• Title/Summary/Keyword: A549 cell

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Antitumor Effect of Asterina pectinifera Lectin on Ascitic Tumor (별불가사리 렉틴의 복수암에 대한 항암효과)

  • Shon, Yun-Hee;Jeune, Kyung-Hee;Choi, Soo-Jeong;Chung, See-Ryun
    • YAKHAK HOEJI
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    • v.42 no.4
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    • pp.388-394
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    • 1998
  • The lectin from starfish, Asterina pectinifera, was purified and tested for its potential antitumor activity. It was shown to possess considerable toxicity toward various tumor cell lines. Concentration of Asterina pectinifera lectin (APL) at 4mg/$5{\times}10^5$ cells resulted in 28% death of Ehrlich ascites tumor cell, 40% of L929, 60% of A549, and 52% of HeLa cells after 48 hours incubation. Toxicity of APL to L929, Ehrlich ascites, A549, and HeLa cells revealed a reduction in cell viability of approximately 70% at APL concentration of 8mg/$5{\times}10^5$ cells after 48 hours incubation. Administration of APL ($100{\mu}g/day$ or $300{\mu}g/day$) inhibited the growth of Ehrlich ascites cells in vivo. Mice given only Ehrlich cells survived an average of $15{\pm}1$ (S.E.) days. Mice given Ehrlich cells and $100{\mu}g\;or\;300{\mu}g$ APL had 58% and 67% survival, respectively, after 20 days. These results suggest that APL has antitumor activity.

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Induction of Apoptosis by Curcuma aromatica on Lung Cancer Cells(A549), Cervical Cancer Cells(HeLa), Glioma Cancer Cells(A172) and Prostate Cancer Cells(PC3) (울금(鬱金)이 폐암(肺癌), 자궁암(子宮癌), 신경교종(神經膠腫) 및 전립선암(前立腺癌)에 대한 세포자살유도(細胞自殺誘導)에 미치는 영향(影響))

  • Park, Sang-Hyun;Kim, Jin-Sung;Yoon, Sang-Hyub;Ryu, Bong-Ha
    • The Journal of Internal Korean Medicine
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    • v.27 no.2
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    • pp.379-393
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    • 2006
  • Objectives: We are aimed to identify anti-tumor effects of Curcuma aromatics on some kinds of cancer cells through molecular biologic methods. Materials & Methods: We used 4 kinds of cancer cell lines such as lung cancer cells(AS49), cervical cancer cells(HeLa), glioma cancer cells(A172) and prostate cancer cells(PC3). We treated the boiled extract of Curcuma aromatica $5{\mu}g,\;10{\mu}g$ to cultural media(ml) for 24 hours. We measured the cytotoxicitv on 4 kinds of cancer cells through tryphan blue exclusion test and the suppressive effect on viability of 4 kinds of cancer cells via MTT assay. We measured change of mitochondria membrane potential via flow cytometry. The quantitative RT-PCR was used to examine the effect on the revelation of Bcl-2 and Bax which are genes related to apoptosis. We examined the effect on the revelation of Bcl-2 Protein and Bar protein by western blot analysis. Results : In the experiment of tryphan blue exclusion test, the extract of Curcuma aromatica showed more significant killing effect on AS49, HeLa than the control group with density dependent manner, which was statistically significant. In the experiment of MTT assay the extract of Curcuma aromatica showed more suppressive effect on viability of A549, HeLa than the control group with density dependent manner, which was statistically significant. Curcuma aromatica induced apoptosis by decreasing the membrane potential of mitochondria in A549, HeLa. In the experiment of the revelation of genes related to apoptosis, the revelation of Bcl-2 decreased and the revelation of Bax increased in A549, HeLa treated with Curcuma aromatica with dose dependent manner. In the experiment of the revelation of protein related to apoptosis, the protein levels of Bcl-2 decreased and the protein levels of Bax increased in AS49, HeLa treated with Curcuma aromatica with dose dependent manner. Conclusions: From this study, we can infer that Curcuma aromatica has anti-tumor effect on lung cancer cells and uterine carcinoma cells but not on glioma cells and prostate cancer cells.

