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유방암세포 성장과 Bmi-1 발현에 대한 레스베라트롤의 억제 효과
박현주(Hyun-Joo Park),박광제(Kwang Je Bak),옥창엽(Chang Youp Ok),장혜옥(Hye-Ock Jang),배문경(Moon-Kyoung Bae),배수경(Soo-Kyung Bae) 한국생물공학회 2017 KSBB Journal Vol.32 No.3
Resveratrol has been actively investigated as an anticancer drug since it induces cell growth inhibition and apoptosis in many cancer cells. Resveratrol acts through modulation of multiple pathways and genes. In this study, we found resveratrol reduced cell growth and mammosphere formation in MDA-MB-231 triple-negative human breast cancer cells. This suppressive effect of resveratrol is accompanied by a reduction in Bmi-1 gene expression. We also observed that knockdown of Bmi-1 gene by small interfering RNA effectively sensitizes breast cancer cells to resveratrol treatment. Our data demonstrate, for the first time, that resveratrol down-regulates Bmi-1 expression in human breast cancer cells and suggest that specific molecular targeting of Bmi-1 can be combined with a chemotherapeutic strategy to improve the response of breast cancer cells to resveratrol.
JD005 화합물이 인간치수유래줄기세포의 상아질 모세포 분화에 미치는 영향에 관한 연구
김다솔(Da-Sol Kim),이남걸(Nam-Geol Lee),장혜옥(Hye-Ock Jang),안진희(Jin-Hee Ahn),김형룡(Hyung-Ryong Kim) 대한치과의사협회 2021 대한치과의사협회지 Vol.59 No.11
Preservation of natural teeth and their structure is critical for chewing, swallowing, and better speech. Dentin and dental tissues are crucial in maintaining natural teeth and their structure, but treatment of dental tissue and dentin fracture is challenging for dentistry. Hence, scientific understanding needs to be translated to discover novel dental treatments. Dental pulp stem cells (DPSCs) are mesenchymal stem cells (MSCs) isolated from the third molar pulp. These cells have similar characteristics to MSCs with a unique property where DPSCs can differentiate into dentin forming odontoblast-like cells. Here, we made an effort to evaluate the potential substrate that induces odontoblastic differentiation of DPSCs. In this study, JD005, A MODIFIED A2A antagonist from ZM-241385, was determined to enhance OD. Specifically, JD005 treatment significantly enhanced the OD markers like alkaline phosphatase (ALP), runt-related transcription factor 2 (RUNX2), OPN, dentin sialophosphoprotein (DSPP), and dentin matrix protein 1 (DMP1). Additionally, the DPSCs treated with JD005 showed enhanced SMAD phosphorylatin associated with differentiation. There observations distinctively suggest that JD005 potentially contributes to dentin regeneration via odontoblast differentiation.
돌연변이 p53 단백질의 Silencing에 의한 사람유방암세포의 in vivo 항종양 효과
박원익(Won Ick Park),박세라(Se-Ra Park),박현주(Hyun-Joo Park),배윤희(Yun-Hee Bae),유현수(Hyun Su Ryu),장혜옥(Hye-Ock Jang),배문경(Moon-Kyoung Bae),배수경(Soo-Kyung Bae) 한국생물공학회 2016 KSBB Journal Vol.31 No.1
Mutant p53 (R280K) is highly expressed in MDAMB-231 triple-negative human breast cancer cells. Currently, we reported the role of mutant p53-R280K in mediating the survival of MDA-MB-231 cells in vitro. The present study was undertaken to determine whether mutant p53-R280K affects breast cancer cell growth in vivo. To this end, we used small interfering RNA to knockdown the level of mutant p53- R280K in MDA-MB-231 cells. Silencing of mutant p53- R280K in MDA-MB-231 cells causes substantial tumor regression of established xenografts in vivo. In xenograft model for breast cancer, silencing of mutant p53-R280K in MDAMB-231 cells significantly inhibited the tumor growth. Moreover, TUNEL assay showed more occurrence of apoptotic cells in mutant p53-R280K silenced tumors compared to control. Our data indicate that mutant p53-R280K has an important role in mediating tumor growth of MDA-MB-231 cells in vivo. Taken together, this study suggests that endogenous mutant p53-R280K could be used as a therapeutic target for breast cancer cells harboring this TP53 missense mutation.
박선영(Seon-Yeong Park),강용규(Yong-Gyu Kang),배윤희(Yun-Hee Bae),김수륜(Su-Ryun Kim),박현주(Hyun-Joo Park),강영순(Young-Soon Kang),김미경(Mi-Kyoung Kim),위희준(Hee-Jun Wee),장혜옥(Hye-Ock Jang),배문경(Moon-Kyoung Bae),우재석(Jae Suk 한국생물공학회 2013 KSBB Journal Vol.28 No.1
Curcumin has diverse anticancer activities that lead to tumor growth inhibition of cancer cells and induction of apoptosis. Curcumin is involved in the regulation of multiple genes via transcription factors including NF-kB, STATs, AP1, and SP. Notch signaling plays critical roles in maintaining the balance between cell proliferation, differentiation and apoptosis, and thereby may contribute to the development of various cancers involving breast cancer. This study was to investigate the effects of curcumin on Notch1 gene expression and to explore the underlying mechanism. Here, we found that curcumin decreased the levels of Notch1 mRNA and protein in MDA-MB-231 human breast cancer cells, along with the downregulation of Sp family genes (Sp1, Sp2, Sp3, and Sp4). The repressive effect of curcumin on Notch1 gene transcription was confirmed by performing Notch1 promoter- driven reporter assay and three Sp-binding sites were identified on Notch1 promoter that may act as curcumin-respose elements. Moreover, treatment with mitramycin A, a specific Sp inhibitor, decreased the levels of Notch1 mRNA and protein in human breast cancer cells. Taken together, our results indicate that Notch1 gene expression is downregulated by curcumin, at least in part, through the suppression of Sp family, which may lead to apoptosis in human breast cancer cells.