• Korean Journal of Ichthyology
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• v.12 no.3
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• pp.173-179
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• 2000

Effects of Estradiol-$17\beta(E_2)$ and 2, 4-dichlorophenoxy acetic acid (2, 4-D) on vitellogenin(VTG) production were investigated in primary hepatocyte culture of olive flounder, Paralichthys olivaceus. Highest survival rate of hepatocyte were observed at $27^{\circ}C$, which markedly declined equal to 50% of those of $15^{\circ}C$. Vitellogenin production peaked at the concentration of $10^{-6}M\;E_2$. No effect was observed on VTG production at various concentrations of 2, 4-D. However, a low concentration of 2, 4-D (ie, $10^{-8}M$) only appeared increased VTG production. $E_2$ or $10^{-8}M$ 2, 4-D-primed VTG production was markedly inhibited by the addition of $10^{-6}M$ tamoxifen to the culture medium(P<0.01). Inhibition was not affected by combinational treatment with $10^{-6}M$ $E_2$ and $10^{-6}M$ 2, 4-D. These results from the current investigation suggest that 2, 4-D mimics $E_2$, but the mechanism of reaction in inducing the $E_2$ receptor are different in VTG production in oliver flounder hepatocytes.

• Journal of Life Science
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• v.17 no.8 s.88
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• pp.1053-1062
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• 2007

In the present work, we show that tamoxifen(Tam)-induced cytotoxicity is due to the mitochondrial-dependent pathway triggered by the intracellular $Ca^{2+}$ increase in MCF-7 human breast cancer cells. Tam induced the intracellular $Ca^{2+}$ increase. According to the experimental results with $Ca^{2+}$ channel blockers, Tam-induced $Ca^{2+}$ uptake seemed to depend on the voltage-sensitive $Ca^{2+}$ channel at the early stage, but at later stages the intracellular $Ca^{2+}$ increases are more likely due partly to the release of stored $Ca^{2+}$ and partly to the capacitative $Ca^{2+}$ or other entry pathways. Tam-induced $Ca^{2+}$ increase led to the release of cytochrome c from mitochondria into the cytosol and the change of mitochondrial membrane potential. In MCF-7 cells, caspase-7 plays a key role in the downstream of apoptosis because caspase-3 is absent. In the cells treated with Tam, caspase-7 cleavage was increased almost two-fold. There was no marked alteration in the level of anti-apoptotic Bcl-2 protein; however, the cells showed increased expression of pro-apoptotic Bax protein more than two-fold in response to Tam. These results imply that the apoptotic signaling pathway activated by Tam is likely to be mediated via the mitochondrial-dependent pathway.

• Clinical and Experimental Reproductive Medicine
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• v.26 no.2
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• pp.149-156
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• 1999

Steroid hormone is known to cause the dynamic changes of mammalian uterus during reproductive cycle, which are modulated via hypothalamus-pituitary -gonad reproductive endocrine axis. Although there were so many studies about estrogenic regulation of uterine growth and differentiation. There is little information about the effect of estrogen on the expression of various transcription factors involved in gene expression. Thus the present study was designed to demonstrate E induced expression of c-fos, c-jun, hsp25 mRNA in rat uterus. Employing Northern blot analysis, we studied the temporal expressions of c-fos, c-jun, and hsp25 messenger RNAs (mRNAs) elicited by a single 17beta-estradiol (E) treatment in the uteri of bilaterally ovariectomized adult rats. c-fos, c-jun, and hsp25 mRNA levels were increased and peaked at 3h after E administration, and then c-fos and c-jun mRNA levels were rapidly decreased to basal control level while, increased hsp25 mRNA levels were sustained till 12h post E treatment. To test the estrogenic effect on the increase of c-fos, c-jun, and hsp25 mRNA levels, we also examined the effects of antiestrogen (tamoxifen). Pretreatment with tamoxifen effectively blocked the E-induced increase of c-fos, c-jun, and hsp25 mRNA levels at 3h post E treatment. Present results suggest that transient increase of c-fos and c-jun protooncogene mRNA at the early time and simultaneous expression of hsp25 mRNA contribute to the response of uterine tissues to E in adult female rats.

