• Title/Summary/Keyword: Apoptosis

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AN EXPERIMENTAL STUDY ON MISTLETOE EXTRACT-INDUCED APOPTOSIS IN ORAL SQUAMOUS CELL CARCINOMA (구강편평세포암종에서 미슬토 추출물의 Apoptosis 유도 효과에 대한 실험적 연구)

  • Heo, Gyun-Haeng;Lee, Jae-Hoon;Kim, Chul-Hwan
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • v.31 no.1
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    • pp.13-23
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    • 2005
  • This study was performed to investigate mistletoe extract-induced apoptosis in oral squamous cell carcinoma. In vivo study, HN22 cells were xenografted in nude mice. After tumor was experimentally induced, mistletoe extract was directly injected on the tumor mass. The specimens were evaluated using light and transmission electron microscopes. In vitro study, HN22 cells were cultured and exposed to mistletoe extract. The cells were evaluated using transmissin electron microscope. To evaluate apoptotic cells, flow cytometric analysis was done. The results were obtained as follows: 1. Light microscopic view of tumor mass showed necrosis at 2-4 weeks. 2. Transmission electron micrographs of tumor mass showed apoptosis and necrosis. 3. In TEM view of cell lines, necrosis and apoptosis were shown with mistletoe extract at $300{\mu}g/ml$, apoptosis was shown with mistletoe extract at $100{\mu}g/ml$. 4. In flow cytometric analysis, early and late apoptosis was shown when using caspase-3Ab and annexin-V, but no significant change was noted when using mebstain and Apo2.7 Ab. In this study, mistletoe extract induced necrosis and apoptosis in the tumor mass was induced by HN22 cells, early and late apoptosis in vitro study. Mistletoe extract was likely to induce cell death in oral squamous cell carcinoma through apoptosis.

Olibanum-induced Apoptosis Signaling in Human Cervical Carcinoma HeLa Cells (자궁경부암세포(子宮經部癌細胞)(HeLa cell)에서 유향(乳香) 세포고사(細胞枯死) 기전(機轉) 연구(硏究))

  • Park, Kyung-Mi;Kong, Bok-Cheul;Lee, Su-Jung;Choe, Chang-Min;Yoo, Sim-Keun
    • The Journal of Korean Obstetrics and Gynecology
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    • v.19 no.2
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    • pp.92-106
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    • 2006
  • Purpose : To address the ability of Olibanum to induce cell death, we investigated the effect of olibanum on cell apoptosis. Twenty-four hours later, apoptosis occurred following olibanum exposure in a dose-dependent manner. Methods : We culture HeLa cell which is human metrocarcinoma cell in D-MEM included 10% fetal bovine serum(Hyclone Laboratories) below $37^{\circ}C$, 5% CO2. Then we observed apoptosis of log phage cell which is changed cultivation liquid 24 Hours periodically. Results : The treatment of BAPTA-AM regulated olibanum-induced apoptosis in HeLa human cervical carcinoma cells. The 24 hr-earlier -thapsigargin-pretreated cell showed the resistance against olibanum-induced apoptosis and the Ru360-mitochondrial uniporter-inhibited olibanum-induced apoptosis, too. It means that olibanum leads to the accumulation of calcium and the resultant apoptosis in HeLa cells. Immunoblotting data also shows that the expression of GRP78, ER stress marker protein, was induced by the olibanum. Bcl-2, anti-apototic protein, was decreased and that the expression of Bax, pro-apoptotic protein, was increased by the addition of olibanum. Interestingly, the olibanum increased the activity of caspase-8 as well as calpain cysteine pretense in HeLa cervical carcinoma cells. Calpain inhibitor-calpastatin as well as caspase-8C/A expression abrogated olibanum-induced apoptosis in the carcinoma cells. The inhibition of caspase-8 regulated olibanum-induced calpain activation but the inhibition of calpain did not have any effect on the caspase-8 activation in HeLa human cervical carcinoma cells. Conclusion : We conclude that olibanum induces the accumulation of calcium and the resultant apoptosis in which caspase-8 and calpain are involved.

