• 제목/요약/키워드: lung carcinoma A549

검색결과 164건 처리시간 0.029초

사독의 인체 폐암세포(A549)에 대한 Natural Killer 세포 세포독성 촉진 효과 (Snake Venom-enhanced Cytotoxic Effect of Natural Killer Cells on A549 Human Lung Cancer Cell Growth)

  • 이지인;송호섭
    • Journal of Acupuncture Research
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    • 제32권1호
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    • pp.79-88
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    • 2015
  • Objectives : The purpose of this research was to investigate the cytotoxic effect of Natural Killer(NK)-92 cell and Snake Venom, and to elucidate its mechanism on human lung carcinoma cell A549. Methods : In order to figure out whether Snake Venom enhances the cytotoxic effect of NK-92 cell in A549 cell, Cell Viability Assay was conducted. Also, in order to observe the changes of Caspase-3 and Caspase-8, both of which are proteinases that advance apoptosis, and the changes of TNRF and DR3, which are Death Receptors of the extrinsic pathway of apoptosis, Western Blot Analysis was conducted. By conducting RT-PCR analysis, we have tried to confirm Perforin, Granzyme B, and GADPH, all of which are cytotoxic-related proteins. Lastly, in order to observe the effect of Snake Venom on NO formation within human lung carcinoma cells, NO determination was conducted. Results : 1. After conducting Cell Viability Assay, Snake Venom enhanced the cytotoxic effect of NK-92 cell and inhibited the growth of A549. 2. Western Blot Analysis caused proteinases Caspase-3 and Caspase-8, which advance apoptosis, to increase in the combined treatment group, but not in treatment groups that focused only on either Snake Venom or NK-92 cell in A549 lung carcinoma cells. 3. Western Blot Analysis caused an expression of TNFR2 and DR3, both of which are Death Receptors of the apoptosis extrinsic pathway, in the combined treatment group, but not intreatment groups that focused only on either Snake Venom or NK-92 cell in A549 human lung carcinoma cells. 4. After conducting NO determination, NO formation within A549 cell showed no significant changes in both treatment groups that focused NK-92 cell and combined treatment group. 5. After conducting RT-PCR, the expression of Granzyme B and Perforin, which are cytotoxic-related proteins within A549 human lung carcinoma cells, showed growth in the combined treatment group, but not the treatment group that focused only on NK-92 cell. Conclusion : It has been indicated that, when it comes to the A549 cell, Snake Venom enhances the increase of Death Receptor expression and continuous apoptosis reaction, leading to the enhancement of the cancer cell cytotoxic effect of the NK-92 cell. It is expected that Snake Venom can be used with the NK-92 cell for further lung cancer treatment.

길경이 인체 폐암세포에 미치는 영향에 대한 실험적 연구 (Apoptotic Cell Death of Human Lung Carcinoma A549 Cells by an Aqueous Extract from the Roots of Platycodon grandiflorum)

  • 이성열;김원일;박동일
    • 동의생리병리학회지
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    • 제17권4호
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    • pp.1019-1030
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    • 2003
  • Platycodi Radix, the root of Platycodon grandiflorum, commonly known as Doraji, is used as a traditional oriental medicine. Extracts from the roots of P. grandiflorum have been reported to have wide ranging health benefits. In the present study, we investigated the effects of an aqueous extract from the roots of P. grandiflorum (AEPG) on the growth of human lung carcinoma A549 cells. Results obtained are as fellow; AEPG treatment resulted in the inhibition of the cell viability of A549 cells in a concentration-dependent manner. Upon treatment with AEPG, A549 cells developed many of the hallmark features of apoptosis, including condensation of chromatin. Flow cytometry analysis confirmed that AEPG increased populations of apoptotic-sub G1 phase. Western blot and RT-PCR analyses indicated that the expressions of Bcl-2 was down-regulated but Bax was up-regulated in AEPG-treated A549 cells. AEPG-induced apoptotis of A549 cells was associated with rroteolytic cleavage and activation of caspase-3, release of cytochrome c from mitochondria into cytosol and down-regulation of Akt and phospho-Akt proteins in a dose-dependent manner. Induction of apoptosis by AEPG treatment was associated with inhibition and/or degradation of apoptotic target proteins such as poly(ADP-ribose) polymerase, β-catenin and phospholipase C-γ 1. AEPG treatment inhibited the levels of cyclooxygenases protein of A549 cells, which was associated with the inhibition of prostaglandin E2 accumulation in a concentration-dependent fashion. Taken together, these findings suggest that P. grandiflorum has strong potential for development as an agent for prevention against human lung cancer.