• Journal of KIISE:Computing Practices and Letters
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• v.9 no.1
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• pp.1-12
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• 2003

Recently, many researches into distributed processing on Internet, and multimedia data processing have been performed. Rapid and convenient multimedia services supplied with high quality and high speed are to be needed. In this paper, we design and implement clip-based video retrieval system on the Web enviroment in real-time. Our system consists of the content-based indexing system supporting convenient services for video content providers, and the Web-based retrieval system in order to make it easy and various information retrieval for users in the Web. Three important methods are used in the content-based indexing system, key frame extracting method by dividing video data, clip file creation method by clustering related information, and video database construction method by using clip unit. In Web-based retrieval system, retrieval method ny using a key word, two dimension browsing method of key frame, and real-time display method of the clip are used. In this paper, we design and implement the system that supports real-time display method of the clip are used. In this paper, we design and implement the system that supports real-time retrieval for video clips on Web environment and provides the multimedia service in stability. The proposed methods show a usefulness of video content providing, and provide an easy method for serching intented video content.

• The Journal of Korean Obstetrics and Gynecology
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• v.37 no.1
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• pp.1-22
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• 2024

목 적: 본 연구의 목적은 유방암 세포(MCF-7) 이식 누드 마우스 모델을 이용하여 육종용 열수 추출물의 면역활성 효과를 통한 항암 활성을 체계적으로 평가하는 것이다. 육종용 열수 추출물은 유방암 치료제로 자주 사용되는 대표적인 경구용 항암제인 tamoxifen 경구 투여군과 비교하여 분석 연구하였다. 방 법: 총 110마리의 6주령 암컷 누드 마우스를 준비하여, 7일간 적응 후 체중이 일정한 마우스를 선정하여 우측 둔부 피하부위에 MCF-7 세포를 이식하였다. 종양세포 이식을 한 지 20일 후, 종양 크기 및 체중을 기준으로 그룹 당 8마리씩 본 실험에 사용하였다. MCF-7 이종 이식 21일 후부터 매일 1회씩 35일간 육종용 열수 추출물을 10 ml/kg의 용량(400, 200 및 100 mg/kg)으로 경구 투여하였으며, tamoxifen 역시 10 ml/kg의 용량(20 mg/kg)으로 경구 투여하였고, 정상 및 종양 이식 매체 대조군에서는 멸균증류수만 종양 이식 21일 후부터 동일한 방법으로 35일간 경구 투여 하였다. 결 과: 본 실험의 결과, MCF-7 세포 이식을 함으로써 현저한 비장 및 하악하 림프절 무게, 혈중 IFN-γ의 함량, IL-1β 및 IL-10의 함량, 비장내 TNF-α, 비장세포 및 복강 대식구의 활성의 감소가 관찰되었고, 비장 및 하악하 림프절의 림프구 감소에 의한 조직병리학적 위축 또한 관찰되었다. 그리고 체중 및 증체량의 감소 역시 관찰되었으며, 혈중 IL-6 함량의 증가, 난소 주위의 지방 무게의 감소 및 조직병리학적으로 난소 주위의 축적 지방 조직 위축 현상이 인정되어, 종양 이식 후에 전형적인 종양과 관련된 면역억제와 악액질 현상이 유발된 것으로 판단되었다. 한편 육종용 열수 추출물 400, 200 및 100 mg/kg 경구 투여군에서는 종양 이식 대조군에 비해 유의성 있는 현저한 항암활성이 투여 용량 의존적으로 관찰되었다. 또한 tamoxifen 20 mg/kg 경구 투여군에서는 종양 관련 악액질 소견이 오히려 악화되는 반면, 육종용 열수 추출물 경구 투여군에서는 면역활성 및 악액질 억제 효과가 관찰되었다. 결 론: 본 연구 결과, 육종용 열수 추출물의 적절한 경구 투여는 심각한 부작용 없이, 종양 관련 악액질 소견을 포함하여, 효과적인 유방암 치료 수단을 제공할 수 있을 것으로 기대된다.

