• 제목/요약/키워드: Caspase-3/7

검색결과 403건 처리시간 0.032초

수수 추출물에 의한 primary 전립선 암세포의 caspase 의존성 apoptosis 유도 및 대식세포 면역활성 증가 (Sorghum Extract Enhances Caspase-dependent Apoptosis in Primary Prostate Cancer Cells and Immune Activity in Macrophages)

  • 조현동;김정호;홍성민;이주혜;이용석;김두현;서권일
    • 생명과학회지
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    • 제26권12호
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    • pp.1431-1437
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    • 2016
  • 본 연구에서는 수수 에탄올 추출물(ethanol extract of Sorghum bicolor L., SE)을 이용하여 RC-58T/h/SA#4 primary 인체 전립선 암세포에 대한 apoptosis 유도효과 및 RAW 264.7 마우스 대식세포에 대한 면역활성 증진효능에 대해 알아보고자 하였다. SE의 처리는 RC-58T/h/SA#4 세포의 증식을 억제하였으며 세포수축을 통한 형태학적 변화를 유발하였다. 또한 apoptosis 관련 지표현상인 apoptotic body 및 핵의 형태변화를 관찰할 수 있었다. RC-58T/h/SA#4 세포에 SE를 처리하였을 때 caspase-8, -9, -3 단백질 활성을 증가시켰으며 pro-apoptotic 단백질인 Bax, p53, 분절된 PARP 및 세포질의 cytochrome c 단백질은 증가시킨 반면, anti-apoptotic 단백질인 Bcl-2 단백질은 감소시켰다. 이는 z-VAD-fmk로 caspase 활성을 억제시켰을 때 SE에 의한 세포증식 억제효과가 감소되었으며 이를 통해 SE에 의한 세포증식 억제효과는 caspase 의존적임을 확인할 수 있었다. 면역반응에서 nitric oxide(NO)의 증가는 면역활성 지표로 여겨지며, 본 연구에서 SE를 처리하였을 때 RAW 264.7 세포에서 NO 생성능이 증가하는 것으로 나타났다. 본 연구의 결과들은 SE가 primary 전립선 암세포에서 caspase 의존형 apoptosis를 유도하며 대식세포의 면역활성을 증가시킨다는 것을 나타낸다. 따라서 수수를 전립선 암 예방 및 면역활성을 증진효능이 있는 기능성 식품 소재로 활용할 수 있을 것으로 생각된다.

사람혀편평세포암종세포에서 Chios gum mastic과 eugenol의 병용처리가 미치는 세포자멸사 효과에 관한 연구 (Apoptotic Effect of Co-Treatment with Chios Gum Mastic and Eugenol on SCC25 Human Tongue Squamous Cell Carcinoma Cell Line)

  • 손현진;예병호;김인령;박봉수;정성희;안용우;고명연
    • Journal of Oral Medicine and Pain
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    • 제36권3호
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    • pp.147-160
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    • 2011
  • Chios gum mastic (CGM)은 그리이스 키오스 섬에서만 자생하는 Pistiacia lentiscus L. var. Chia. 의 잎과 줄기로부터 추출되어진 식물성 수지이며, 과거 수세기 동안 지중해와 중동 지역 국가들에서 음식 첨가물과 위궤양, 십이지장궤양 등의 민간 치료약재로서 사용되어져 왔다. 정향나무에서 추출하는 페놀화합물인 eugenol은 zinc oxide eugenol의 구성성분으로 치과치료를 위해 많이 사용되고 있다. 본 연구는 사람혀편평세포암종세포(SCC25 cells)에서 천연물질인 CGM과 eugenol을 병용처리한 후 세포자멸사 효과가 있는지를 알아보기 위해 수행하였다. CGM과 eugenol의 병용처리가 단독처리에 비해서 효과적인 세포생존율 감소가 있는지 확인하기 위하여 MTT법을 시행하였고, 세포자멸사의 유도와 증가를 알기 위하여 Hoechst 염색법, TUNEL 염색법, DNA hypoploidy법을 사용하였다. 그리고 세포자멸사에 관계하는 단백질의 발현 변화와 세포내에서의 이동을 밝혀내기 위하여 Western blot 분석과 면역형광염색법을 수행하였다. 본 연구에서는 CGM과 eugenol이 병용처리된 SCC25 세포에서 핵의 농축, DNA분절, Bax의 증가와 Bcl-2의 감소, DNA양의 감소, cytochrome c의 세포질로의 유리, AIF와 DFF40 (CAD)의 핵으로의 이동, caspase-3, caspase-6, caspase-7, caspase-9, PARP, Lamin A/C 그리고 DFF45 (ICAD)의 활성화와 같은 다양한 세포자멸사 증거를 보였다. 반면에 CGM과 eugenol이 각각 단독 처리된 SCC25 세포에서는 세포자멸사 현상이 미미하였다. 24시간 동안 40 ${\mu}g$/ml의 CGM과 0.5 mM의 eugenol을 각기 단독처리 한 결과에서는 세포자멸사를 거의 유도하지 못했으나, 병용처리 한 결과에는 아주 탁월한 세포자멸사의 유도를 보였다. 그러므로 본 실험결과는 사람구강편평세포암종 환자들에게 CGM과 eugenol의 병용요법이 새로운 치료전략으로서의 가능성을 줄 수 있다고 생각한다.

