• Asian Pacific Journal of Cancer Prevention
• /
• 제17권7호
• /
• pp.3281-3287
• /
• 2016

Bioactive compounds extracted from leaves and twigs of Goniothalamus griffithii include pinocembrin (PCN) and goniothalamin (GTN). The objectives of this study were to investigate the cytotoxic activities of PCN and GTN and their influence on molecular signaling for cell death in several human cancer cell lines compared to normal murine fibroblast NIH3T3 cells. GTN exhibited the most potent cytotoxicity against MCF-7 > HeLa > HepG2 > NIH3T3 cells with $IC_{50}$ values of 7.33, 14.8, 37.1 and $65.4{\mu}M$, respectively, whereas PCN was cytotoxic only to HepG2 cells with $IC_{50}$ values of ${\sim}80{\mu}M$. Apoptotic cell death was confirmed by staining the cells with annexin V-FITC and propidium iodide (PI) employing flow cytometry. Apoptosis was shown by externalization of phosphatidylserine in goniothalamin-treated MCF-7 cells in a dose response manner. Positive PI-stained cells with the typical morphology of apoptotic cells were increased dose-dependently. Furthermore, reduction of mitochondrial transmembrane potential was found in goniothalamin-treated MCF-7, HepG2 and HeLa cells. GTN treatment in MCF-7 increased caspase-3, -8 and -9 activities while GTN-induced HeLa cells showed an increase of both caspase-3 and -9 activities. But an increased caspase-8 activity was demonstrated in GTN- and PCN-treated MCF-7 and HepG2 cells, respectively. Taken together, GTN- and PCN-induced human cancer cell apoptosis was through different molecular mechanisms or signaling pathways, which might be due to different machineries in different types of cancer cells, as evidenced by the compound-modulated caspase activities in both intrinsic and/or extrinsic pathways.

• 생명과학회지
• /
• 제18권10호
• /
• pp.1435-1441
• /
• 2008

본 연구는 MCF-7 유방암 세포에 대한 유자(CJP)와 탱자 (PTP) 과피 추출물의 항암 활성과 환경호르몬에 의해 유도된 암세포의 증식 억제 효과에 대하여 조사하였다. CJP와 PTP를 300 mg/ml 농도에서 72시간 처리하였을 경우, 암세포의 성장을 저해하였고 세포사멸을 유도하였다. MCF-7 유방암 세포의 형태학적 변화는 CJP와 PTP를 500 mg/ml 농도에서 7시간 처리하였을 경우 관측되었고 세포사멸은 capase-3의 활성화에 의하여 유도되었다. 환경호르몬에 의해 유도된 MCF-7 유방암 세포의 증식은 CJP와 PTP의 처리로 인하여 농도 의존적으로 감소하였으며, 300 mg/ml 농도에서는 대조군과 비교하였을 때 각각 70%와 80% 이상 감소하였다.

• 대한한방부인과학회지
• /
• 제20권3호
• /
• pp.35-44
• /
• 2007

Purpose: This study was conducted to investigate the anti-proliferative effects of Ulmi Pumilae Cortex Extracts(UPCE) on MCF-7(human, breast, adenocaecinoma) and NIH3T3 (human, murine, fibroblast). Methods: MCF-7 cells and NIH3T3 cells were cultured and seeded in cell culture plates, respectively. UPC was extracted with hot water and then further fractionated it into five types: hexane, chloroform, ethyl acetate, butanol, and water soluable fractions. These five different fractions from UPCE were tested for their anti-proliferative effects on MCF-7 cells and NIH3T3 cells by MMT assay. Results: Among the five solvent-fractions of UPCE, n-hexane fraction and ethyl acetate fraction showed a strong anti-proliferative effects on MCF-7 cells but they displayed significant cytotoxicity on NIH3T3 cells, too. On the other hand, chloroform fraction showed a marked anti-proliferative effects on MCF-7 cells and low cytotoxicity on NIH3T3 cells. Conclusion: Chloloform fraction from UPCE showed selective anti-cancer activities on human breast cancer cell MCF-7 relatively to the other fractions.

• 대한한방부인과학회지
• /
• 제27권2호
• /
• pp.12-22
• /
• 2014

Objectives: This study aimed to evaluate the effects of Cuscutae Semen water extract (CS) on MCF-7 human breast cancer cells. Methods: To clarify the results, we cultivated MCF-7 cells in cell culture plates. And then we extracted each of $100{\mu}g/ml$, $300{\mu}g/ml$, $600{\mu}g/ml$ CS, gave it to MCF-7 cell. After these process we performed MTT assay to elucidate the ability of apoptosis. The result of mRNA was analyzed by RT-PCR. Results: Each of concentrated extracts CS decreased the survival rate of MCF-7 cells. CS decreased Bcl-2 which is known as a blocking cell apoptosis. Bax, caspase-3, P21 and RIP-1 that accelerate apoptogenic activity factors increased by CS. CS did not change the condition of caspase-8, caspase-9, P53 factors on MCF-7 cells. Furthermore caspase-8, caspase-9, P53 factors on MCF-7 cells does not make it more active but turn it on. Conclusions: According to the above results, we could suggest that CS can occur the apoptosis on MCF-7 cells.