천금위경탕의 인체 폐암세포 증식억제에 관한 연구 (Anti-proliferative Effects of Cheonkumwikyung-tang In A549 Human Lung Carcinoma Cells)

  • 박봉규;박동일
    • 동의생리병리학회지
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    • 제18권4호
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    • pp.1147-1152
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    • 2004
  • To investigate the anti-cancer effects of aqueous extract of Cheonkumwikyung-tang (CKWKT) on the growth of human lung carcinoma cell line A549, we performed various biochemical experiments such as the effects of CKWKT on the cell proliferation and viability, the morphological changes, the effects on expression of apoptosis and cell growth-regulatory gene products. Results obtained are as follow; CKWKT treatment declined the cell viability and proliferation of A549 cells in a concentration-dependent manner. The anti-proliferative effect by CKWKT treatment in A549 cells was associated with morphological changes such as membrane shrinking and cell rounding up. CKWKT treatment induced apoptotic cell death of A549 cells in a concentration-dependent manner, which was associated with inhibition and/or degradation of apoptotic target proteins such poly(ADP-ribose) polymerase, β-catenin and phospholipase C-γ1. Western blot analysis revealed that the levels cyclin-dependent kinase inhibitor p21 expression were induced by CKWKT treatment in A549 cells. Taken together, these findings suggest that CKWKT-induced inhibition of human lung cancer cell proliferation is associated with the induction of apoptotic cell death via regulation of several major growth regulatory gene products and CKWKT may have therapeutic potential in human lung cancer.

동충하초의 인체 폐암세포 증식억제에 관한 연구 (Induction of Apoptotic Cell Death by an Aqueous Extract of Cordyceps militaris in A549 Human Lung Carcinoma Cells)

  • 홍상훈;감철우;박동일
    • 동의생리병리학회지
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    • 제18권4호
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    • pp.1102-1106
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    • 2004
  • To investigate the anti-proliferative effects of an aqueous extract of Cordyceps militaris (AECM) on the growth of human lung carcinoma cell line A549, we performed various biochemical experiments such as the effects of AECM on the cell proliferation and viability, the morphological changes, the effects on expression of apoptosis and cell growth-regulatory gene products. Results obtained are as follow; AECM treatment declined the cell viability and proliferation of A549 cells in a concentration-dependent manner. The anti-proliferative effect by AECM treatment in A549 cells was associated with morphological changes such as membrane shrinking and cell rounding up. Taken together, these findings suggest that AECM-induced inhibition of human lung cancer cell proliferation is associated with the induction of apoptotic cell death via regulation of several major growth regulatory gene products, and C. militaris may have therapeutic potential in human lung cancer.

인체폐암세포에서의 prostaglandin E2 생성과 Telomere 활성에 미치는 청조구폐탕의 영향에 관한 연구 (Antiproliferative effect of Chungjogupae-tang treatment was associated with the inhibition of prostaglandin E2 release and Telomere active in human lung carcinoma cells)

  • 김훈;박동일
    • 한방안이비인후피부과학회지
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    • 제19권2호
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    • pp.26-39
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    • 2006
  • Objective : The effect of water extract of Chungjogupae-tang (CJGPT) was investigated on the growth of human lung carcinoma A549 cells. Methods : MTT assay and fluorescent microscope performed to compare and examine the efficacy of CJGPT treatment on the cytostaticity of lung cancer cells in proportion to time and doses, and DAPI staining and Western blot analysis were used to examine their effect on apoptosis. In addition the quantitative RT-PCR was used to examine to lung cancer cells growth and Progtaglandin E2 and Telomerase activity were measured Results : Exposure of A549 cells to CJGPT resulted in the growth inhibition and apoptosis in a dose-dependent manner as measured by MTT assay and fluorescent microscope. The antiuoliferative effect by CJGPT treatment in A549 cells was associated with morphological changes such as membrane shrinking and cell rounding up. CJGPT treatment resulted in an up-regulation of cyclin-dependent kinase inhibitor p21(WAF1/CIPl) in a p53-independent fashion. We found that CJGPT treatment decreased the levels of cyclooxygenase (COX)-2 and inducible nitric oxide synthease (iNOS) expression without significant changes in the expression of COX-1, which was correlated with a decrease in protaglandin E2 (PGE2) synthesis. CJGPT treatment also inhibited the levels of human telomerase reverse transcriptase (hTERT) and telomerase-associated protein (TEP)-1 mRNA expression, however the activity of telomerase was slightly increased by CJGPT treatment. Conclusion : These findings suggested that CJGPT-induced inhibition of human lung carcinoma A549 cell growth was connected with the induction of apoptotic cell death and the results provided important new insights into the possible molecular mechanisms of the anti-cancer activity of CJGPT.