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Synthesis and Structure-activity Relationship of Cytotoxic $5,2^I,5^I$-Trihydroxy-7,8-dimethoxyflavanone Analogues

  • Min, Byung-Sun;Ahn, Byung-Zun;Bae, Ki-Hwan
    • Archives of Pharmacal Research
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    • v.19 no.6
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    • pp.543-550
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    • 1996
  • Analogues of $2(S)-5, 2^{l}, 5^{l}$-trihydroxy-7, 8-dimethoxyflavanone, a naturally-occurring compound, which had been reported to have potent antitumor activity, were synthesized and examined for the cytotoxicity against three cancer cell lines. Among the intermediate chalcones and synthetic 5-hydroxy-7, 8-dimethoxyflavanone analogues, $({\pm})2^{l}, 5^{l}-dibenzyloxy-5, 7, 8-trimethoxyflavanone$ exhibited about 2-8 times stronger activity than $2(S)-5, 2^{l}, 5^{l}$-trihydroxy-7, 8-dimethoxyflavanone against L1210, K562 and A549 cancer cell lines. In the structure-activity relationship, it is suggested that among analogues of 5-hydroxy-7, 8-dimethoxyflavanone, the existence of two oxygenated groups of para-relation at $C-2^{I} and C-5^{I}$ positions on flavanone B-ring, may be necessary to exhibit effective cytotoxic activity.

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Antitumor Activity of Gamdutang Aqua-Acupuncture Solution (감두약침액의 암세포 성장 저해 효과)

  • 조경희;한상훈;임종국;손윤희;이임태;남경수
    • Journal of Life Science
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    • v.9 no.6
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    • pp.677-683
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    • 1999
  • Gamdutang aqua-acupuncture solution (GAS), Gamdutang water-extracted solution (GWS) and Dae-Gamdutang aqua-acupuncture solution (DGAS) were prepared and tested for antitumor activities. It was shown to possess considerable toxicity toward various tumor cell lines. Concentration of 5 $\times$ and 10$\times$ of GAS resulted in more than 70% inhibition of growth in Ehrlich ascites tumor cells (EATC), Hepa1c1c7 and A549. GAS at concentrations of 5$\times$ and 10$\times$ revealed more than 60% inhibition in HeLa. GWS showed more than 50% inhibition of growth with EATC and HeLa at concentrations of 5$\times$ and 10$\times$, respectively. Toxicity assay with GWS in Hepa1c1c7 and A549 revealed that more than 80% inhibition of growth at the concentration of 5$\times$ and 10$\times$. In morphological study, the number of cells were decreased, and the shape of cells was round-form in EATC, Hepa1c1c7, A549, HeLa with GAS.

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Liripois Tuber contributes to the chemotaxis of eosinophils and secretion of cytokines in A549 human epithelial cells (맥문동(麥門冬)이 천식유발 cytokine 분비와 호산구 chemotaxis에 미치는 영향)

  • Jung, Hae-Jun;Jung, Gee-Jae;Jung, Sung-Ki;Rhee, Hyung-Koo
    • The Journal of Korean Oriental Chronic Disease
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    • v.10 no.1
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    • pp.1-20
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    • 2005
  • Background and Objective: The importance of the presence of eosinophils in the airways of patients with fetal asthma has long been recognized, but the mechanism by which these cells are recruited and retained in the lung are only now being elucidated. Eotaxin is a potent and specific eosinophil chemoattractant that is mobilized in the respiratory epithelium after allergic stimulation. Material and Methods: We used water extracts of Liripois Tuber and pulmonary epithelial cell lines A549(human typeII-like epithelial cells) and human eosinophils. We estimated cytotoxic effects of Liripois Tuber via MTS assay, and estimated the effects of Liripois Tuber on chemokines from prestimulated A549 cells by sandwich ELISA and RT-PCR. We conducted chemotaxis assay on prestimulated eosinophils treated with Liripois Tuber. Result: In this study we demonstrated that $TNF-{\alpha}$, IL-4 and $IL-1{\beta}$ induced the accumulation of chemokines mRNA in the pulmonary epithelial cell lines A549 in dose-dependent manner. Chemokines were inhibited by Liripois Tuber in dose-dependent manner. The eosinophil migration was inhibited at high concentration of Liripois Tuber. Conculusion: These findings indicate that the supression of the expression of chemokines can be accomplished by Liripois Tuber treatment, raising the possibility that Liripois Tuber might be of therapeutic value in diseases such as asthma.