Rice Bran Phytic Acid Induced Apoptosis Through Regulation of Bcl-2/Bax and p53 Genes in HepG2 Human Hepatocellular Carcinoma Cells

  • Al-Fatlawi, Atheer Abbas;Al-Fatlawi, Anees Abbas;Irshad, Md.;Zafaryab, Md.;Alam Rizvi, M. Moshahid;Ahmad, Ayaz
    • Asian Pacific Journal of Cancer Prevention
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    • 제15권8호
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    • pp.3731-3736
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    • 2014
  • Phytic acid (PA) has been reported to have positive nutritional benefits and prevent cancer formation. This study investigated the anticancer activity of rice bran PA against hepatocellular carcinoma (HepG2) cells. Cytotoxicty of PA (0.5 to 4mM) was examined by MTT and LDH assays after 24 and 48h treatment. Apoptotic activity was evaluated by expression analysis of apoptosis-regulatory genes [i.e. p53, Bcl-2, Bax, Caspase-3 and -9] by reverse transcriptase-PCR and DNA fragmentation assay. The results showed antioxidant activity of PA in Fe3+ reducing power assay ($p{\leq}0.03$). PA inhibited the growth of HepG2 cells in a concentration dependent manner ($p{\leq}0.04$). After 48h treatment, cell viability was recorded 84.7, 74.4, 65.6, 49.6, 36.0 and 23.8% in MTT assay and 92.6, 77.0%, 66.8%, 51.2, 40.3 and 32.3% in LDH assay at concentrations of 1, 1.5, 2.0, 2.5, 3.0, and 3.5mM, respectively. Hence, treatment of PA for 24h, recorded viability of cells 93.5, 88.6, 55.5, 34.6 and 24.4% in MTT assay and 94.2, 86.1%, 59.7%, 42.3 and 31.6%, in LDH assay at concentrations of 1, 2.2, 3.0, 3.6 and 4.0mM, respectively. PA treated HepG2 cells showed up-regulation of p53, Bax, Caspase-3 and -9, and down-regulation of Bcl-2 gene ($p{\leq}0.01$). At the $IC_{50}$ (2.49mM) of PA, the p53, Bax, Caspase-3 and-9 genes were up-regulated by 6.03, 7.37, 19.7 and 14.5 fold respectively. Also, the fragmented genomic DNA in PA treated cells provided evidence of apoptosis. Our study confirmed the biological activity of PA and demonstrated growth inhibition and induction of apoptosis in HepG2 cells with modulation of the expression of apoptosis-regulatory genes.

Involvement of miR-Let7A in inflammatory response and cell survival/apoptosis regulated by resveratrol in THP-1 macrophage

  • Song, Juhyun;Jun, Mira;Ahn, Mok-Ryeon;Kim, Oh Yoen
    • Nutrition Research and Practice
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    • 제10권4호
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    • pp.377-384
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    • 2016
  • BACKGROUND/OBJECTIVES: Resveratrol, a natural polyphenol, has multiple functions in cellular responses including apoptosis, survival, and differentiation. It also participates in the regulation of inflammatory response and oxidative stress. MicroRNA-Let-7A (miR-Let7A), known as a tumor suppressor miRNA, was recently reported to play a crucial role in both inflammation and apoptosis. Therefore, we examined involvement of miR-Let7A in the modulation of inflammation and cell survival/apoptosis regulated by resveratrol. MATERIALS/METHODS: mRNA expression of pro-/anti-inflammatory cytokines and sirtuin 1 (SIRT1), and protein expression of apoptosis signal-regulating kinase 1 (ASK1), p-ASK1, and caspase-3 and cleaved caspase-3 were measured, and cell viability and Hoechst/PI staining for apoptosis were observed in Lipopolysaccharide (LPS)-stimulated human THP-1 macrophages with the treatment of resveratrol and/or miR-Let7A overexpression. RESULTS: Pre-treatment with resveratrol ($25-200{\mu}M$) resulted in significant recovery of the reduced cell viabilities under LPS-induced inflammatory condition and in markedly increased expression of miR-Let7A in non-stimulated or LPS-stimulated cells. Increased mRNA levels of tumor necrosis $factor-{\alpha}$ and interleukin (IL)-6 induced by LPS were significantly attenuated, and decreased levels of IL-10 and brain-derived neurotrophic factor were significantly restored by resveratrol and miR-Let7A overexpression, respectively, or in combination. Decreased expression of IL-4 mRNA by LPS stimulation was also significantly increased by miR-Let7A overexpression co-treated with resveratrol. In addition, decreased SIRT1 mRNA levels, and increased p-ASK1 levels and PI-positive cells by LPS stimulation were significantly restored by resveratrol and miR-Let7A overexpression, respectively, or in combination. CONCLUSIONS: miR-Let7A may be involved in the inflammatory response and cell survival/apoptosis modulated by resveratrol in human THP-1 macrophages.

