• Biomolecules & Therapeutics
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• 제22권5호
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• pp.384-389
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• 2014

Adiponectin, an adipokine predominantly secreted from adipose tissue, exhibits diverse biological responses, including metabolism of glucose and lipid, and apoptosis in cancer cells. Recently, adiponectin has been shown to modulate autophagy as well. While emerging evidence has demonstrated that autophagy plays a role in the modulation of proliferation and apoptosis of cancer cells, the role of autophagy in apoptosis of cancer cell caused by adiponectin has not been explored. In the present study, we demonstrated that globular adiponectin (gAcrp) induces both apoptosis and autophagy in human hepatoma cell line (HepG2 cells) and breast cancer cells (MCF-7), as evidenced by increase in caspase-3 activity, Bax, microtubule-associated protein light chain 3-II (LC3 II) protein levels, and autophagosome formation. Interestingly, gene silencing of LC3B, an autophagy marker, significantly enhanced gAcrp-induced apoptosis in both HepG2 and MCF-7 cell lines, whereas induction of autophagy by rapamycin, an mTOR inhibitor, significantly prevented gAcrp-induced apoptosis in hepatoma cells HepG2. Furthermore, modulation of autophagy produced similar effects on gAcrp-induced Bax expression in HepG2 cells. These results implicate that induction of autophagy plays a regulatory role in adiponectin-induced apoptosis of cancer cells, and thus inhibition of autophagy would be a novel promising target to enhance the efficiency of cancer cell apoptosis by adiponectin.

• 셀메드
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• 제13권2호
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• pp.2.1-2.9
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• 2023

CPS219, a new concept compound composed of coffee (CO), Pueraria Tomsonii flower (PF), and Sambou bamboo salt^TM (BS), was developed as a coffee beverage to alleviate menopausal symptoms. The purpose of this study is to evaluate the anti-oxidant and menopausal alleviating effects of CPS219 combined as the optimal ratio of each component selected through sensory evaluation and blind consumer test. For CPS219, the optimal ratio of CO, PF, and BS was determined to be 1:0.1:0.017 through various sensory evaluations and blind consumer tests. CPS219 significantly enhanced the superoxide dismutase-like activity compared to the CO or CO plus PF (CP). The proliferation of MCF-7 cells was considerably increased after 24 hours by treatment with CO, CP, or CPS219, but only CPS219 significantly boosted the proliferation of MCF-7 cells after 48 hours. Moreover, CPS219 had an estrogen-like effect by dramatically increasing the expression of estrogen receptor-β mRNA in MCF-7 cells but not CO and CP. Treatment of MCF-7 cells with CO, CP, or CPS219 did not cause any cytotoxicity. In conclusion, these findings imply that anti-oxidant and estrogen-like properties of CPS219 can be used to prevent and cure postmenopausal symptoms.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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• pp.223.1-223.1
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• 2003

Many studies have identified the phosphatidylinositol 3-kinase (PI3K) as a key regulator for various cellular functions including cell survival, growth and motility. We have previously shown that H-ras, but not N-ras. induces invasiveness and motility in human breast epithelial cells (MCF10A), while both H-ras and N-ras induce transformed phenotype. In the present study, we wished to investigate the functional role of PI3K pathway in H-ra-induced invasive phenotype and motility of MCF10A cells. (omitted)

• 생명과학회지
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• 제31권3호
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• pp.266-279
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• 2021