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.10a
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• pp.202-202
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• 2001

Stable MCF-7-ERE cells, in which pERE-Luc reporter gene has been stably integrated into the genome of the MCF-7 cells, were used to detect the estrogenic activity of various dietary flavonoids.in either pure chemical or mixtures. Estradiol (E2) induced luciferase activity in dose dependent manner and this activity was inhibited by tamoxifen (Tam) concomitant treatment.(omitted)

• 대한임상약리학회:학술대회논문집
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• 2002.12a
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• pp.30-30
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• 2002

• BMB Reports
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• v.41 no.3
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• pp.210-216
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• 2008

CSE1L/CAS, a microtubule-associated, cellular apoptosis susceptibility protein, is highly expressed in various cancers. Microtubules are the target of paclitaxel-induced apoptosis. We studied the effects of increased or reduced CAS expression on cancer cell apoptosis induced by chemotherapeutic drugs including paclitaxel. Our results showed that CAS overexpression enhanced apoptosis induced by doxorubicin, 5-fluorour-acil, cisplatin, and tamoxifen, but inhibited paclitaxel-induced apoptosis of cancer cells. Reductions in CAS produced opposite results. CAS overexpression enhanced p53 accumulation induced by doxorubicin, 5-fluorouracil, cisplatin, tamoxifen, and etoposide. CAS was associated with $\alpha$-tubulin and $\beta$-tubulin and enhanced the association between $\alpha$-tubulin and $\beta$-tubulin. Paclitaxel can induce G2/M phase cell cycle arrest and microtubule aster formation during apoptosis induction, but CAS overexpression reduced paclitaxel-induced G2/M phase cell cycle arrest and microtubule aster formation. Our results indicate that CAS may play an important role in regulating the cytotoxicities of chemotherapeutic drugs used in cancer chemotherapy against cancer cells.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.6
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• pp.3419-3423
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• 2013

Of all gynecologic cancers, endometrial cancer is the most common cancer in the US and Europe. In addition, it is presently the second most common gynecologic cancer in the world. As a result of increasing menopausal, obese and tamoxifen use women, the incidence of the cancer seems to be on the increase. Surgery is the major treatment, whereas postoperative radiation therapy in high-intermediate risk patients many prevent locoregional recurrence. Adjuvant chemotherapy can improve progression free survival in advanced or recurrent cancers. Molecular targeted therapies are now a focus of attention including anti-vascular endothelial growth factor (VEGF), mammalian target of rapamycin (mTOR) inhibitor and tyrosine kinase inhibitor (TKI). They may provide useful future strategies for control of endometrial malignancies in developing countries and across the world.

• Journal of Life Science
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• v.26 no.12
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• pp.1383-1391
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• 2016

Anti-estrogen drugs such as tamoxifen have been used for treating patients with ER-positive, early breast cancer. However, resistance to anti-estrogen treatment is inevitable in most patients. Breast cancer anti-estrogen resistance-3 (BCAR3) has been identified as the protein responsible for the induction of tamoxifen resistance in estrogen-dependent human breast cancer. We have previously reported that BCAR3 regulates the cell cycle progression and the signaling pathway of EGF and insulin leading to DNA synthesis. In this study, we investigated the functional role of BCAR3 in regulating c-Jun transcription in non-tumorigenic human breast epithelial MCF-12A cells. A transient transfection of BCAR3 increased both the mRNA and protein of c-Jun expression, and stable expression of BCAR3 increased c-Jun protein expression. The overexpression of BCAR3 directly activated the promoter of c-jun, AP-1, and SRE but not that of $NF-{\kappa}B$. Furthermore, single-cell microinjection of BCAR3 expression plasmid in the cell cycle-arrested MCF-12A cells induced c-Jun protein expression, and co-injection of dominant negative mutants of Ras, Rac, and Rho suppressed the transcriptional activity of c-Jun in the presence of BCAR3. Furthermore, stable expression of BCAR3 increased the proliferation of MCF-12A cells. The microinjection of inhibitory materials such as anti-BCAR3 antibody and siRNA BCAR3 inhibited EGF-induced c-Jun expression but did not affect IGF-1 induced upregulation of c-Jun. Taken together, we propose that BCAR3 plays a crucial role in c-Jun protein expression and cell proliferation and that small GTPases (e.g., Ras, Rac, and Rho) are required for the BCAR3-mediated activation of c-Jun expression.