조성대 교수
Sung-Dae Cho
서울대학교 · 생화학·유전·분자생물학
연구실 소개
조성대 교수 연구실은 항암제 개발을 목표로, 자연유래 화합물과 신약 후보 물질이 암세포에 미치는 세포 사멸 유도 및 세포주기 정 arrest 작용을 중심으로 연구를 진행하고 있습니다. 특히, 난소암, 대장암, 전립선암 등 다양한 암세포주에서 Nur77, Sp1, 사멸수용체 등 핵심 전사인자와 사멸 경로를 타겟으로 한 약리적 작용 메커니즘을 규명하고 있습니다. 또한, 식물 유래 천연물(시리마린, 에보디아민 등)과 화합물(설퍼프라프란, DIM-C-Ph 등)의 항암 메커니즘을 분자생물학적·세포생물학적 방법으로 규명하고 있습니다. 이는 암 예방 및 치료제 개발에 기여할 수 있는 기초적이고 임상적 응용가치가 높은 연구입니다.
연구 현황
연구 성과 추이
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
주요 논문
15Tolfenamic acid (Tol) is a non-steroidal anti-inflammatory drug that was reported to exhibit anticancer activity in pancreatic and colorectal cancer models. This study examined the role of Tol in the death regulation of PC-3 and DU145 human androgen-independent prostate cancer cells. The results showed that Tol inhibited cell growth and induced apoptosis, as evidenced by nuclear fragmentation and cleaved caspase 3 and poly(ADP-ribose) polymerase. Tol suppressed the specificity protein 1 (Sp1) pr
Evodiamine, a bioactive alkaloid, has been regarded as having antioxidant, antiinflammatory, and anticancer properties. In the present study, we explored the effects of evodiamine on cell growth and apoptosis in human oral cancer cell lines. Our data revealed that evodiamine significantly inhibited the proliferation of human oral cancer cells and resulted in the cleavages of PARP (poly (ADP‐ribose) polymerase) and caspase‐3, in addition to causing the typical characteristics of apoptosis. Evodia
Earlier studies have shown that tolfenamic acid (Tol) exhibits anticancer activity in several cancer models by inhibiting tumor growth and angiogenesis. However, the chemopreventive effect of Tol on a cervical cancer model and the underlying mechanism of action are unknown. In this study, Tol was found to inhibit cell proliferation by inducing apoptosis without affecting cyclo-oxygenase 2 expression, but ampiroxicam did not. Tol decreases the specificity protein 1 (Sp1) mRNA and its promoter act
Sodium butyrate (NaBu) is known to exhibit anti-cancer effects via the differentiation and apoptosis of various carcinoma cells. However, the mechanism by which NaBu induces apoptosis and the involvement of protein kinases during apoptosis is not completely understood. To investigate the underlying pathways, we performed cell culture experiments in androgen-independent human prostate cancer (DU145 cells) focusing on various protein kinases. NaBu causes concentration-dependent cell detachment and
In the present study, we examined the effects of methanol extracts of Picrasma quassioides (MEPQ) on apoptosis in human cervical cancer cells. The results showed that MEPQ decreased the viability and induced caspase-dependent apoptosis in HEp-2 cells. MEPQ decreased specificity protein 1 (Sp1) in HEp-2 cells, whereas Sp1 mRNA was not changed. We found that MEPQ reduced Sp1 protein through proteasome-dependent protein degradation, but not the inhibition of protein synthesis. Also, MEPQ increased
Our findings suggest that NC triggers apoptosis via lysosome-dependent Mcl-1 protein degradation and could be chosen as a promising chemotherapeutic candidate against human OSCCs.
These suggest that MEAG and WA may be potential natural materials for the treatment of HNSCC.
Norcantharidin (NCTD), a demethylated analog of cantharidin isolated from blister beetles, has been used as a promising anticancer agent; however, the underlying function of NCTD against human oral squamous cell carcinoma (OSCC) has not been fully understood. Here, this study was aimed to investigate the apoptotic effect and molecular targets of NCTD in human OSCC in vitro and in vivo. The anticancer effects of NCTD and its related molecular mechanisms were evaluated by trypan blue exclusion ass
These results suggest that MEIB may serve as a potential drug candidate for the treatment of human OSCC.
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