LINC01272 Suppressed Cell Multiplication and Induced Apoptosis Via Regulating MiR-7-5p/CRLS1 Axis in Lung Cancer

  • Ma, Xuan;Liu, Yang;Tian, Hao;Zhang, Bo;Wang, Meiling;Gao, Xia
    • Journal of Microbiology and Biotechnology
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    • 제31권7호
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    • pp.921-932
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    • 2021
  • LINC01272 is a long non-coding RNA (lncRNA) that has been considered as a biomarker for many diseases including lung squamous cell carcinoma. Here, we investigated the function and mechanism of LINC01272 on lung cancer (LC). The differential expression of LINC01272 in LC and normal samples was analyzed by GEPIA based on the data from TCGA-LUAD database, as survival prognosis was analyzed through Kaplan-Meier Plotter. LINC01272 overexpression plasmid and miR-7-5p mimic were transfected into A549 and PC-9 cells. LINC01272, miR-7-5p and cardiolipin synthase 1 (CRLS1) mRNA expression was measured by quantitative reverse transcription-polymerase chain reaction. Cell viability was detected through MTT assay. Cell multiplication was evaluated by cell formation assay. Cell apoptosis was assessed through flow cytometry assay. Through bioinformatics, the target miRNA of LINC01272 and downstream genes of miR-7-5p were predicted. The targeting relationship was tested by dual luciferase reporter analysis. CRLS1, B-cell lymphoma-2 (Bcl-2), BCL2-associated X (Bax) and cleaved caspase-3 protein levels were detected through western blot. LINC01272 was downregulated in LC and low LINC01272 expression had poor prognosis. In A549 and PC-9 cells, LINC01272 inhibited cell viability and multiplication and induced apoptosis. LINC01272 negatively regulated miR-7-5p and CRLS1 was a target of miR-7-5p. MiR-7-5p reversed the effect of LINC01272 on viability, multiplication, apoptosis and expression of miR-7-5p and CRLS1 as well as apoptosis-related factors (Bcl-2, Bax and cleaved caspase-3). LINC01272 suppressed cell multiplication and induced apoptosis via regulating the miR-7-5p/CRLS1 axis in LC.

무선 센서 네트워크에서 RF 전송 레벨을 이용한 위치 측정 기법 (A Localization Method Using RF Transmission Levels in Wireless Sensor Networks)