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Changes in Mitogen-activated Protein Kinase Activities During Acidification-induced Apoptosis in CHO Cells

  • Kim, Jin-Young;Jeong, Dae-Won;Roh, Sang-Ho;Min, Byung-Moo
    • International Journal of Oral Biology
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    • v.30 no.3
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    • pp.85-90
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    • 2005
  • Homeostatic pH is very important for various cellular processes, including metabolism, survival, and death. An imbalanced-pH might induce cellular acidosis, which is involved in many abnormal events such as apoptosis and malignancy. One of several factors contributing to the onset of metabolic acidosis is the production of lactate and protons by lactate dehydrogenase (LDH) in anaerobic glycolysis. LDH is an important enzyme that catalyzes the reversible conversion of pyruvate to lactate. This study sought to examine whether decreases in extracellular pH induce apoptosis of CHO cells, and to elucidate the role of mitogen-activated protein kinases (MAPKs) in acidification-induced apoptosis. To test apoptotic signaling by acidification we used CHO dhfr cells that were sensitive to acidification, and CHO/anti-LDH cells that are resistant to acidification-induced apoptosis and have reduced LDH activity by stable LDH antisense mRNA expression. In the present study, cellular lactic acid-induced acidification and the role of MAPKs signaling in acidification-induced apoptosis were investigated. Acidification, which is caused by $HCO{_3}^-$-free conditions, induced apoptosis and MAPKs (ERK, JNK, and p38) activation. However, MAPKs were slightly activated in acidic conditions in the CHO/anti-LDH cells, indicating that lactic acid-induced acidification induces activation of MAPKs. Treatment with a p38 inhibitor, PD169316, increased acidification-induced apoptosis but apoptosis was not affected by inhibitors for ERK (U0126) or JNK (SP600125). Thus, these data support the hypothesis that activation of the p38 MAPK during acidification-induced apoptosis contributes to cell survival.

MicroRNAs regulate granulosa cells apoptosis and follicular development - A review

  • Gong, Zhuandi;Yang, Juan;Bai, Shengju;Wei, Suocheng
    • Asian-Australasian Journal of Animal Sciences
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    • v.33 no.11
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    • pp.1714-1724
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    • 2020
  • Objective: MicroRNAs (miRNAs) are the most abundant small RNAs. Approximately 2,000 annotated miRNAs genes have been found to be differentially expressed in ovarian follicles during the follicular development (FD). Many miRNAs exert their regulatory effects on the apoptosis of follicular granulosa cells (FGCs) and FD. However, accurate roles and mechanism of miRNAs regulating apoptosis of FGCs remain undetermined. Methods: In this review, we summarized the regulatory role of each miRNA or miRNA cluster on FGCs apoptosis and FD on the bases of 41 academic articles retrieved from PubMed and web of science and other databases. Results: Total of 30 miRNAs and 4 miRNAs clusters in 41 articles were reviewed and summarized in the present article. Twenty nine documents indicated explicitly that 24 miRNAs and miRNAs clusters in 29 articles promoted or induced FGCs apoptosis through their distinctive target genes. The remaining 10 miRNAs and miRNAs of 12 articles inhibited FGCs apoptosis. MiRNAs exerted modulation actions by at least 77 signal pathways during FGCs apoptosis and FD. Conclusion: We concluded that miRNAs or miRNAs clusters could modulate the apoptosis of GCs (including follicular GCs, mural GCs and cumulus cells) by targeting their specific genes. A great majority of miRNAs show a promoting role on apoptosis of FGCs in mammals. But the accurate mechanism of miRNAs and miRNA clusters has not been well understood. It is necessary to ascertain clearly the role and mechanism of each miRNA or miRNA cluster in the future. Understanding precise functions and mechanisms of miRNAs in FGCs apoptosis and FD will be beneficial in developing new diagnostic and treatment strategies for treating infertility and ovarian diseases in humans and animals.

Enhancement of TRAIL-Mediated Apoptosis by Genistein in Human Hepatocellular Carcinoma Hep3B Cells: Roles of p38 MAPK Signaling Pathway (인체간암세포에서 genistein의 TRAIL에 의한 apoptosis 유도 상승효과에서 미치는 p38 MAPK signaling pathway의 영향)