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Protective Effects of Socheongryong-tang on Elastase-Induced Lung Injury (Elastase로 유도된 폐손상에 대한 소청룡탕(小靑龍湯)의 보호효과)

  • Lee, Ju-Guan;Yang, Su-Young;Kim, Min-Hee;NamGung, Uk;Park, Yang-Chun
    • The Journal of Korean Medicine
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    • v.32 no.4
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    • pp.83-99
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    • 2011
  • Objective: This study aimed to evaluate the protective effects of Socheongryong-tang (SCRT) on elastase-induced lung injury. Materials and Methods: The extract of SCRT was treated to A549 cells and elastase-induced COPD mice model. Then, various parameters such as cell-based cytoprotective activity and histopathological findings were analyzed. Results: SCRT showed a protective effect on elastase-induced cytotoxicity in A549 cells. This effect was correlated with analysis for caspase 3 levels, collagen and elastin contents, and gene expression of TNF-${\alpha}$ and IL-$1{\beta}$ in A549 cells. SCRT treatment also revealed the protective effect on elastase-induced COPD mice model. This effect was evidenced via histopathological findings including immunofluoresence stains against elastin, collagen, and caspase 3, and protein level of Cdc2, cyclin B1, and phospho-Erk1/2 in lung tissue. Conclusion: These data suggest that SCRT has pharmaceutical properties on COPD. This study provides scientific evidence for the efficacy of SCRT for clinical application to patients with COPD.

H9 Inhibits Tumor Growth and Induces Apoptosis via Intrinsic and Extrinsic Signaling Pathway in Human Non-Small Cell Lung Cancer Xenografts

  • Kim, Min-Je;Kwon, Sae-Bom;Ham, Seung Hoon;Jeong, Eui-Suk;Choi, Yang-Kyu;Choi, Kang Duk;Hong, Jin Tae;Jung, Seung Hyun;Yoon, Do-Young
    • Journal of Microbiology and Biotechnology
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    • v.25 no.5
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    • pp.648-657
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    • 2015
  • H9, a novel herbal extract, demonstrated cytotoxicity in A549 non-small cell lung cancer (NSCLC) cell lines. In this study, we investigated whether H9, and/or co-treatment with an anticancer drug, pemetrexed (PEM), inhibited tumor growth in BALB/c nude mice models bearing A549 NSCLC cells. The mice were separated into groups and administered H9 and PEM for 2 weeks. Protein and mRNA levels were detected using western blotting and reverse transcription polymerase chain reaction, respectively; immunohistochemistry (IHC) was also performed on the tumor tissues. H9 and co-treatment with PEM induced the cleavage of proapoptotic factors, such as caspase-3, caspase-8, caspase-9, and poly(ADP)-ribose polymerase (PARP). Expression levels of cell-death receptors involving Fas/FasL, TNF-related apoptosisinducing ligands (TRAIL), and TRAIL receptors were increased by H9 and co-treatment with PEM. Furthermore, analysis of levels of cell-cycle modulating proteins indicated that tumor cells were arrested in the G1/S phase. In addition, the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/Akt survival signaling pathways were inhibited by H9 and co-treatment with PEM. In conclusion, H9 and co-treatment with PEM inhibited tumor growth in BALB/c nude mice models bearing A549 NSCLC cells. These results indicate that H9 and co-treatment with PEM can be used as an anticancer therapy in NSCLC.

Antiproliferative Effect of Mistletoe Extract Added Kimchi in Human Lung Carcinoma A549 Cells (겨우살이 물추출물 첨가 김치의 A549 인체 폐암 세포 증식저해 효과)

  • Kil, Jung-Ha
    • Journal of Life Science
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    • v.27 no.12
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    • pp.1507-1514
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    • 2017
  • The purpose of this study aimed at examining the antiproliferative effect of kimchi (kimchi B) adding mistletoe extract known as an anticancer function to improve the functions of kimchi. The study investigated the antiproliferative effect through hemocytometer counts and MTT assay, apoptosis induction through DAPI staining, and mRNA expression through RT-PCR using human lung carcinoma A549 cells. The standardized kimchi (Kimchi A) was used as a control group. As a result of hemocytometer counts and the MTT assay, it was found that kimchi samples inhibited the growth of A549 cells in a concentration-dependent manner. Kimchi B induced apoptosis in A549 cells through DAPI staining. The apoptosis induced by kimchi B was associated with the increase in the expression of pro-apoptotic Bax and with the decrease in the expression of anti-apoptotic Bcl-2 and Bcl-xL. Also, kimchi B influenced the increase in the expression of p21 mRNA, but did not have the effect on the expression of p53 mRNA. In conclusion, the antiproliferative effect of kimchi B was due to apoptosis induced by increasing Bax and decreasing Bcl-2, and increasing p21. The findings will be utilized to develop kimchi with the improved function for the patients having cancer.

