• Title, Summary, Keyword: A549 lung cancer cells

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Toll-like Receptor 5 Agonist Inhibition of Growth of A549 Lung Cancer Cells in Vivo in a Myd88 Dependent Manner

  • Zhou, Shi-Xiang;Li, Feng-Sheng;Qiao, Yu-Lei;Zhang, Xue-Qing;Wang, Zhi-Dong
    • Asian Pacific Journal of Cancer Prevention
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    • v.13 no.6
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    • pp.2807-2812
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    • 2012
  • The purpose of this study was to examine the effect of a Toll-like receptor 5 (TLR5) agonist, CBLB502, on the growth and radiosensitivity of A549 lung cancer cells in vivo. Expression of myeloid differentiation factor 88 (MyD88) or TLR5 was stably knocked down in human lung cancer cells (A549) using lentivirus expressing short hairpin RNA targeting human MyD88 or TLR5. Lack of MyD88 or TLR5 expression enhanced tumor growth in mouse xenografts of A549 lung cancer cells. CBLB502 inhibited the growth of A549 lung cancer cells, not A549-MyD88-KD cells in vivo in the murine xenograft model. Our results showed that the inhibition of A549 by CBLB502 in vivo was realized through regulating the expression of neutrophil recruiting cytokines and neutrophil infiltration. Finally, we found that activation of TLR5 signaling did not affect the radiosensitivity of tumors in vivo.

Effects of Ribosomal Protein L39-L on the Drug Resistance Mechanisms of Lung Cancer A549 Cells

  • Liu, Hong-Sheng;Tan, Wen-Bin;Yang, Ning;Yang, Yuan-Yuan;Cheng, Peng;Liu, Li-Juan;Wang, Wei-Jie;Zhu, Chang-Liang
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.7
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    • pp.3093-3097
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    • 2014
  • Background: Cancer is a major threat to the public health whether in developed or in developing countries. As the most common primary malignant tumor, the morbidity and mortality rate of lung cancer continues to rise in recent ten years worldwide. Chemotherapy is one of the main methods in the treatment of lung cancer, but this is hampered by chemotherapy drug resistance, especially MDR. As a component of the 60S large ribosomal subunit, ribosomal protein L39-L gene was reported to be expressed specifically in the human testis and human cancer samples of various tissue origins. Materials and Methods: Total RNA of cultured drug-resistant and susceptible A549 cells was isolated, and real time quantitative RT-PCR were used to indicate the transcribe difference between amycin resistant and susceptible strain of A549 cells. Viability assay were used to show the amycin resistance difference in RPL39-L transfected A549 cell line than control vector and null-transfected A549 cell line. Results: The ribosomal protein L39-L transcription level was 8.2 times higher in drug-resistant human lung cancer A549 cell line than in susceptible A549 cell line by quantitative RT-PCR analysis. The ribosomal protein L39-L transfected cells showed enhanced drug resistance compared to plasmid vector-transfected or null-transfected cells as determined by methyl tritiated thymidine (3H-TdR) incorporation. Conclusions and Implications for Practice: The ribosomal protein L39-L gene may have effects on the drug resistance mechanism of lung cancer A549 cells.

Kanahia Laniflora Methanolic Extract Suppressed Proliferation of Human Non-Small Cell Lung Cancer A549 Cells

  • Alfaif, Mohammad Yahya
    • Asian Pacific Journal of Cancer Prevention
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    • v.17 no.10
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    • pp.4755-4759
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    • 2016
  • Introduction: Lung cancer is one of the most common cancers worldwide. In certain countries such as United States of America, it is the leading cause of related cancer mortality among both men and women. Natural products play an important role in overcoming the limitations of chemotherapy and radiotherapy. Objectives: In this study, we investigated the antiproliferative and apoptotic activities of Kanahia laniflora methanolic extract against human non-small cell lung cancer cells (A549). Methods: Sulforhodamine B colorimetric assays were used to determine the inhibitory effects of a leaf methanolic extract against A549 cells. Results: The extract showed strong cytotoxic activity against A549 cells with an $IC_{50}$ value of $0.13{\mu}g/ml$ compared to $0.21{\mu}g/ml$ for doxorubicin. The extract also significantly increased the percentage of apoptotic cells to 49.7% as compared to 1.4% and 47.4% for control and doxorubicin respectively. Conclusion: These results showed, for the first time, that a methanolic extract of Kanahia laniflora leaves can inhibit the proliferation of human non-small cell lung cancer cells (A549). Further attention to its potential as a new effective anticancer agent is warranted.

Inhibitory Effects of Bee Venom on Growth of A549 Lung Cancer Cells via Induction of Death Receptors

  • Jang, Dong Min;Song, Ho Sueb
    • Journal of Acupuncture Research
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    • v.30 no.1
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    • pp.57-70
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    • 2013
  • This study was to investigated the effects of the bee venom on inhibition of cell growth via upregulation of death receptor expression in the A549 human lung cancer cells. Bee venom(1-5 ${\mu}g$/ml) inhibited the growth of A549 lung cancer cells by the induction of apoptotic cell death in a dose dependent manner. Consistent with apoptotic cell death, expression of TNFR1, Fas, death receptors(DR) 3, 4 and 6 was increased in the cells. Expression of DR downstream pro-apoptotic proteins including caspase-3, -9 and Bax was concomitantly increased, but the expression of Bcl-2, NF-${\kappa}B$ were inhibited by treatment with bee venom in A549 cells. Moreover, deletion of DR3, DR4 by small interfering RNA significantly reversed bee venom-induced cell growth inhibitory effect, whereas Apo3L strengthened anti-proliferative effect of bee venom through enhancement of DR3 expression. These results suggest that bee venom should exert anti-tumor effect through induction of apoptotic cell death in lung cancer cells via enhancement of death receptor expression, and that bee venom could be a promising agent for preventing and treating lung cancer.