  • Jin, Cheng-Yun;Park, Cheol;Park, Sang-Eun;Hong, Sang-Hoon;Choi, Yung-Hyun
    • Journal of Life Science
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    • v.21 no.11
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    • pp.1549-1557
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    • 2011
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can selectively induce apoptosis in many types of transformed cells; however, some human hepatocellular carcinoma cells are particularly resistant to the effects of TRAIL. Although genistein, a natural isoflavonoid phytoestrogen, has been shown to have pro-apoptotic activity against human cancer cell lines, little is known about the mechanism of genistein in terms of TRAIL-induced apoptosis. In the present study, it was investigated whether or not combined treatment with genistein and TRAIL synergistically induced apoptosis in Hep3B hepatocarcinoma cells. Results indicate that treatment with TRAIL in combination with nontoxic concentrations of genistein sensitized TRAIL-resistant Hep3B cells to TRAIL-induced apoptosis, which was associated with mitochondrial dysfunction. Further, the inhibition of p38 mitogen-activated protein kinase (MAPK) activation markedly decreased genistein and TRAIL-induced cell viability and apoptosis by enhanced truncation of Bid, increase of pro-apoptotic Bax, decrease of anti-apoptotic Bcl-2, and release of cytochrome c from mitochondria to cytoplasm. Activation of caspases and degradation of poly (ADP-ribose) polymerase induced by the combined treatment was also markedly increased by the inhibition of p38 MAPK, through the mitochondrial amplification step. In conclusion, our data suggest that genistein sensitizes TRAIL-induced-apoptosis via p38 MAPK-dependent pathway.

The Sanguinarine Apoptosis Induction of Hep3B Human Hepatocellular Carcinoma Cells is Dependent on the Activation of Caspase (Sanguinarine에 의한 Hep3B 인체 간암세포의 apoptosis 유도에 관한 연구)

  • Han, Min Ho;Choi, Sung Hyun;Hong, Su Hyun;Park, Dong Il;Choi, ung Hyun
    • Journal of Life Science
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    • v.27 no.11
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    • pp.1340-1348
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    • 2017
  • Sanguinarine is a benzophenanthridine alkaloid derived from the roots of Sanguinaria canadensis L., which is used for the purpose of treating various diseases. Although studies of anticancer activities have been performed using various cancer cell lines, the phenomenon of inducing apoptosis in cancer cells by using sanguinarine requires more research. Therefore, this study investigated the anti-cancer activities and related mechanisms of sanguinarine used with Hep3B human hepatocellular carcinoma cells in terms of the regulation of apoptosis. Sanguinarine inhibited the proliferation of Hep3B cells in a concentration-dependent manner, which was associated with the induction of apoptosis. Sanguinarine also increased the activity of caspase-3, which is a typical effector caspase, and the activities of caspase-8 and caspase-9, which are key when initiating extrinsic and intrinsic apoptosis pathways, respectively. In addition, sanguinarine increased the expression of death receptor-related genes and pro-apoptotic BAX, which belongs to the Bcl-2 family, while suppressing the expression of anti-apoptotic Bcl-2. Sanguinarine promoted the truncation of Bid and enhanced the release of cytochrome c from the mitochondria to the cytoplasm due to a loss of mitochondrial membrane potential. Furthermore, the reduction of a survival rate that was induced by sanguinarine and the induction of apoptosis disappeared with the inhibition of artificial caspase activity. Therefore, the results of the study indicated that sanguinarine-induced apoptosis in Hep3B cells involves both extrinsic and intrinsic pathways; such apoptosis is a caspase-dependent phenomenon.

Effect of Glycyrrhizin on Apoptosis of Transplanted-L1210 cells in mice (글리시르히진이 생쥐에 이식된 L1210 세포의 아포프토시스에 미치는 영향)

  • Eun, Jae-Soon;Kwon, Jin;Oh, Chan-Ho
    • YAKHAK HOEJI
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    • v.42 no.3
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    • pp.324-329
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    • 1998
  • These experiments were conducted to investigate effects of glycyrrhizin (GL) on apoptosis of transplanted-L1210 cells in mice. GL induced apoptosis of transplanted-Ll2lO cells. GL increased nitric oxide production from peritoneal macrophages of L1210 cells-transplanted mice. NOC12, nitric oxide donor, induced apoptosis of L1210 cells in vitro. The apoptosis of L1210 cells were enhanced by co-culture of the peritoneal macrophages of GL-administered mice and L1210 cells in vitro, and was inhibited by L-NMMA. These results suggest that the apoptosis of transplanted-Ll2lO cells is partly induced by nitric oxide produced from peritoneal macrophages in GL-administered mice.