본 연구에서는 다양한 사람의 암세포주(A-549, MCF-7, MDA-MB-231, U87-MG, AGS, MKN-74 및 SNU-601 세포)와 정상세포주(MRC-5 섬유아세포 및 사랑니 유래 중간엽성 줄기세포에 토복령 추출물(Smilax china L. extract, SCLE)을 처리하여 세포 사멸 효과를 조사하였다. SCLE 처리 후, MTT 분석에서 여러 암세포주는 정상세포주보다 유의적으로 휠씬 낮은 반억제농도값을 나타내었고, 세포는 세포부착력의 소실로 인한 세포사멸(anoikis)이 관찰되었다. 또한, SCLE를 처리한 A-549, AGS 및 MCF-7 암세포주에서 세포의 생존성과 말단소립 복원효소의 활성도를 조사하였을 때, SCLE 처리 후 4일째에 세포의 생존성과 말단소립 복원효소의 활성도가 현저히 줄어드는 것을 관찰하였다. 또한, SCLE를 처리한 A-549, AGS 및 MCF-7 암세포주에서 세포 주기의 G1기에서 세포 성장이 정지되었고,세포 사멸이 유의적으로 증가하는 것을 알 수 있었다. 그러나, SCLE 처리는 rho 단백질의 활성과 관련 없는 세포부착력의 소실과 세포 사멸이 유도되는 것을 관찰하였다. 이 연구의 결과를 바탕으로 토복령 추출물은 정상 세포보다는 암세포에 특이적으로 세포부착력의 소실과 세포 사멸을 유도하여, 이 추출물에 포함된 물질을 이용한 항암 연구에 응용될 수 있을 것으로 판단된다.

• Asian Pacific Journal of Cancer Prevention
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• 제16권6호
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• pp.2351-2354
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• 2015

In this study, the antiproliferative effects of the metformin was evaluated on MCF-7 Cells (human breast adenocarcinoma cell line). For this purpose cell kinetic parameters including cell proliferation assay, mitotic index and labelling index analysis were used. $30{\mu}M$, $65{\mu}M$ and $130{\mu}M$ Metformin doses were applied to cells for 24, 48 and 72 hours. The results showed that there was a significant decrease in cell proliferation, mitotic index and labelling index for all experimental groups (p<0.05) for all applications.

• 생명과학회지
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• 제22권10호
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• pp.1277-1285
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• 2012

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)은 암세포 선택적으로 작용하므로서 유용한 항암제로 주목 받고 있다. 그러나, TRAIL 에 내성을 나타내는 암세포도 많이 존재한다. 그러므로 TRAIL 내성을 극복할 수 있는 방법을 고안하는 연구는 암 치료 요법에 매우 중요하다. 본 연구에서는 SIRT1 siRNA 또는 SIRT1 inhibitor인 amurensin G를 사람 유방암세포에 처리하면 DR5및 c-Myc의 발현 증강과 c-$FLIP_{L/S}$ 및 Mcl-1 발현 억제를 유도하므로서, TRAIL 에 내성을 나타내는 사람유방암세포 MCF-7 세포의 TRAIL 감수성을 증강시킴을 알 수 있었다. 또한, SIRT1 억제에 의한 caspase 활성화, PARP cleavage 및 Bcl-2 발현감소를 나타내었다. 이러한 연구결과는 SIRT1 저해에 의한 DR5 유도와 함께 c-FLIP 발현 억제가 TRAIL 내성 암세포의 TRAIL 반응성 증강에 유용한 기전으로 사용 될 수 있음을 시사하였다.

• Journal of Microbiology and Biotechnology
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• 제28권9호
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• pp.1563-1572
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• 2018