  • 채상윤;한주선;하란
    • 한국정보과학회:학술대회논문집
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    • 한국정보과학회 2007년도 가을 학술발표논문집 Vol.34 No.2 (D)
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    • pp.366-371
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    • 2007
  • 무선 센서 네트워크는 경제적, 환경적 목적으로 다양한 방면에서 활용되고 있다 이 때, 배치된 각 센서의 위치를 파악하는 것은 센서 네트워크에서 가장 기본적이며 가장 중요한 문제 중의 하나이다. 기존 논문에서 제안된 센서 위치 측정 방법은 특별한 장비를 장착하거나 특정한 환경의 지역에 한정시킨 방범으로 제한하고 있는 경우가 대부분이다. 하지만 어떠한 관심 지역의 환경은 언제라도 바뀔 수 있다. 또한, 센서가 위치할 환경의 기온, 풍속 등을 미리 안다는 것은 비현실적인 가정이다. 더구나 각각의 센서에 특별한 장비를 장착한다는 것은 비용 절감을 이유로 센서 네트워크를 운영하는 경우 오히려 그것을 이용하지 않는 경우보다 비용이 더 들 수도 있다. 이에 본 논문에서는 센서 노드의 기본적인 통신 기능은 이용하여, 환경에 순응적으로 센서의 위치를 측정할 수 있는 방법을 제안하고자 한다. 센서 노드에서 기본적으로 제공하는 통신 기능은 RF 전파를 보낼 때 전송 레벨을 달리하여 보낼 수 있다. 이러한 기본적인 기능을 이용하여 위치를 측정하게 되면 전체적인 센서 네트워크의 비용이 절감될 뿐만 아니라 환경에 순응적인 위치 측정이 가능하게 된다. 또한, 각 노드의 위치가 정해진 후 다른 노드와 통신할 때 전파의 세기를 조정함으로써 RF 통신에서 소모되는 전력량을 줄일 수 있다. 따라서 본 논문에서 제안하는 전송 레벨을 이용한 위치 측정 방법은 단순히 위치를 측정한다는 의미뿐 아니라 환경에 순응적으로 작동한다는 장점이 있다. 향후 네트워크 내에서 통신에 소비되는 전력을 줄일 수 있다는 점에서도 중요한 의미를 지닌다.를 집행하는 caspase의 활성 형태인 cleaved caspase-8, -9, -7, -3의 단백질 수준이 목향 헥산추출물의 처리에 의해 증가하였고 caspase-3의 표적 단백질 중 하나인 PARP의 불활성 형태인 cleaved PARP의 단백질 수준도 현저하게 증가하였다. 이 결과들은 목향 헥산 추출물이 LNCaP 세포의 apoptosis를 유도함으로써 전립선 암세포의 증식을 억제함을 보여주는 것이며 목향 헥산추출물에 의한 apoptosis 유도는 caspase 활성 증가와 Bak 및 t-Bid 단백질의 증가에 의한 것임을 제시한다. 따라서 앞으로 항암효과를 나타내는 성분의 동정 및 동물실험을 통하여 좀 더 면밀한 기전 연구가 수행된다면 목향 헥산추출물은 화학적 암예방 물질이나 치료제로 개발될 수 있을 것으로 사료된다.적 분해층과 마모질이가 가장 깊은 것으로 나타났으며 flowable type의 복합레진과 컴포머는 표면 경도와 마모도에서 양호한 결과를 보였다. 이상의 결과 복합레진과 컴포머의 평가요소로서 마모도와 함께 가수분해도 고려되어야 할 것으로 사료된다.증후군 환자에서 대조군에 비해 높은 비율을 보였다.er thinning은 3 군모두에서 관찰되었고 항암 3 일군이 가장 심하게 나타났다. 이상의 실험결과를 보면 술전 항암제투여가 초기에 시행한 경우에는 조직의 치유에 초기 5 일정도까지는 영향을 미치나 7 일이 지나면 정상범주로 회복함을 알수 있었고 실험결과 항암제 투여후 3 일째 피판 형성한 군에서 피판치유가 늦어진 것으로 관찰되어 인체에서 항암 투여후 수술시기는 인체면역계가 회복하는 시기를 3

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Curdione Inhibits Proliferation of MCF-7 Cells by Inducing Apoptosis

  • Li, Juan;Bian, Wei-He;Wan, Juan;Zhou, Jing;Lin, Yan;Wang, Ji-Rong;Wang, Zhao-Xia;Shen, Qun;Wang, Ke-Ming
    • Asian Pacific Journal of Cancer Prevention
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    • 제15권22호
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    • pp.9997-10001
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    • 2014
  • Background: Curdione, one of the major components of Curcuma zedoaria, has been reported to possess various biological activities. It thus might be a candidate anti-flammatory and cancer chemopreventive agent. However, the precise molecular mechanisms of action of curdione on cancer cells are still unclear. In this study, we investigated the effect of curdione on breast cancer. Materials and Methods: Xenograft nude mice were used to detect the effect of curdione on breast cancer in vivo; we also tested the effect of curdione on breast cancer in vitro by MTT, Flow cytometry, JC-I assay, and western blot. Results: Firstly, we found that curdione significantly suppressed tumor growth in a xenograft nude mouse breast tumor model in a dose-dependent manner. In addition, curdione treatment inhibited cell proliferation and induced cell apoptosis. Moreover, after curdione treatment, increase of impaired mitochondrial membrane potential occurred in a concentration dependent manner. Furthermore, the expression of apoptosis-related proteins including cleaved caspase-3, caspase-9 and Bax was increased in curdione treatment groups, while the expression of the anti-apoptotic Bcl-2 was decreased. Inhibitors of caspase-3 were used to confirm that curdione induced apoptosis. Conclusions: Overall, our observations first suggested that curdione inhibited the proliferation of breast cancer cells by inducing apoptosis. These results might provide some molecular basis for the anti-cancer activity of curdione.

