• The Journal of Korean Obstetrics and Gynecology
• /
• v.31 no.2
• /
• pp.18-30
• /
• 2018

Objective: This study was designed to investigate the anti-cancer effects of AAH on ovarian cancer in vitro and by using allograft model in vivo. Methods: In this experiment, the effects of AAH on proliferation rates, cell morphology, cell death type, cell cycle, caspase activities and p38 mitogen-activated protein kinase (MAPK) pathway were investigated in A2780, human ovarian cell line. Results: AAH inhibited proliferation of A2780 cells in a dose dependent manner. In addition, AAH induced apoptosis but did not affect cell cycle of A2780 cells. AAH also effectively inhibited caspase 3 and caspase 9 activities respectively. In allograft tumor model, AAH reduced tumor volume and expanded life span in a dose dependent manner. Conclusion: It can be inferred that AAH can induce apoptosis in ovarian cancer cells and has possibility as an anticancer agent for ovarian cancer.

• Asian Pacific Journal of Cancer Prevention
• /
• v.15 no.12
• /
• pp.4995-5000
• /
• 2014

Background: Cancer constitutes a key pressure on public health regardless of the economy state in different countries. As a kind of highly malignant epithelial tumor, lacrimal gland adenoid cystic carcinoma can occur in any part of the body, such as salivary gland, submandibular gland, trachea, lung, breast, skin and lacrimal gland. Chemotherapy is one of the key treatment techniques, but drug resistance, especially MDR, seriously blunts its effects. As an element of the 60S large ribosomal subunit, the ribosomal protein L39-L gene appears to be documented specifically in the human testis and many human cancer samples of different origins. Materials and Methods: Total RNA of cultured drug-resistant and susceptible lacrimal gland adenoid cystic carcinoma cells was seperated, and real time quantitative RT-PCR were used to reveal transcription differences between amycin resistant and susceptible strains of lacrimal gland adenoid cystic carcinoma cells. Viability assays were used to present the amycin resistance difference in a RPL39-L transfected lacrimal gland adenoid cystic carcinoma cell line as compared to control vector and null-transfected lacrimal gland adenoid cystic carcinoma cell lines. Results: The ribosomal protein L39-L transcription level was 6.5-fold higher in the drug-resistant human lacrimal gland adenoid cystic carcinoma cell line than in the susceptible cell line by quantitative RT-PCR analysis. The ribosomal protein L39-L transfected cells revealed enhanced drug resistance compared to plasmid vector-transfected or null-transfected cells as determined by methyl tritiated thymidine (3H-TdR) incorporation. Conclusions: The ribosomal protein L39-L gene could possibly have influence on the drug resistance mechanism of lacrimal gland adenoid cystic carcinoma cells.

• The Journal of the Korean Society for Microbiology
• /
• v.35 no.1
• /
• pp.9-18
• /
• 2000

Immunological mechanisms involving the release of inflammatory factors by HIV-1 infected microglia in the brain have been implicated in the pathogenesis of HIV dementia (HIVD). Since the regulation of matrix metalloproteinases (MMPs) activity can be influenced by variety of inflammatory mediators, this study was undertaken to look for a correlation between the MMP-9 release and the production of TNF-${\alpha}$ in response to HIV-1 p24 in the human monocyte cell line THP-1 as a model for microglia. First, it was shown that HIV-l core p24 antigen induced THP-1 to secrete MMP-9 in a dose response manner while it elicited a little effect on MMP-2 release in human astroglial cell line T98G. Next, it was found that p24 induced THP-1 to secrete TNF-${\alpha}$ without prior differentiation into macrophages by phorbol myristate acetate (PMA) treatment. Furthermore, anti-TNF-${\alpha}$ neutralizing antibodies significantly blocked p24-induced MMP-9 release in a dose dependent manner. Our data indicate that p24 antigen induces monocytic MMP-9 release by triggering up-regulation of TNF-${\alpha}$ secretion.

• Microbiology and Biotechnology Letters
• /
• v.32 no.1
• /
• pp.72-77
• /
• 2004

