${\alpha}$-induced cell death in parkin expressing cells is inhibited by using a MMP-3 inhibitor. These results suggest that parkin expression induces prolonged expression of MMP-3 via MEK-1, PI3K, MAPK, and JNK pathway in HeLa cells allowing the HeLa cells to become sensitive to TNF-${\alpha}$-induced cell death. These results implicate a role of MMP-3 in parkin-induced cell death in TNF-${\alpha}$ treated HeLa cells.

• 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.

• Advances in Traditional Medicine
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• v.3 no.3
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• pp.151-156
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• 2003

The leaves of Mirabilis jalapa L contains protein fraction presumed ribosome-inactivating protein (RIP). RIP is a group of protein that has RNA N-glycosidase activity that is capable to inhibit protein synthesis. Protein fraction of the plant was shown to be cytotoxic on HeLa cell-line, however, the mechanism by which the protein kill the cells is not identified yet, whether trough apoptosis, necrosis, or other mechanism. This research aim to study the mechanism of cell death caused by the protein fraction isolated from the leaves of this plant on HeLa and Raji cell-line, as representative of different kind of cancer cells. Results showed that protein fraction isolated from the leaves of Mirabilis jalapa L was more cytotoxic to HeLa cell-line (LC50: 0.65 mg/ml) than to Raji cell-line (1.815 mg/ml) on 48 hours incubation time. Moreover, it was demonstrated that the death of HeLa cells caused by the protein fraction was due to induction of apoptosis, while on Raji cell-line was due to non-apoptosis way, presumably via necrosis.