• Journal of Nutrition and Health
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• v.35 no.4
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• pp.439-445
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• 2002

This study was undertaken to investigate the inhibitory effect of prunus fume extracts on the growth of Hep G2 and HeLa cells. Prunus mums was extracted using the following solvents hexane, chloroform, ethylacetate, methanol, and hot water. The effect on the growth of each cancer cell line was examined by MTT (3-[4, 5-dimethylthiaeol-2-yl)-2,5-diphenyl tetrazolium bromide) assay, cytotoxicity testing, and microscopic observation. The ethylacetate extracts of Prunus muse at the concentration of 250 $\mu\textrm{g}$/ml exhibited the greatest inhibitory effect on the growth of Hep G2 in the MW assay. In cytotoxicity testing, the treatment of the Hep G2 cells with ethylacetate extracts (1000 $\mu\textrm{g}$/ml for 72 hrs) destroyed 75% of the cells, and morphological changes were also observed. futhermore, the hexane extracts of Prunes muse at the concentration of 250 $\mu\textrm{g}$/ml exhibited the greatest inhibitory effect on the growth of HeLa cells in the MTT assay. The treatment of the HeLa cells with the hexane extracts (1000 $\mu\textrm{g}$/ml for 72 hrs) resulted in the destruction of 68% of the cells. Fibroblasts were not affected by either ethylacetate or hexane extracts of prunus muse.

• The Korean Journal of Zoology
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• v.38 no.4
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• pp.457-464
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• 1995

Hela cells, a transformed human epithelial cell line, attach to various substrata but subsequent spreading is specific to collagen or gelatin. The spreading is initiated by the activation of phospholipase $A_2$ (PLA$_2$) which produces arachidonic acid (AA) as a consequence of cell surface collagen receptor clustering. This study examines the mechanism of PLA$_2$activation and which phospholipids are hydrolyzed by PIA$_2$ to release AA in response to Hela cell adhesion to a gelatin substratum. The levels of phosphatidyicholine decreases, among various phospholipids, during attachment and spreading of Hela cells. Lysophosphatidyicholine Is the only lysophospholipids formed during ileLa cell adhesion indicating that clustered collagen receptors activate PLA$_2$to hydrolyze posphatidylcholine to AA and lysophosphatidylcholine. Among various molecular entitles which are known to regulate PLA$_2$ activation, we have previously shown that PLA2 activation is not mediated by either changes in $Ca_2$+ levels, alkalinization of cytoplasmic p11, or activation of protein hinase C. It is also likely that PIA2 activation is not mediated by either pertussis or cholera toxinsensitive G proteins as those toxins do not affect both AA release and cell spreading.

• Journal of Life Science
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• v.27 no.2
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• pp.164-171
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• 2017

Our previous study suggested that S-allylcysteine (SAC) inhibits the proliferation of the human cervical cancer cell line, HeLa, at least in part through the induction of apoptosis and cell cycle arrest. To further analyze the specific molecular mechanism(s) by which SAC mediates its antiproliferative effects, this study examined the role of SAC in regulating the protein expression of initiator caspase (caspase-9), effector caspases (caspase-3 and caspase-7), and poly-ADP-ribose polymerase (PARP) in HeLa. Western blot analysis showed that when cells were treated with 50 mM SAC for 48 hr, the expression of procaspase-3, -7, and -9 and PARP was reduced by 94%, 38%, 95%, and 64%, respectively, as compared to the untreated control. In contrast, the expression of caspase-3, -7, and -9 and cleaved-PARP was markedly increased by SAC treatment. The SAC-mediated changes in the expression of these proteins were correlated with the concomitant inhibition of cellular proliferation by SAC. The cell proliferation assay showed that HeLa treatment with more than 20 mM SAC for 6-48 hr resulted in both concentration- and time-dependent inhibition of cellular proliferation. These results indicate that the SAC-induced antiproliferative effect in HeLa may be mediated at least in part through the activation of caspase-9, followed by the activation of caspase-3 and caspase-7 as well as the inactivation of PARP, thus leading to cellular apoptosis.