The Extract from Artemisia annua Linné. Induces p53-independent Apoptosis through Mitochondrial Signaling Pathway in A549 Lung Cancer Cells (A549 폐암세포에서 미토콘드리아 경로를 통한 개똥쑥 추출물의 apoptosis 유도 효과)

  • Kim, Bo-Min;Kim, Guen-Tae;Kim, Eun-Ji;Lim, Eun-Gyeong;Kim, Sang-Yong;Kim, Young-Min
    • Journal of Life Science
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    • v.26 no.8
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    • pp.887-894
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    • 2016
  • The extract from Artemisia annuain L.(AAE) is known as a medicinal herb that is effective against cancer. Apoptosis is the process of programmed cell death, and mitochondria are known to play a central role in cell death control. In this study, we evaluated the p53-independent apoptosis of extract of AAE through downregulation of Bcl-2 and the mitochondrial pathway in A549 (lung cancer cells). AAE may exert cancer cell apoptosis through regulating p-Akt, Cox-2, p53 and mitochondria-mediated apoptotic proteins. p-Akt/cox-2 is known to play an important role in cell proliferation and cell survival. The Bcl-2 pro-apoptotic proteins (such as Bax, Bak and Bim) mediate the permeabilization of the mitochondrial outer membrane. Treatment of AAE reduces p-Akt, p-Mdm2, cox-2 and anti-apoptotic proteins (such as Bcl-2), while tumor suppressor p53 and pro-apoptotic proteins. Activation of Bax/Bak releases cytochrome c from mitochondria to the cytosol to activate a caspase. Caspase-3 is the major effector caspase associated with apoptotic pathways. Caspase-3 generally exists in cytoplasm in the form of a pro-enzyme. In the initiation stage of apoptosis, caspase-3 is activated by proteolytic cleavage and activated caspase-3 cleaves poly (ADP-ribose) polymerase (PARP). We treated Pifithrin-α (p53 inhibitor) and Celecoxib (Cox-2 inhibitor) to learn the relationship between the signal transduction of proteins associated with apoptosis. These results suggest that AAE induces apoptosis through a p53-independent pathway in A549.

Gallic Acid Hindered Lung Cancer Progression by Inducing Cell Cycle Arrest and Apoptosis in A549 Lung Cancer Cells via PI3K/Akt Pathway

  • Ko, Eul-Bee;Jang, Yin-Gi;Kim, Cho-Won;Go, Ryeo-Eun;Lee, Hong Kyu;Choi, Kyung-Chul
    • Biomolecules & Therapeutics
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    • v.30 no.2
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    • pp.151-161
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    • 2022
  • This study elucidates the anti-cancer potential of gallic acid (GA) as a promising therapeutic agent that exerts its effect by regulating the PI3K/Akt pathway. To prove our research rationale, we used diverse experimental methods such as cell viability assay, colony formation assay, tumor spheroid formation assay, cell cycle analysis, TUNEL assay, Western blot analysis, xenograft mouse model and histological analysis. Treatment with GA inhibited cell proliferation in dose-dependent manner as measured by cell viability assay at 48 h. GA and cisplatin (CDDP) also inhibited colony formation and tumor spheroid formation. In addition, GA and CDDP induced apoptosis, as determined by the distribution of early and late apoptotic cells and DNA fragmentation. Western blot analysis revealed that inhibition of the PI3K/Akt pathway induced upregulation of p53 (tumor suppressor protein), which in turn regulated cell cycle related proteins such as p21, p27, Cyclin D1 and E1, and intrinsic apoptotic proteins such as Bax, Bcl-2 and cleaved caspase-3. The anti-cancer effect of GA was further confirmed in an in vivo mouse model. Intraperitoneal injection with GA for 4 weeks in an A549-derived tumor xenograft model reduced the size of tumor mass. Injection of them downregulated the expression of proliferating cell nuclear antigen and p-Akt, but upregulated the expression of cleaved caspase-3 in tumor tissues. Taken together, these results indicated that GA hindered lung cancer progression by inducing cell cycle arrest and apoptosis, suggesting that GA would be a potential therapeutic agent against non-small cell lung cancer.