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인체폐암세포의 증식 및 prostaglandin E2 생성에 미치는 청조구폐탕의 영향에 관한 연구 (Antiproliferative Effect of Chungjogupae-tang Treatment was Associated with the Inhibition of Prostaglandin E2 Release in Human Lung Carcinoma Cells)

  • 임재형;김훈;변미권;감철우;박동일
    • 동의생리병리학회지
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    • 제20권4호
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    • pp.966-972
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    • 2006
  • The effect of water extract of Chungjogupae-tang (CJGPT) was investigated _on the growth of human lung carcinoma A549 cells. Methods: MTT assay and fluorescent microscope peformed to compare and examine the efficacy of CJGPT treatment on the cytostaticity of lung cancer cells in proportion to time and doses, and DAPI staining and Western blot analysis were used to examine their effect on apoptosis. In addition, the quantitative RT-PCR was used to examine to lung cancer cells growth, and Prostaglandin E2 activity were measured. Results: Exposure of A549 cells to CJGPT respited in the growth inhibition and apoptosis in a dose-dependent manner as measured by MTT assay and fluorescent microscope. The antiproliferative effect by CJGPT treatment in A549 cells was associated with morphological changes such as membrane shrinking and cell rounding up. CJGPT treatment resulted in an up-regulation of cyclin-dependent kinase inhibitor p21 (WAFl/CIPl) in a p53-independent fashion. We found that CJGPT treatment decreased the levels of cyclooxygenase (COX)-2 and inducible nitric oxide synthease (iNOS) expression without significant changes in the expression of COX-1 , which was correlated with a decrease in prostaglandin E2 (PGE2) synthesis. Conclusion: These findings suggested that CJGPT-induced inhibition of human lung carcinoma A549 cell growth was connected with the induction of apoptotic cell death and the results provided important new insights into the possible molecular mechanisms of the anti-cancer activity of CJGPT.

A549 폐암 세포주에 대한 정력대조사폐탕 및 정력탕의 Apoptosis 효과 (Apoptotic Effects of Junglyeokdaejosape-tang and Junglyeok-tang on A549 lung Cancer Cells)

  • 유병길;김명동;황태준;유영민;이선구
    • 동의생리병리학회지
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    • 제19권5호
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    • pp.1204-1212
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    • 2005
  • Lung cancer is one of the common malignant tumors in the world. It occurs more increasingly due to the serious air pollution, heavy smoking, expoure to ionized radiation, pollution with heavy metal, and owing to well advanced diagnostic skill, etc. Also lung cancer has the limitation of medical care because metastasis is already shown up in more than half cases when it is first detected through medical examination. Although it is treated with chemoradiation, the rate of deaths from lung cancer is high as well, because blood has a lot of toxicity which give side effects. So it has a low rate of cure. So, the ways of various treatment is being researched to raise the rate of care and decrease the side effects recently, and one of the results is inducing apoptosis which makes use of molecularbiologic diagnosis of lung cancer's cell and using oriental medicine drugs. The purpose of this study is whether apoptosis would happen on the human lung carcinoma cell by treated with Junglyeokdaejosape-tang, Junglyeok-tang Junglyeokdaejosape-tang and Junglyeok-tang has been prescribed for cough, chest pain, and many other similar cases. Cough and chest pain is shown in early lung cancer. That is why we used these prescriptions. Apoptosis happend on the human lung carcinoma A549 cells treated with Jeongiyeokdaejosapye-tang, Jeonglyeok-tang. The concentration-dependent inhibition of cell viability was observed and apoptosis was confirmed by DNA fragmentation. Bcl-2 and COX-2 mRNA expression decreased, but Bax mRNA expression increased, so it was identified with the case of indomethacin known to enhance apoptotic DNA fragmentation. Also expression of the p21, p53, cyclin E, cyclin D1, cytochrome c, caspase-3, and caspase-9 protein increased and the activity of caspase-3 increased, as well. Last, fragmentation of the PARP was shown. The previous and present results indicated that apoptosis of A549 cells by above-mentioned drugs is associated with the blockage of G1/S progression.