Previously, we synthesized a novel Cyclin-dependent kinase inhibitor, MCS-5A. Also, we investigated the involvement of cell cycle regulatory events during MCS-5A-mediated apoptosis in HL-60(+p16/-p53) cells with up-regulation of p16 protein expression. In contrast, apoptosis was not observed in A549(-p16/+p53) cells. Therefore we propose that $p16^{INK4A}$ is a key enzyme for inducing apoptosis. In the present studies, we have explored the mechanism of $p16^{INK4A}$ -mediated cytotoxicity and the role of p16.sup INK4A/ overexpression in the induction of apoptosis in human tumor cells. The tumor suppressor gene $p16^{INK4A}$ is known as a cyclin-dependent kinase inhibitor (CKI) and cell cycle regulator. We expressed wild type $p16^{INK4A}$ in pcDNA3.1 vector and then transfected into non-small cell lung cancer (NSCLC) cell expressing different statue of p16$^{INK4A}$, p53 gene〔A549(-p16/+p53), H1299(-p16/-p53) and HeLa(+pl6/+p53) cell line〕. TUNEL assay (including propidium iodide staining following transfection of these cell line with pcDNA3.1-pl6) indicate that p16$^{INK4A}$-mediated cytotoxicity was associated with apoptosis. This is supported by studies demonstrating an induction of caspase 3 cleavage due to the transfection of A549, H1299 and HeLa cells with pcDNA3.1-pl6. These results suggest that p16$^{INK4A}$ has a new function of inducing apoptosis which is not related with the function of tumor suppressor gene p53.

• Imaging Science in Dentistry
• /
• v.30 no.1
• /
• pp.71-79
• /
• 2000

Purpose : This study was aimed to evaluate the cell cycle arrest and apoptosis induction after irradiation and epidermal growth factor (EGF) treatment in three human epithelial tumor cell lines (A431, Siha, KB). Materials and Methods: Single irradiation of 2, 5 and 10 Gy was done on three cell lines with 5.38 Gy/min dose rate using Cs-137 irradiator at room temperature. Also, EGF of 10 ng/ml was added immediately after 10 Gy irradiation. Cell growth was evaluated by counting the living cell number using a hemocytometer at 1 day, 2 days, 3 days, 4 days and 5 days after irradiation. Cell cycle arrest and apoptosis induction were assayed with the flow cytometry at 8 hours, 12 hours, 1 day, 2 days, 3 days, 4 days and 5 days after irradiation. Results : Growth of irradiated three cell lines were inhibited in proportion to radiation dose. EGF treatment after irradiation showed various results according to cell lines. On all cell lines, G2 arrest was detected after 8 hours and maximized after 12 hours or 1 day. Amount of G2 arrest was positively dose dependent. However, EGF showed no significant change on G2 arrest. G2 arrest was recovered with time at 2 Gy and 5 Gy irradiation. However, at 10 Gy irradiation, G2 arrest was continued. Apoptosis was detected at 10 Gy irradiation. On EGF treated group after irradiation, A431 and Siha cell lines showed slightly increased apoptosis but there was no statistically significant difference. KB cell line showed no marked change of apoptosis induction. Conclusion : Irradiation effects on cell cycle arrest and apoptosis induction in three human epithelial tumor cell lines, however epidermal growth factor doesn't effect on.

• Asian Pacific Journal of Cancer Prevention
• /
• v.16 no.4
• /
• pp.1575-1579
• /
• 2015

Some microRNAs (miRNAs) have been shown to act as oncogenes or tumor suppressor genes in human melanomas. miR-328 is upregulated in blood cells of melanoma patients compared to in healthy controls. This suggests a role for miR-328 in melanoma that warrants investigation. In this study, we demonstrated miR-328 levels to be dramatically decreased in human melanoma cell lines. Moreover, forced expression of miR-328 inhibited proliferation and induced G1-phase arrest of the SK-MEL-1 melanoma cell line. We identified TGFB2 as a direct target gene for miR-328 using a fluorescent reporter assay and western blotting. Levels of TGFB2 were dramatically increased in human melanoma cell lines and were inversely correlated with the miR-328 expression level. Our findings provide new insights into the mechanisms of human melanoma development, indicating that miR-328 has therapeutic potential for this disease.

• The Korean Journal of Physiology and Pharmacology
• /
• v.13 no.2
• /
• pp.115-121
• /
• 2009

Functional defects in mitochondria are involved in the induction of cell death in cancer cells. We assessed the toxic effect of camptothecin against the human cervical and uterine tumor cell line SiHa with respect to the mitochondria-mediated cell death process, and examined the combined effect of camptothecin and anticancer drugs. Camptothecin caused apoptosis in SiHa cells by inducing mitochondrial membrane permeability changes that lead to the loss of mitochondrial membrane potential, decreased Bcl-2 levels, cytochrome c release, caspase-3 activation, formation of reactive oxygen species and depletion of GSH. Combination of camptothecin with other anticancer drugs (carboplatin, paclitaxel, doxorubicin and mitomycin c) or signaling inhibitors (farnesyltransferase inhibitor and ERK inhibitor) did not enhance the camptothecin-induced cell death and caspase-3 activation. These results suggest that camptothecin may cause cell death in SiHa cells by inducing changes in mitochondrial membrane permeability, which leads to cytochrome c release and activation of caspase-3. This effect is also associated with increased formation of reactive oxygen species and depletion of GSH. Combination with other anticancer drugs (or signaling inhibitors) does not appear to increase the anti-tumor effect of camptothecin against SiHa cells, but rather may reduce it. Combination of camptothecin with other anticancer drugs does not seem to provide a benefit in the treatment of cervical and uterine cancer compared with camptothecin monotherapy.