• 한국융합학회논문지
• /
• 제12권9호
• /
• pp.179-183
• /
• 2021

본 연구는 다양한 항암성분을 함유한 Celeriac Extract의 암세포 증식에 미치는 영향을 살펴보기 위하여 실시되었다. 실험에 사용한 암 세포주는 5종으로 폐암세포 A549, 전립샘암세포 DU-145, 자궁암세포 HeLa, 유방암세포 MCF-7, 간암세포 SNU-182 로 모두 인체 유래 암 세포주를 사용하였으며 Celeriac Extract 10ug/mL, 100ug/mL, 1000ug/mL 에 대한 암세포의 증식 억제는 CCK-8 방법을 이용하여 측정하였다. 암세포 증식 억제를 살펴본 결과 Celeriac Extract 1000ug/mL는 폐암세포 A549, 전립샘암세포 DU-145, 자궁암세포 HeLa, 간암세포 SNU-182에서 유의한 증식 억제를 보였으며 농도 의존성을 나타냈다. 그러나 유방암세포 MCF-7 에서는 농도 의존적인 감소만 보였다. 결론적으로, 다양한 인간유래 암 세포주를 이용한 Celeriac Extract의 세포 증식 억제기전들은 암 예방효과 및 치료제 개발의 잠재력을 제공한다고 볼 수 있다.

• Asian Pacific Journal of Cancer Prevention
• /
• 제15권18호
• /
• pp.7919-7923
• /
• 2014

20(S)-Protopanaxadiol (PPD), a ginsenoside isolated from Pananx quinquefolium L., has been shown to inhibit growth and proliferation in several cancer cell lines. The aim of this study was to evaluate its anticancer activity in human breast cancer cells. MCF-7 cells were incubated with different concentrations of 20(S)-PPD and cytotoxicity was evaluated by MTT assay. Occurrence of apoptosis was detected by DAPI and Annexin V-FITC/PI double staining. Mitochondrial membrane potential was measured with Rhodamine 123. The Bcl-2 and Bax expression were determined by Western blot analysis. Caspase activity was measured by colorimetric assay. 20(S)-PPD dose-dependently inhibited cell proliferation in MCF-7 cells, with an $IC_{50}$ value of $33.3{\mu}M$ at 24h. MCF-7 cells treated with 20(S)-PPD presented typical apoptosis, as observed by morphological analysis in cell stained with DAPI. The percentages of annexin V-FITC positive cells were 8.92%, 17.8%, 24.5% and 30.5% in MCF-7 cells treated with 0, 15, 30 and $60{\mu}M$ of 20(S)-PPD, respectively. Moreover, 20(S)-PPD could induce mitochondrial membrane potential loss, up-regulate Bax expression and down-regulate Bcl-2 expression. These events paralleled activation of caspase-9, -3 and PARP cleavage. Apoptosis induced by 20(S)-PPD was blocked by z-VAD-fmk, a pan-caspase inhibitor, suggesting induction of caspase-mediated apoptotic cell death. In conclusion, the 20(S)-PPD investigated is able to inhibit cell proliferation and to induce cancer cell death by a caspase-mediated apoptosis pathway.

• Asian Pacific Journal of Cancer Prevention
• /
• 제17권2호
• /
• pp.581-590
• /
• 2016

Resistance to anoikis, a cell-detachment induced apoptosis, is one of the malignant phenotypes which support tumor metastasis. Molecular mechanisms underlying the establishment of this phenotype require further investigation. This study aimed at exploring protein expression profiles associated with anoikis resistance of a metastatic breast cancer cell. Cell survival of suspension cultures of non-metastatic MCF-7 and metastatic MDA-MB-231 cells were compared with their adherent cultures. Trypan blue exclusion assays demonstrated a significantly higher percentage of viable cells in MDA-MB-231 than MCF-7 cell cultures, consistent with analysis of annexin V-7-AAD stained cells indicating that MDA-MB-231 possess anti-apoptotic ability 1.7 fold higher than MCF-7 cells. GeLC-MS/MS analysis of protein lysates of MDA-MB-231 and MCF-7 cells grown under both culture conditions identified 925 proteins which are differentially expressed, 54 of which were expressed only in suspended and adherent MDA-MB-231 but not in MCF-7 cells. These proteins have been implicated in various cellular processes, including DNA replication and repair, transcription, translation, protein modification, cytoskeleton, transport and cell signaling. Analysis based on the STITCH database predicted the interaction of phospholipases, PLC and PLD, and 14-3-3 beta/alpha, YWHAB, with the intrinsic and extrinsic apoptotic signaling network, suggesting putative roles in controlling anti-anoikis ability. MDA-MB-231 cells grown in the presence of inhibitors of phospholipase C, U73122, and phospholipase D, FIPI, demonstrated reduced ability to survive in suspension culture, indicating functional roles of PLC and PLD in the process of anti-anoikis. Our study identified intracellular mediators potentially associated with establishment of anoikis resistance of metastatic cells. These proteins require further clarification as prognostic and therapeutic targets for advanced breast cancer.