• Biomedical Science Letters
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• v.2 no.2
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• pp.153-158
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• 1996

Verapamil, a potent calcium channel blocker, has been proved to be one of the modulators to overcome drug resistance in cancer chemotherapy. In the present experiment, the possibility of verapamil as a MDR modulator was investigated by using MTT assay. Sole treatment of verapamil on the HeLa and Caski cervical cancer cell line revealed dose dependent cytotoxicity within a range of tested dose. Combined treatment of verapamil with 5-FU, DDP on two human cervical cancer cell line led to a significant synergistic cytotoxicity. Therefore , these studies showed that verapamil had a possibility to be applicable to cancer chemotherapy in gynecological oncology.

• Journal of Life Science
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• v.21 no.12
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• pp.1746-1751
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• 2011

This study examined the effects of estrogen, progesterone and tamoxifen at different concentrations and treatment periods on proliferation of a human cervical carcinoma cell line, HeLa, in culture, based on MTT assay. Estrogen did not have an effect on the cellular proliferation in concentrations up to $1{\mu}g$/ml for treatment periods of between 2.5 and 6 days, but significantly inhibited proliferation at a higher concentration of $10{\mu}g$/ml in a progressive manner with increasing treatment periods. Also, treatment of HeLa with more than $10{\mu}g$/ml of progesterone for 2.5 days significantly inhibited proliferation and caused a concentration-dependent inhibition with 4 days of treatment. However, longer treatment with progesterone for 6 days abolished the concentration-dependent inhibitory effect on cellular proliferation observed with the 4-day treatment period. Furthermore, tamoxifen required a higher concentration ($100{\mu}g$/ml) than estrogen to bring about the inhibitory effect on the HeLa proliferation. These results suggest that high concentrations of estrogen, progesterone and tamoxifen may suppress proliferation of HeLa, and both the concentration and the treatment period may also influence their inhibitory effects on cellular proliferation.

• KSBB Journal
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• v.16 no.6
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• pp.579-591
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• 2001

The cell growth inhibitor effect of cervical cancer cells was investigated by liposome mediated transfection (pRcCMVp53/lipofectin) and by transfection using adenovirus (AdCMVp57). The papilloma virus cancer cell lines we used in this study were HPV16 positive, having inhibiter gene, wild p53 gene, CaSki, SiHa, HPV18 positive HeLa, HeLaS3 and HPV negative C33A, HT3. LacZ gene of E.coli was used as the marker gene for the transfection efficiency. The effect on the inhibition of tumor cell growth was measured by cell count and cell viability though ELISA analysis and MTT assay. The inhibition of tumor cell growth was confirmed by measuring each assay for six days, comparing with the normal control cell growth. The cell growth of cervical cancer calls by transfection was significantly reduced and showed tittle differences among the cell lines. To eliminate the potential problem of Ad(adenovirus) contamination during rAAV production, rAAV can be produced by a triple transfection of vector plasmic, packaging plasmid, and adenovirus helper plasmid. To examine the helper functions of Ad plasmids on the production of rAAV vector, we carried out cotransfection of three plasmids, AAV vector, packaging construct, and Ad helper plasmids. The optimized transfection condition for calcium phosphate method is 25ug of total DNA per 10-cm-diameter plate of 293 cell. We found that rAAV yields peaked at 48hr after Ad infection. The titer of rAAV was measured by the dot blot analysis to measure the number of particles/ml based on the quantification of viral DNA. Recent1y, Kombucha(fungi) was identified as a very potent antileukefic agent. In the present study, effect of natural toxin(plankton) and Kombucha is PSP(GTXI-3, neoSTX), on various MTT assay cervical cancer cell line. Toxin(GTX 1-3, neoSTX) also inhibited the proliferation in primary cervical cancer calls in a dose-dependent toxin concentration. These results showed that toxin was very potent in inhibiting the proliferation of cervical cancer calls in vitro. Toxins and Kombuoha exhibited a dose dependent inhibition of cellular proliferation in cancer cell line.

• Polymer(Korea)
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• v.33 no.3
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• pp.213-218
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• 2009

A cationic lipid emulsion containing 1,2-dioleoyl-3-trimethylammonium-propane(DOTAP), Tween80, squalene has been prepared as a gene delivery system. In order to increase the transfection efficiency of gene carrier, folate was used as the tumor-targeting ligand that was attached on PEG-DPPE. HeLa and 293 cells were used for the in vitro transfection experiment. HeLa cell is a folate-positive cell line. The mean particle sizes of polymeric lipid system and DNA/lipid complex system were 206.6 nm and 150.5 nm, respectively. The transfection efficiencies of our carriers(4:l(w:w) complex ratio)were 100 times higher than that of DOTAP only emulsion due to the targeting effect of folate.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.8
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• pp.3797-3803
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• 2016

