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- 저자 : 손현진(Hyeon-Jin Sohn) (검색결과 3 건)
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손현진,예병호,김인령,박봉수,정성희,안용우,고명연,Sohn, Hyeon-Jin,Yea, Byeong-Ho,Kim, In-Ryoung,Park, Bong-Soo,Jeong, Sung-Hee,Ahn, Yong-Woo,Ko, Myung-Yun Korean Academy of Orofacial Pain and Oral Medicine 2011 Journal of Oral Medicine and Pain Vol.36 No.3
Eugenol (4-allyl-2-methoxyphenol) is a natural phenolic constituent extensively used in dentistry as a component of zinc oxide eugenol cement and is applied to the mouth environment. Chios gum mastic (CGM) is a resinous exudate obtained from the stem and the main leaves of Pistacia lenticulus tree native to Mediterranean areas. This study was undertaken to investigate the synergistic apoptotic effect of co-treatment with a natural product, CGM and natural phenolic compound, eugenol on SCC25 human tongue squamous cell carcinoma cell line. To investigate whether the co-treatment with eugenol and CGM compared to each single treatment efficiently reduces the viability of SCC25 cells, MTT assay was conducted. Induction and augmentation of apoptosis were confirmed by Hoechst staining, TUNEL staining and DNA hypoploidy. Westen blot analysis and immunofluorescent staining were performed to study the alterations of the expression level and the translocation of apoptosis-related proteins in co-treatment. In this study, co-treatment of with eugenol and CGM on SCC25 cells showed several lines of apoptotic manifestation such as nuclear condensations, DNA fragmentation, the increase and decrease of Bax and Bcl-2, decrease of DNA content, the release of cytochrome c into cytosol, translocation of AIF and DFF40 (CAD) onto nuclei, and activation of caspase-3, caspase-6 caspase-7, caspase-9, PARP, Lamin A/C and DFF45 (ICAD) whereas each single treated SCC25 cells did not show or very slightly these patterns. Although the single treatment of 40 ${\mu}g$/ml CGM and 0.5 mM eugenol for 24 h did not induce apoptosis, the co-treatment of these reagents prominently induced apoptosis. Therefore our data provide the possibility that combination therapy with CGM and eugenol could be considered as a novel therapeutic strategy for human oral squamous cell carcinoma.
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김인령,손현진,곽현호,김규천,박봉수,최원철,고명연,안용우,Kim, In-Ryoung,Sohn, Hyeon-Jin,Kim, Gyoo-Cheon,Kwak, Hyun-Ho,Park, Bong-Soo,Choi, Won-Chul,Ko, Myung-Yun,Ahn, Yong-Woo Korean Academy of Orofacial Pain and Oral Medicine 2007 Journal of Oral Medicine and Pain Vol.32 No.3
Bile acids and synthetic its derivatives induced apoptosis in various kinds of cancer cells and anticancer effects. Previous studies have been reported that the synthetic chenodeoxycholic acid (CDCA) derivatives showed apoptosis inducing activity on various cancer cells in vitro. It wasn't discovered those materials have apoptosis induced effects on YD9 human oral squamous carcinoma cells. The present study was done to examine the synthetic bile acid derivatives(HS-1199, HS-1200) induced apoptosis on YD9 cells and such these apoptosis events. We administered them in culture to YD9 cells. Tested YD9 cells showed several lines of apoptotic manifestation such as activation of caspase-3, degradation of DFF, production of poly (ADP-ribose) polymerase(PARP) cleavage(HS-1200 only), DNA degradation(HS-1200 only), nuclear condensation, inhibition of proteasome activity, reduction of mitochondrial membrane potential(HS-1200 only) and the release of cytochrome c and AIF to cytosol. Between two synthetic CDCA derivatives, HS-1200 showed stronger apoptosis-inducing effect than HS-1199. Therefore HS-1200 was demonstrated to have the most efficient antitumor effect. Taken collectively, we demonstrated that a synthetic CDCA derivative HS-1200 induced caspases-dependent apoptosis via mitochondrial pathway in human oral sqauamous carcinoma cells in vitro. Our data therefore provide the possibility that HS-1200 could be considered as a novel therapeutic strategy for human orall squamous carcinoma from its poweful apoptosis-inducing activity.