Growth Inhibition of Human Head and Neck Squamous Cell Carcinomas by Angelica decursiva Extracts

  • Shin, Woo-Cheol;Kim, Chun-Sung;Kim, Heung-Joong;Lee, Myoung-Hwa;Kim, Hye-Ryun;Kim, Do-Kyung
    • International Journal of Oral Biology
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    • 제35권4호
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    • pp.153-158
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    • 2010
  • Angelica decursiva has been used in Korean traditional medicine as an antitussive, an analgesic, an antipyretic and a cough remedy. However, the anti-cancer properties of Angelica decursiva have not yet been well defined. In our current study the cytotoxic activity of ethanol extracts of Angelica decursiva root (EEAD) and the mechanism of cell death exhibited by EEAD were examined in FaDu human head and neck squamous cell carcinoma cells. The cytotoxic effects of EEAD upon the growth of FaDu cells were examined with an MTT assay. In addition, the mechanism of cell death induced by EEAD was evaluated by DNA fragmentation analysis, immunoblotting and caspase activation measurements. EEAD induced apoptotic cell death in FaDu cells in a concentration- and time-dependent manner, as determined by MTT assay and DNA fragmentation analysis. Furthermore, the proteolytic processing of caspase-3, -7 and -9 was increased by EEAD treatment of FaDu cells. In addition, the activation of caspase-3 and -7 was detected in living FaDu cells by fluorescence microscopy. These results suggest that EEAD can induce apoptosis and suppress cell growth in cancer cells and may have utility as a future anticancer therapy.

Modulating Effect of Lupeol on the Expression Pattern of Apoptotic Markers in 7, 12-Dimethylbenz(a)anthracene Induced Oral Carcinogenesis

  • Manoharan, S.;Palanimuthu, D.;Baskaran, N.;Silvan, S.
    • Asian Pacific Journal of Cancer Prevention
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    • 제13권11호
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    • pp.5753-5757
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    • 2012
  • Apoptosis, also known as cell suicide or programmed cell death, removes unwanted and genetically damaged cells from the body. Evasion of apoptosis is one of the major characteristic features of rapidly proliferating tumor cells. Chemopreventive agents inhibit or suppress tumor formation through apoptotic induction in target tissues. The aim of the present study was to investigate the pro-apoptotic potential of lupeol during 7,12-dimethylbenz(a) anthracene (DMBA) induced hamster buccal pouch carcinogenesis. Topical application of 0.5% DMBA three times a week for 14 weeks in the buccal pouches of golden Syrian hamsters resulted in oral squamous cell carcinoma. The expression pattern of apoptotic markers was analyzed using immunohistochemistry (p53, Bcl-2, Bax) and ELISA reader (caspase 3 and 9). In the present study, 100% tumor formation with defects in apoptotic markerexpression pattern was noticed in hamsters treated with DMBA alone. Oral administration of lupeol at a dose of 50mg/kg bw completely prevented the formation oral tumors as well as decreased the expression p53 and Bcl-2, while increasing the expression of Bax and the activities of caspase 3 and 9. The present study thus indicated that lupeol might inhibit DMBA-induced oral tumor formation through its pro-apoptotic potential in golden Syrian hamsters.

Antiproliferative Effect of Trichostatin A and HC-Toxin in T47D Human Breast Cancer Cells

  • Joung, Ki-Eun;Kim, Dae-Kee;Sheen, Yhun-Yhong
    • Archives of Pharmacal Research
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    • 제27권6호
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    • pp.640-645
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    • 2004
  • Histone deacetylase inhibitors are new class of chemotherapeutic drugs able to induce tumor cell apoptosis and/or cell cycle arrest. Trichostatin A, an antifungal antibiotic, and HC-toxin are potent and specific inhibitors of histone deacetylase activity. In this study, we have examined the antiproliferative activities of trichostatin A and HC-toxin in estrogen receptor positive human breast cancer, T47D cells. Both trichostatin A and HC-toxin showed potent antiprolifer-ative efficacy and cell cycle arrest at $G_2/M$ in T47D human breast cancer cells in a dose-dependent manner. Trichostatin A caused potent apoptosis of T47D human breast cancer cells and trichostatin A-induced apoptosis might be involved in an increase of caspase-3/7 activity. HC-toxin evoked apoptosis of T47D cells and HC-toxin induced apoptosis might not be medi-ated through direct increase in caspase-3/7 activity. We have identified potent activities of anti-proliferation, apoptosis, and cell cycle arrest of trichostatin A and HC-toxin in estrogen receptor positive human breast cancer cell line T47D.