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A Comparison of Hydrated versus Dehydrated Gels for Evaluation of Apoptosis in Comet Assay Slides (Comet assay slides 에서 나타난 apoptosis 평가에서 함수 및 탈수 겔의 비교)

  • 최민철;수즌엠러루;에드워드엘질럿
    • Journal of Veterinary Clinics
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    • v.13 no.2
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    • pp.158-162
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    • 1996
  • Comet assay 는 포유류 세포에서 DNA의 파괴를 측정하는데 있어 신속하고 단순하며 시각적이고 민감한 방법이다. Apoptosis에서는 세포핵의 광범위한 DNA의 붕괴가 일어나므로 comet assay는 종양세포에서 apoptosis가 발생되었는가를 알아내는데 유용하다. 본 연구는 apoptosis 연구의 결과가 변화되지 않도록 comet assay slides를 좀 더 오래 보관할 수 있는 방법을 개발하고자 시행되었다. 개의 종양세포를 가지고 alkali comet assay를 끝낸 뒤 slides를 진공 건조기에서 꺼내서 증류수로 점적하여 10-20분간 침수시키고 현광현미경하에서 육안적으로 관찰하였다. 건조후 3-4일, 1주, 2주, 3주, 4주 및 7주의 slides에서 apoptosis 회복율(%)은 각각 98.1, 98.3, 99.4, 80.8 및 35.2%이었다. 3주 이내의 slides에서 대조군과 비교하여 apoptosis 회복율에서 차이가 없었으나 4주 이상의 slides를 건조후 침수시키는 방법을 이용하였을 때 apoptosis 평가에서 건조 후 3주간까지는 처음의 결과와 차이가 없으며, 이 방법을 이용하여 comet slide의 좀 더 긴 기간이 보관과 보관후의 재평가에서 이용될 수 있는 좋은 방법이 된다.

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Development of Apoptosis Model and Bioimmune Responses in Experimental Animal I. Induction and Indicator of Apoptosis and Hepatic Tumorigenesis (실험동물에서 Apoptosis의 모델개발과 생체면역반응 및 형태학적 특징 I. Apoptosis 및 Hepatic Tumorigenesis의 유도 및 관련지표의 검색)

  • 강정부;하우송;김지경
    • Journal of Veterinary Clinics
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    • v.16 no.1
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    • pp.100-107
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    • 1999
  • Apoptosis is now widely recognized as a common form of cell death and represents mechanism of cell clearance in many physiological situations where deletion of cells is required. In vivo administration of bacterial lipopolysaccharide (LPS) to Balb/c mice induced DNA fragmentation in the thymus. DNA fragmentation in the thymus was roughly dependent on the dose of LPS injected and reached the peak 18 hours after injection. This apoptosis in the thymus might be mediated due to LPS stimulant. DEN (diethylnitrosamine) has been shown to cause liver cancer in experimental animals and humans. The hepatic tumorigenesis was induced by ad libitum feeding of DEN only. It was suggested that DEN induced hepatic tumorgenesis in rat is a good reproducible model for studying biochemical and pathophysiological changes associated with the development of hepatic tumorigenesis and apoptosis.

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Apigenin Sensitizes Huh-7 Human Hepatocellular Carcinoma Cells to TRAIL-induced Apoptosis

  • Kim, Eun-Young;Kim, An-Keun
    • Biomolecules & Therapeutics
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    • v.20 no.1
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    • pp.62-67
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    • 2012
  • TNF-related apoptosis-inducing ligand (TRAIL) is a promising agent for management of cancer because of its selective cytotoxicity to cancer cells. However, some cancer cells have resistance to TRAIL. Accordingly, novel treatment strategies are required to overcome TRAIL resistance. Here, we examined the synergistic apoptotic effect of apigenin in combination with TRAIL in Huh-7 cells. We found that combined treatment of TRAIL and apigenin markedly inhibited Huh-7 cell growth compared to either agent alone by inducing apoptosis. Combined treatment with apigenin and TRAIL induced chromatin condensation and the cleavage of poly (ADP-ribose) polymerase (PARP). In addition, enhanced apoptosis by TRAIL/apigenin combination was quantified by annexin V/PI flow cytometry analysis. Western blot analysis suggested that apigenin sensitizes cells to TRAIL-induced apoptosis by activating both intrinsic and extrinsic apoptotic pathway-related caspases. The augmented apoptotic effect by TRAIL/apigenin combination was accompanied by triggering mitochondria-dependent signaling pathway, as indicated by Bax/Bcl-2 ratio up-regulation. Our results demonstrate that combination of TRAIL and apigenin facilitates apoptosis in Huh-7 cells.