http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Lee, Ju-Hye,Won, Yeong-Seon,Park, Ki-Hun,Lee, Mi-Kyung,Tachibana, Hirofumi,Yamada, Koji,Seo, Kwon-Il Rapid Science Publishers ; Kluwer Academic Publish 2012 Apoptosis Vol.17 No.12
<P>Celastrol has been reported to possess anticancer effects in various cancers; however, the precise mechanism underlying ROS-mediated mitochondria-dependent apoptotic cell death triggered by celastrol treatment in melanoma cells remains unknown. We showed that celastrol effectively induced apoptotic cell death and inhibited tumor growth using tissue culture and in vivo models of B16 melanoma. In addition to apoptotic cell death in B16 cells, several apoptotic events such as PARP cleavage and activation of caspase were confirmed. Pretreatment with caspase inhibitor modestly attenuated the celastrol-induced increase in PARP cleavage and sub-G1 cell population, implying that caspases play a partial role in celastrol-induced apoptosis. Moreover, ROS generation was detected following celastrol treatment. Blocking of ROS accumulation with ROS scavengers resulted in inhibition of celastrol-induced Bcl-2 family-mediated apoptosis, indicating that celastrol-induced apoptosis involves ROS generation as well as an increase in the Bax/Bcl-2 ratio leading to release of cytochrome c and AIF. Importantly, silencing of AIF by transfection of siAIF into cells remarkably attenuated celastrol-induced apoptotic cell death. Moreover, celastrol inhibited the activation of PI3K/AKT/mTOR signaling cascade in B16 cells. Our data reveal that celastrol inhibits growth and induces apoptosis in melanoma cells via the activation of ROS-mediated caspase-dependent and -independent pathways and the suppression of PI3K/AKT signaling.</P>
Hyung-Jin Lim,Jaehoon Bae,Seon Gyeong Bak,Nisansala Chandimali,Eun Hyun Park,Sang-Ik Park,Hirofumi Tachibana,Yeong-Seon Won,이승재 한국식품영양과학회 2023 Journal of medicinal food Vol.26 No.10
The discovery of limocitrin in Sedum sarmentosum Bunge, a compound known for its potent antitumor activity, hassparked interest in understanding its molecular mechanisms and bioactive effects. Breast cancer, particularly triple-negative breastcancer (TNBC), presents a challenging prognosis with a higher likelihood of recurrence, metastasis, and lower survival ratescompared tomost other cancer types. This study aimed to explore the anticancer potential of limocitrin on two different human breastcancer cell lines. The results of the study revealed that limocitrin effectively reduced the viability of breast cancer cells, with IC50values of 29.33 – 0.010 and 28.70 – 0.030 lM for MDA-MB-231 and MCF-7 cells, respectively. Further investigations demonstratedthat limocitrin induced apoptotic cell death, characterized by an increase in the population of apoptotic cells and the formationof apoptotic bodies. Limocitrin induced the upregulation of apoptosis-related protein expressions such as apoptosis-inducing factor,Bax, endonuclease G, and cleaved-poly ADP-ribose polymerase, while downregulating the expression of proteins associated withcell survival, including Akt, Bcl-2, Bid,mTOR, PI3K, procaspases, and p70 S6 kinase.Notably, the response to limocitrin treatmentvaried between the two types of breast cancer cells, indicating a differential effect of limocitrin on the intracellular signalingpathways related to cell survival in breast cancer.These findings open up avenues for further research and exploration of limocitrin asa potential therapeutic agent for breast cancer treatment, especially for challenging subtypes like TNBC.