• 한국식품위생안전성학회지
• /
• 제25권3호
• /
• pp.209-214
• /
• 2010

Metastasis is the primary cause of from breast cancer mortality. Cell migration and invasion play important roles in neoplastic metastasis. Matrix metalloproteinase-9 (MMP-9), which degrades the extracellular matrix (ECM), plays an important role in cancer cell invasion. NF-${\kappa}B$ is transcription factor important in the regulation of MMP-9, as the promoter of MMP-9 gene contains binding sites for NF-${\kappa}B$. Brazilin, an active component of sappan wood (Caesalpinia sappan), decreases TPA-induced MMP-9 expression and invasion in MCF-7 cells. Also, brazilin suppressed NF-${\kappa}B$ activation in TPA-treated MCF-7 cells. Taken together, we demonstrated that the inhibition of TPA-induced MMP-9 expression and cell invasion by brazilin is mediated by the suppression of the NF-${\kappa}B$ pathway in MCF-7 cells. This result suggest brazilin provide a potential therapeutic app roach for the treatment of breast cancer.

• International Journal of Industrial Entomology and Biomaterials
• /
• 제27권2호
• /
• pp.228-236
• /
• 2013

Breast cancer is one of the most common cancers among women worldwide. Recently anticancer agents have been developed using natural substances. To evaluate the anticancer effect of hydrolysates of silk fibroin (HSF), we investigated the effect of HSF on cell viability and apoptosis of a breast cancer cell line, MCF-7, induced through the mitochondrial pathway. The result showed that HSF decreased cell viability in MCF-7 cells in a dose- and time-dependent manner, resulting in an increase in the sub-G1 phase cell population. HSF increased the level of the pro-apoptotic Bax protein and decreased the levels of the anti-apoptotic Bcl-2 protein. In addition, HSF induced apoptosis in MCF-7 cells through a mitochondria-dependent pathway by increasing levels of cytochtome c, and cleavage of PARP. Taken together, these findings suggest that HSF inhibits the proliferation of MCF-7 breast cancer cells through a mitochondria and caspase dependent apoptotic pathway.

• Asian Pacific Journal of Cancer Prevention
• /
• 제14권10호
• /
• pp.5719-5723
• /
• 2013

Pharmacological and preventive properties of Petroselinum sativum seed extracts are well known, but the anticancer activity of alcoholic extracts and oil of Petroselinum sativum seeds on human breast cancer cells have not been explored so far. Therefore, the present study was designed to investigate the cytotoxic activities of these extracts against MCF-7 cells. Cells were exposed to 10 to $1000{\mu}g/ml$ of alcoholic seed extract (PSA) and seed oil (PSO) of Petroselinum sativum for 24 h. Post-treatment, percent cell viability was studied by 3-(4, 5-dimethylthiazol-2yl)-2, 5-biphenyl tetrazolium bromide (MTT) and neutral red uptake (NRU) assays, and cellular morphology by phase contrast inverted microscopy. The results showed that PSA and PSO significantly reduced cell viability, and altered the cellular morphology of MCF-7 cells in a concentration dependent manner. Concentrations of $50{\mu}g/ml$ and above of PSA and $100{\mu}g/ml$ and above of PSO were found to be cytotoxic in MCF-7 cells. Cell viability at 50, 100, 250, 500 and $1000{\mu}g/ml$ of PSA was recorded as 81%, 57%, 33%, 8% and 5%, respectively, whereas at 100, 250, 500, and $1000{\mu}g/ml$ of PSO values were 90%, 78%, 62%, and 8%, respectively by MTT assay. MCF-7 cells exposed to 250, 500 and $1000{\mu}g/ml$ of PSA and PSO lost their typical morphology and appeared smaller in size. The data revealed that the treatment with PSA and PSO of Petroselinum sativum induced cell death in MCF-7 cells.