Gold nanoparticles (AuNP) and their conjugates have been gaining a great deal of recognition in the medical field. Meanwhile, extended-spectrum ${\beta}$-lactamases (ESBL)-producing bacteria are also demonstrating a challenging problem for health care. The aim of this study was the biosynthesis of AuNP using Rosa damascenes petal extract and conjugation of ceftriaxone antibiotic (Cef-AuNP) in inhibiting ESBL-producing bacteria and study of in vitro anticancer activity. Characterization of the synthesized AuNP and Cef-AuNP was studied. ESBL-producing strains, Acinetobacter baumannii ACI1 and Pseudomonas aeruginosa PSE4 were used for testing the efficacy of Cef-AuNP. The cells of MCF-7 breast cancer were treated with previous AuNP and Cef-AuNP at different time intervals. Cytotoxicity effects of apoptosis and its molecular mechanism were evaluated. Ultraviolet-visible spectroscopy and Fourier transform infrared spectroscopy established the formation of AuNP and Cef-AuNP. Transmission electron microscope demonstrated that the formed nanoparticles were of different shapes with sizes of 15~35 nm and conjugation was established by a slight increase in size. Minimum inhibitory concentration (MIC) values of Cef-AuNP against tested strains were obtained as 3.6 and $4{\mu}g/ml$, respectively. Cef-AuNP demonstrated a decrease in the MIC of ceftriaxone down to more than 27 folds on the studied strains. The biosynthesized AuNP displayed apoptotic and time-dependent cytotoxic effects in the cells of MCF-7 at a concentration of $0.1{\mu}g/ml$ medium. The Cef-AuNP have low significant effects on MCF-7 cells. These results enhance the conjugating utility in old unresponsive ceftriaxone with AuNP to restore its efficiency against otherwise resistant bacterial pathogens. Additionally, AuNP may be used as an alternative chemotherapeutic treatment of MCF-7 cancer cells.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2002년도 Molecular and Cellular Response to Toxic Substances
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• pp.141-141
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• 2002

Transforming growth factor-${\beta}$ (TGF-${\beta}$), a hormonally active polypeptide found in normal and transformed tissues, regulates cellular growth and phenotyphic plasticity. We have previously shown that H-ras, but not N-ras, induces invasive phenotype in MCF10A human breast epithelial cells.(omitted)

• BMB Reports
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• 제51권9호
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• pp.450-455
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• 2018

Tamoxifen (TAM) is commonly used to treat estrogen receptor (ER)-positive breast cancer. Despite the remarkable benefits, resistance to TAM presents a serious therapeutic challenge. Since several HOX transcription factors have been proposed as strong candidates in the development of resistance to TAM therapy in breast cancer, we generated an in vitro model of acquired TAM resistance using ER-positive MCF7 breast cancer cells (MCF7-TAMR), and analyzed the expression pattern and epigenetic states of HOX genes. HOXB cluster genes were uniquely up-regulated in MCF7-TAMR cells. Survival analysis of in slico data showed the correlation of high expression of HOXB genes with poor response to TAM in ER-positive breast cancer patients treated with TAM. Gain- and loss-of-function experiments showed that the overexpression of multi HOXB genes in MCF7 renders cancer cells more resistant to TAM, whereas the knockdown restores TAM sensitivity. Furthermore, activation of HOXB genes in MCF7-TAMR was associated with histone modifications, particularly the gain of H3K9ac. These findings imply that the activation of HOXB genes mediate the development of TAM resistance, and represent a target for development of new strategies to prevent or reverse TAM resistance.

• Asian Pacific Journal of Cancer Prevention
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• 제13권4호
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• pp.1431-1437
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• 2012

The growth of many breast tumors is stimulated by IGF-1, which activates signal transduction pathways inducing cell proliferation. $ER{\alpha}$ is important in this process. The aim of the study was to investigate relationships in vitro among inhibitory effects of luteolin on the growth of MCF-7 cells, IGF-1 pathway and $ER{\alpha}$. Our results showed that luteolin could effectively block IGF-l-stimulated MCF-7 cell proliferation in a dose- and time-dependent manner and block cell cycle progression and induce apoptosis evidenced by the flow cytometric detection of sub-G1DNA content. Luteolin markedly decreased IGF-l-dependent IGF-IR and Akt phosphorylation without affecting Erk1/2 phosphorylation. Further experiments pointed out that $ER{\alpha}$ was directly involved in IGF-l induced cell growth inhibitory effects of luteolin, which significantly decreased $ER{\alpha}$ expression. Knockdown of $ER{\alpha}$ in MCF-7 cells by an $ER{\alpha}$-specific siRNA decreased the IGF-l induced cell growth inhibitory effects of luteolin. $ER{\alpha}$ is thus a possible target of luteolin. These findings indicate that the inhibitory effect of luteolin on the growth of MCF-7 cells is via inhibiting IGF-l mediated PI3K-Akt pathway dependent of $ER{\alpha}$ expression.