Bax 및 Cdk inhibitor p21WAF1/CIP1 발현 증가에 의한 bee venom의 A549 인체폐암세포 성장억제 (Anti-proliferative Effects of Bee Venom through Induction of Bax and Cdk Inhibitor p21WAF1/CIP1 in Human Lung Carcinoma Cells)

  • 최영현
    • 동의생리병리학회지
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    • 제19권1호
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    • pp.167-173
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    • 2005
  • To investigate the possible molecular mechanism (s) of bee venom as a candidate of anti-cancer drug, we examined the effects of the compound on the growth of human lung carcinoma cell line A549. Bee venom treatment declined the cell growth and viability of A549 cells in a concentration-dependent manner, which was associated with induction of apoptotic cell death. Bee venom down-regulated the levels of anti-apoptotic genes such as Bcl-2 and Bcl-XS/L, however, the levels of Bax, a pro-apoptotic gene, were up-regulated. Bee venom treatment induced not only tumor suppressor p53 but also cyclin-dependent kinase inhibitor p21WAF1/CIP1 expression in a dose-dependent manner. Furthermore, bee venom treatment induced the down-regulation of telomerase reverse transcriptase mRNA and telomeric repeat binding factor expression of A549 cells, however, the levels of telomerase-associated protein-1 and c-myc were not affected. Taken together, these findings suggest that bee venom-induced inhibition of human lung cancer cell growth is associated with the induction of apoptotic cell death via regulation of several major growth regulatory gene products, and bee venom may have therapeutic potential in human lung cancer.

Gallotannin regulates apoptosis and COX-2 expression via Akt and p38kinase pathway in human lung cancer cell line, A549

  • Yu, Seon-Mi;Gweon, Eun-Jeong;Chung, Ki-Wha;Kim, Kwang-Hoon;Cho, Hong-Sik;Kim, Song-Ja
    • Animal cells and systems
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    • 제16권5호
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    • pp.366-375
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    • 2012
  • Gallotannin (GT) is derived from plant poly phenol and is associated with biological actions in a wide range of cells. In this study, we evaluated the effect of GTon apoptosis and cyclooxygenase-2 (COX-2) expression and attempted to shed light on the mechanism of action in A549 human lung carcinoma cells. We found that GT dramatically induced apoptosis as demonstrated by expression of p53 and active caspase-3 via western blot analysis and fragmented DNA as detected by DNA fragmentation and DAPI staining. We also observed that GT significantly causes COX-2 expression in a dose-dependent manner determined by western blot analysis. Phosphorylation of Akt and p38 was considerably increased by GT in A549 human lung carcinoma cells. Inhibition of Akt and p38kinase with LY294002 or SB203580 suppressed GT-induced apoptosis and COX-2 expression. Furthermore, we have shown that prevention of COX-2 with NS398 or indomethacin does not any effects on apoptosis induced by GT. Taken together, our present results suggest that GT regulates apoptosis and COX-2 expression through Akt and p38kinase pathway in A549, human lung carcinoma cells.

Induction of Cell Cycle Arrest, Apoptosis, and Reducing the Expression of MCM Proteins in Human Lung Carcinoma A549 Cells by Cedrol, Isolated from Juniperus chinensis

  • Yun, Hee Jung;Jeoung, Da Jeoung;Jin, Soojung;Park, Jung-ha;Lee, Eun-Woo;Lee, Hyun-Tai;Choi, Yung Hyun;Kim, Byung Woo;Kwon, Hyun Ju
    • Journal of Microbiology and Biotechnology
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    • 제32권7호
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    • pp.918-926
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    • 2022
  • Proteins related to DNA replication have been proposed as cancer biomarkers and targets for anticancer agents. Among them, minichromosome maintenance (MCM) proteins, often overexpressed in various cancer cells, are recognized both as notable biomarkers for cancer diagnosis and as targets for cancer treatment. Here, we investigated the activity of cedrol, a single compound isolated from Juniperus chinensis, in reducing the expression of MCM proteins in human lung carcinoma A549 cells. Remarkably, cedrol also strongly inhibited the expression of all other MCM protein family members in A549 cells. Moreover, cedrol treatment reduced cell viability in A549 cells, accompanied by cell cycle arrest at the G1 phase, and enhanced apoptosis. Taken together, this study broadens our understanding of how cedrol executes its anticancer activity while demonstrating that cedrol has potential application in the treatment of human lung cancer as an inhibitor of MCM proteins.