• 한국동물학회지
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• 제19권3호
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• pp.113-122
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• 1976

非同時化시킨 HeLa $S_3$ 細胞에 있어 MMS에 의한 $^3 H$-Thymidine Uptake率은 MMS의 頻度증가에 따라 직선적으로 감소하며, BUdR 혹은 IUdR과 二重處理할 경우 그 감소율은 더욱 증가한다. MMS에 의한 $^3 H$-Thymidine Uptake은 thymidine 二重 處理후 얻은 同時化된 HeLa $S_3$ 細胞의 $G_2$ 時期에서 檢出된다. BUdR과 IUdR은 MMS에 의한 $^3 H$-Thymidine Uptake率을 더욱 증가시키며 IUdR은 BUdR에 비해 더효과적인 感受性 物質로 판명되었다.

• 미생물학회지
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• 제36권4호
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• pp.312-315
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• 2000

논꽃동충하초(Paecilomyces tenuipes DGUM 32001)의 자실체를 메탄올로 추출하여 인간 암세포주에 대한 세포독성을 조사하였다. 메탄올 추출물의 암세포주에 대한 세포독성은 매우 우수하였다. 메탄올 추출물의 용매 분획 중, 에틸아세테이트 분획에서 가장 우수한 세포독성을 나타내었으며, HeLa, HeLa S3 및 A-431 암세포주에 대한 $IC_{50}$ 값은 각각 13, 35 및 30 $\mu$ g/ml이었다. 그러나, 이 분획의 HeLa 암세포주에 대한 세포독성은 apoptosis에 의하지 않음을 알 수 있었다. 배양 균사체의 메탄올 추출물은 A-431 암세포주에 대해 우수한 세포독성을 보여주었다.

• 생명과학회지
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• 제17권8호통권88호
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• pp.1027-1033
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• 2007

Paclitaxel이 암세포에서 세포예정사를 유발할지라도, 아직 정확한 기전은 잘 알려져 있지 않다. 이에 본 연구에서는 HeLa $S_{3}$ 자궁암세포에서의 paclitaxel이 어떠한 영향을 미치는지 알아보고자 한다. 그리하여 방법으로는 세포독성검사, apoptotic cells의 형태학적 변화(DAPI 염색 ), western blot 분석법을 사용하여 수행하였다. 본 연구의 결과로 paclitaxel은 HeLa $S_{3}$ 세포에서 세포독성을 보이며 특히 paclitaxel의 $IC_{50}$ 값은 약 1 ${\mu}M$이며, paclitaxel 처리한 HeLa $S_{3}$ 세포에서 형태학적 변화(분절화)를 관찰하였고, flow cytometric 분석에서는 G2/M기가 차단되어 paclitaxel은 세포주기 특히 Sub-$G_{1}$기를 조절함을 알 수 있다. 그리고 Paclitaxel을 처리한 HeLa $S_{3}$ 세포에서는 PARP cleavage를 유발하였고 Bc1-2의 감소와도 관련되었다.

• 대한의용생체공학회:의공학회지
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• 제16권3호
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• pp.331-336
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• 1995

체내 매입후 경시적으로 분해되면서 재생골조직에 의해 치환되는 인공골복합체를 제조하고 복합체가 세포활성에 미치는 영향을 조사하였다. 복합체시편을 세포배양액에 넣고 1주일동안 $37^{\circ}C$에서 배양한 다음, 사람자궁경부암유래 HeLa S3세포와 쥐피하 L929세포를 복합체가 용해된 세포배양액에서 5일간 배양하여 세포성장율을 비교하여 세포특성을 조사하였다. 한편 HeLa S3세포를 배양중인 배양액에 ${Na_2}^{51}CrO_4$를 첨가하여 HeLa S3세포에 $^{51}Cr$를 표식한 다음, 용해된 $^{51}Cr$의 양을 $\gamma$-counter를 이용하여 측정하였다. 세포성장정도의 측정에서는 HeLa S3 세포 및 L929 세포 모두가 특이한 세포독성을 발견할 수 없었으며, 복합체가 용해된 세포배양액내의 표식된 HeLa S3 세포로 부터 용해된 $^{51}Cr$량을 측정한 결과, 세포활성을 저해하지 않은 것으로 관찰되었다.

• 대한한방부인과학회지
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• 제18권4호
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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.

• 대한의생명과학회지
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• 제12권4호
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• pp.349-354
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• 2006

Induction of apoptosis allows the organism to get rid of abnormal cells and also of tumor cells. Understanding the mechanism involved in Ultraviolet radiation (UV) induced apoptosis may improve its therapeutic efficacy. In this study, we present expression of poly (ADP-ribose) polymerase (PARP) during apoptosis induced by UV in HeLa $S_3$ cells. Four different assays were performed in this study: morphological assessment of apoptotic cells and cell viability, DNA fragmentation analysis by agarose gel electrophoresis, quantitative assay of fragmented DNA, and expression of PARP by the western blot analysis. The percentages of apoptotic HeLa $S_3$ cells irradiated with $75J/m^2$ UV was increased continuously from 3 hrs incubation. DNA ladder pattern was appeared at 6 hrs. The amount of nucleosomal DNA fragments in cells treated UV increased from 3 to 12 hrs incubation and gradually decreased. The cleavage of PARP in HeLa $S_3$ cells irradiated with UV was induced, and the cleavage of PARP was more delayed in the cells pretreated with $5J/m^2$ UV and subsequently irradiated with $75J/m^2$ UV. than that in the cells only irradiated with $75J/m^2$ UV. Thus these data suggest that the cleavage of PARP relates with DNA fragmentation associated with apoptosis.

• KSBB Journal
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• 제11권4호
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• pp.438-444
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• 1996

모델 재조합 단백질인 $\beta$galactosidase를 발현하 는 Vaccinia virus를 생산하기 위하여 숙주 동물세 포의 배양조건을 관찰한 결과 감염비 5일 경우 H HeLa는 감염후 60시간 후, HeLa 83는 감염후 40 시간 후에 회수할 때 최 대 의 ${\beta}$-galactosidase 수율 을 얻을 수 있으며, 세포가 대수증식기 일 때 감염하 고 배양온도는 $37^{\circ}C$ 로 하는 것이 최적 배양조건으로 나타났다. 감염후 혈청의 농도는 단백질 수율에 크 게 영향을 미치지는 않으나 3~5% 에서 가장 높은 단백질 수율을 보였으며, 낮은 이온 농도의 용액으 로 세포층을 세척하는 것과 virus 감염시 온도를 20~∼$30^{\circ}C$ 로 낮추는 것은 Vaccinia-HeLa system에서 감염능 증대 효과를 나타내 였다. Dexamethasone 전처리는 HeLa 83에서 ViruS 복제 증대를 HeLa에 서는 virus 복제 감소를 가져왔다.

• 대한의생명과학회지
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• 제12권2호
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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.

• 대한한의학회지
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• 제38권2호
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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.

• 대한의생명과학회지
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• 제17권4호
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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.