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Mechanism Underlying NaF-induced Apoptosis and Cell Cycle Arrest on G361 Human Melanoma Cell Line
김도균(Do-Kyun Kim),손현진(Hyeon-Jin Sohn),김인령(In-Ryoung Kim),김규천(Gyoo-Cheon Kim),박봉수(Bong-Soo Park),곽현호(Hyun-Ho Kwak) 대한체질인류학회 2011 해부·생물인류학 (Anat Biol Anthropol) Vol.24 No.4
불화나트륨(sodium fluoride, NaF)은 치아우식증을 예방하기 위한 치과용 물질로 널리 사용되어 왔다. 치아우식증 예방을 위한 불소의 장기간 섭취가 인체에 미치는 영향에 대해 알려진 것이 거의 없고, 과복용 시 심각하고 치명적인 독성을 일으킬 수 있다는 보고가 있으나 불소의 안전성은 여전히 논쟁요소로 남아 있다. 그러나 불소는 구강건강을 위한 주요 물질로서 인정받고 있는 것이 사실이다. NaF은 몇 가지의 정상세포들에서 세포자멸사를 유도하고, 얼마간의 암세포에서 세포주기 정지와 세포자멸사를 유도한다고 알려져 있다. 이 연구의 목표는 사람구강편평상피세포암종세포(G361 세포)에 NaF 적용 후, 세포자멸사의 유도와 세포자멸사에 대한 분자생물학적 기전을 밝히는 것이다. 사람흑색종세포의 생존율은 MTT법으로, G36l 세포의 성장억제능의 측정은 clonogenic assay를 사용하였다. NaF 적용시, G361 세포에서 세포자멸사가 유도되는 것을 확인하기 위해서 Hemacolor 염색법, Hoechst 염색법, DNA 전기영동법 및 TUNEL법을 사용하였다. 그리고 G361 세포에 NaF을 적용한 후, Western blot 분석, 세포면역화학염색, 공초점레이져주사현미경 검경, FACScan flow cytometry, 사립체막 전위변화, proteasome 활성도 측정 등을 시행하였다. NaF로 처리된 G361 세포는 시간 및 용량의존적인 세포생존율 감소, 용량의존적인 성장억제 및 세포자멸사에 의한 세포죽음을 보였다. 그리고 NaF가 적용된 G361 세포에서 핵농축, DNA 조각남, 사립체막전위와 proteasome 활성도의 감소, DNA양의 감소, cytochrome c의 사립체에서의 세포질로의 유리, AIF와 DFF40(CAD)의 핵으로의 이동, Bax와 Bcl-2의 분율 변화, 그리고 caspase-9, caspase-7, caspase-6, caspase-3, PARP, Lamin A/C, DFF45(ICAD)의 활성화와 같은 다양한 세포자멸사 증거를 보였다. 더 나아가서 NaF에 처리된 G361 세포에서 G1 세포주기에 관계하는 Cyclin D1, Cyclin D3, Cdk2 그리고 Cdk4의 발현의 감소와 p53의 탁월한 발현의 증가를 보였다. 이 연구를 통하여 NaF가 G1 세포주기정지 단백질의 변형 그리고 proteasome, 사립체 및 caspase 경로의 연속 반응을 통해 G361 세포의 세포자멸사를 유도함을 명확하게 증명하였다. Fluoride is widely used in dentistry to prevent dental caries, even though the safety of fluoride is a controversial issue. There are no known adverse effects of long-term fluoride ingestion for caries prevention, but an overdose can cause serious acute toxicity. Nevertheless it is accepted that fluoride is an important material for oral health. This study was undertaken to investigate the modulation of cell cycle-related proteins and apoptosis induction underlying mechanism by NaF treatment on G361 human melanoma cell line. The viability of G361 cells and the growth inhibition of G361 cells were assessed by MTT assay and clonogenic assay respectively. Hoechst staining, DNA electrophoresis and TUNEL staining were conducted to observe G361 cells undergoing apoptosis. G361 cells were treated with NaF, and Western blotting, immunocytochemistry, con-focal microscopy, FACScan flow cytometry, MMP activity and proteasome activity were performed. NaF treatment in G361 cells resulted in a time- and does-dependent decrease of cell viability and a does-dependent inhibition of cell growth, and induced apoptotic cell death. And tested G361 cells showed several lines of apoptotic manifestation such as nuclear condensation, DNA fragmentation, the reduction of MMP and proteasome activity, the decrease of DNA contents, the release of cytochrome c into cytosol, the translocation of AIF and DFF40 (CAD) onto nuclei, a significant shift of Bax/Bcl-2 ratio, and the activation of caspase-9, caspase-7, caspase-6, caspase-3, PARP, Lamin A/C and DFF45 (ICAD). Furthermore, NaF resulted in down-regulation of the G1 cell cycle-related proteins, and up-regulation of p53. Taken collectively, our present findings demonstrate that NaF strongly inhibits cell proliferation by modulating the expression of the G1 cell cycle-related proteins and induces apoptosis via proteasome, mitochondria and cas-pase cascades in G361 cells.
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