Cervical cancer is the second most common malignancy in women worldwide and thus one of the leading causes of mortality in women. Lovastatin, a non polar, anticholesterol drug has previously been reported to exert antitumour activity in vitro. In the present study, lovastatin from Aspergillus terreus (KM017963) was purified by adsoprtion chromatography and evaluated for its anticancer and anti-oxidant properties with a human cervical cancer cell line (HeLa). Growth inhibitory and proapoptotic effects of purified lovastatin on HeLa cells were investigated by determining its influence on cell numbers, mitochondrial membrane potential (MMP), DNA fragmentation and antioxidant properties in terms of hydroxy radical scavenging effects as well as levels of total reduced glutathione. Cell cycle analysis by flow cytometry (propidium iodide staining) confirmed induction of apoptotic cell death and revealed cell cycle arrest in the G0/G1 phase. Results of the study give leads for the anticancer effects of lovastatin and its potential usefulness in the chemotherapy of cervical cancer.

• Molecules and Cells
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• v.21 no.3
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• pp.367-375
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• 2006

We previously identified a novel cancer/testis antigen gene CAGE by screening cDNA expression libraries of human testis and gastric cancer cell lines with sera of gastric cancer patients. CAGE is expressed in many cancers and cancer cell lines, but not in normal tissues apart from the testis. In the present study, we investigated its role in the motility of cells of two human cancer cell lines: HeLa and the human hepatic cancer cell line, SNU387. Induction of CAGE by tetracycline or transient transfection enhanced the migration and invasiveness of HeLa cells, but not the adhesiveness of either cell line. Overexpression of CAGE led to activation of ERK and p38 MAPK but not Akt, and inhibition of ERK by PD98059 or p38 MAPK by SB203580 counteracted the CAGE-promoted increase in motility in both cell lines. Overexpression of CAGE also resulted in a reduction of ROS and an increase of ROS scavenging, associated with induction of catalase activity. Inhibition of ERK and p38 MAPK increased ROS levels in cells transfected with CAGE, suggesting that ROS reduce the motility of both cell lines. Inhibition of ERK and p38 MAPK reduced the induction of catalase activity resulting from overexpression of CAGE, and inhibition of catalase reduced CAGE-promoted motility. We conclude that CAGE enhances the motility of cancer cells by activating ERK and p38 MAPK, inducing catalase activity, and reducing ROS levels.

• Journal of Pharmacopuncture
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• v.18 no.3
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• pp.32-41
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• 2015

Objectives: Condurango (Gonolobus condurango) extract is used by complementary and alternative medicine (CAM) practitioners as a traditional medicine, including homeopathy, mainly for the treatment of syphilis. Condurango bark extract is also known to reduce tumor volume, but the underlying molecular mechanisms still remain unclear. Methods: Using a cervical cancer cell line (HeLa) as our model, the molecular events behind condurango extract's (CE's) anticancer effect were investigated by using flow cytometry, immunoblotting and reverse transcriptase-polymerase chain reaction (RT-PCR). Other included cell types were prostate cancer cells (PC3), transformed liver cells (WRL-68), and peripheral blood mononuclear cells (PBMCs). Results: Condurango extract (CE) was found to be cytotoxic against target cells, and this was significantly deactivated in the presence of N-acetyl cysteine (NAC), a scavenger of reactive oxygen species (ROS), suggesting that its action could be mediated through ROS generation. CE caused an increase in the HeLa cell population containing deoxyribonucleic acid (DNA) damage at the G zero/Growth 1 (G0/G1) stage. Further, CE increased the tumor necrosis factor alpha ($TNF-{\alpha}$) and the fas receptor (FasR) levels both at the ribonucleic acid (RNA) and the protein levels, indicating that CE might have a cytotoxic mechanism of action. CE also triggered a sharp decrease in the expression of nuclear factor kappa-light-chain-enhancer of activated B cells ($NF-{\kappa}B$) both at the RNA and the protein levels, a possible route to attenuation of B-cell lymphoma 2 (Bcl-2), and caused an opening of the mitochondrial membrane's permeability transition (MPT) pores, thus enhancing caspase activities. Conclusion: Overall, our results suggest possible pathways for CE mediated cytotoxicity in model cancer cells.