• YAKHAK HOEJI
• /
• v.59 no.4
• /
• pp.164-169
• /
• 2015

In the present study, we determined the effect of $18{\beta}$-glycyrrhetinic acid ($18{\beta}$-GA) in the mice model bearing xenografts of HT-29 human colon cancer cell line. Data from the cytotoxicity assay displayed that $18{\beta}$-GA induced cell death in HT-29. The cytotoxicity was enhanced as the $18{\beta}$-GA treatment was prolonged. In case of 72 hrs treatment, $LD_{50}$ of $18{\beta}$-GA was approximately $90{\mu}M$, and the efficacy at $100{\mu}M$ of $18{\beta}$-GA appeared to be equivalent to that of doxorubicin at $1{\mu}M$. Based on the in vitro data, we tested the anti-tumor effect of $18{\beta}$-GA in thymic mice (Balb/c strain). Xenograft tumors were generated by subcutaneous injection of HT-29 ($3{\times}10^6cells/mouse$) to mice and the mice were treated intraperitoneally with $18{\beta}$-GA ($50{\mu}g/time/mouse$) every other day for 4 times. The tumor volumes were measured for a period of 14 days. Data displayed that the $18{\beta}$-GA treatment reduced the tumor volumes (P < 0.05) as compared to control mice. However, this activity was demolished when athymic mice (Balb/c nu/nu) were used instead of thymic mice. This observation appeared that T lymphocyte played an important role in the anti-tumor activity. In conclusion, our results indicate that $18{\beta}$-GA has anti-tumor activity in HT-29 tumor-bearing mice, which may be associated with T cells.

• Asian Pacific Journal of Cancer Prevention
• /
• v.16 no.9
• /
• pp.3779-3783
• /
• 2015

Dietary prevention has been known to reduce breast cancer risk. Sesamin is one of the major components in sesame seeds and has been widely studied and proven to have anti-proliferation and anti-angiogenic effects on cancer cells. In this study, the influence of sesamin was tested in the human breast cancer MCF-7 cell line for cell viability (MTT assay) and cell cycling (flow cytometry). Results showed that sesamin dose-dependently (1, 10 and $50{\mu}M$) reduced the cell viability and increased LDH release and apoptosis (TUNEL assay). In addition, there was a significant increase of sub-G1 phase arrest in the cell cycle after sesamin treatment. Furthermore, sesamin increased the expression of apoptotic markers of Bax, caspase-3, and cell cycle control proteins, p53 and checkpoint kinase 2. Taken together, these results suggested that sesamin might be used as a dietary supplement f or prevention of breast cancer by modulating apoptotic signal pathways and inhibiting tumor cell growth.

• Journal of dental hygiene science
• /
• v.7 no.1
• /
• pp.31-35
• /
• 2007

Caesalpinia sappan L. (Leguminosae) is an oriental medicinal herb distributed in China and Taiwan, and its heartwood has been traditionally used as an analgesic, a therapy for thrombosis or tumor. This study was to investigate the proliferation and inhibition effects of Caesalpinia sappan extracts against human epithelial cell and cancer cell lines. The methanol extract of dried C. sappan heartwood was evaporated (KS-6), and then sequentially extracted by hexane (KS-01), chloroform (KS-02), ethyl acetate (KS-03), n-butanol (KS-04), and water (KS-05). After 48 hr of exposure, these fractions at a concentration of $50{\mu}g/ml$ significantly increased, and reduced cell proliferation in both human normal epithelial and cancer cell lines. The ethyl acetate fraction (KS-03) among organic solvent fractions was 120.2% of the most proliferation activity ($50{\mu}g/ml$) against HaCaT human epithelial cell. However, fractions from chloroform, butanolic and methanolic extract had 7.2, 28.7 and 20.8% of antiproliferative effect on HaCaT cell, respectively. In cell proliferation effects of C. sappan extract on HeLa, SiHa and C33A human cervical cancer cells, chloroform fraction (KS-2) was the most antiproliferative activity, its antiproliferative rate (dosage, $50{\mu}g/ml$) relative to control was 25.8, 12.2 and 17.4% for SiHa, HeLa and C33A, respectively. The results indicated that the six extract fractions could induce cell cycle stimulate or arrest in some way. Finally, further investigation is needed to assess the molecular mechanisms mediated anticancer activities of this plant.