Steroidal Saponins from Paris polyphylla Suppress Adhesion, Migration and Invasion of Human Lung Cancer A549 Cells Via Down-Regulating MMP-2 and MMP-9

  • He, Hao;Zheng, Lei;Sun, Yan-Ping;Zhang, Guang-Wei;Yue, Zheng-Gang
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.24
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    • pp.10911-10916
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    • 2015
  • Background: Tumor metastases are the main reasons for oncotherapy failure. Paris polyphylla (Chinese name: Chonglou) has traditionally been used for its anti-cancer actions. In this article, we focus on the regulation of human lung cancer A549 cell metastases and invasion by Paris polyphylla steroidal saponins (PPSS). Materials and Methods: Cell viability was evaluated in A549 cells by MTT assay. Effects of PPSS on invasion and migration were investigated by wound-healing and matrigel invasion chamber assays. Adhesion to type IV collagen and laminin was evaluated by MTT assay. Expression and protease activity of two matrix metalloproteinases (MMPs), MMP-2 and MMP-9, were analyzed by Western blotting and gelatin zymography, respectively. Results: PPSS exerted growth inhibitory effects on A549 cells, and effectively inhibited A549 cell adhesion, migration and invasion in a concentration-dependent manner. Western blotting and gelatin zymography analysis revealed that PPSS inhibited the expression and secretion of MMP-2 and MMP-9 in A549 cells. Conclusions: PPSS has the potential to suppress the migration, adhesion and invasion of A549 cells. PPSS could be a potential candidate for interventions against lung cancer metastases.

Steroidal Saponins from Paris polyphylla Induce Apoptotic Cell Death and Autophagy in A549 Human Lung Cancer Cells

  • He, Hao;Sun, Yan-Ping;Zheng, Lei;Yue, Zheng-Gang
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.3
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    • pp.1169-1173
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    • 2015
  • Background: Paris polyphylla (Chinese name: Chonglou) had been traditionally used for a long time and shown anti-cancer action. Based on the previous study that paris polyphylla steroidal saponins (PPSS) induced cytotoxic effect in human lung cancer A549 cells, this study was designed to further illustrate the mechanisms underlying. Materials and Methods: The mechanisms involved in PPSS-induced A549 cell death were investigated by phase contrast microscopy and fluorescence microscopy, flow cytometry and western blot analysis, respectively. Results: PPSS decreased the proportion of viable A549 cells, and exposure of A549 cells to PPSS led to both apoptosis and autophagy. Apoptosis was due to activations of caspase-8, caspase-3, as well as cleavage of PARP, and autophagy was confirmed by up-regulation of Beclin 1 and the conversion from LC3 I to LC3 II. Conclusions: PPSS was able to induce lung cancer A549 cell apoptosis and autophagy in vitro, the results underlining the possibility that PPSS would be a potential candidate for intervention against lung cancer.

Bufalin Induces Mitochondrial Pathway-Mediated Apoptosis in Lung Adenocarcinoma Cells

  • Ding, Da-Wei;Zhang, Yong-Hong;Huang, Xin-En;An, Qing;Zhang, Xun
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.23
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    • pp.10495-10500
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    • 2015
  • Background: To evaluate the effects of bufalin in A549 human lung adenocarcinoma epithelial cells in vitro and assess the underlying mechanisms. Materials and Methods: Human A549 non-small cell lung cancer (NSCLC) cells were treated with various concentrations of bufalin. Cell proliferation was measured by CCK-8 assay, apoptotic cell percentage was calculated by flow cytometry and morphological change was observed by inverted phase contrast microscopy/transmission electron microscopy. In addition, the membrane potential of mitochondria was detected by JC-1 fluorescence microscopy assay, and the related protein expression of cytochrome C and caspase-3 was analyzed by Western blotting. Results: Bufalin could inhibit the proliferation of A549 cells via induction of apoptosis, with the evidence of characteristic morphological changes in the nucleus and mitochondria. Furthermore, bufalin decreased the mitochondrial membrane potential with up-regulation of cytochrome C in the cytosol, and activation of caspase-3. Conclusions: Bufalin inhibits the proliferation of A549 cells and triggers mitochondria-dependent apoptosis, pointing to therapeutic application for NSCLC.

Preparation of Lysine-Coated Magnetic Fe2O3 Nanoparticles and Influence on Viability of A549 Lung Cancer Cells

  • Ma, Yu-Hua;Peng, Hai-Ying;Yang, Rui-Xia;Ni, Fang
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.20
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    • pp.8981-8985
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    • 2014
  • Objective: To explore the effect of lysine-coated oxide magnetic nanoparticles (Lys@MNPs) on viability and apoptosis of A549 lung cancer cells. Methods: Transmission electron microscopy (TEM), vibrating sample magnetometer (VSM) and Zeta potentiometric analyzer were employed to characterize Lys@MNPs. Then Lys@MNPs and lung cancer A549 cells were co-cultured to study the effect of Lys@MNPs on cell viability and apoptosis. The pathway of Lys@MNPs entering A549 cells was detected by TEM and cell imaging by 1.5 T MRI. Results: Lys@MNPs were 10.2 nm in grain diameter, characterized by small size, positive charge, and superparamagnetism. Under low-dose concentration of Lys@MNPs (< $40{\mu}g/mL$), the survival rate of A549 cells was decreased but remained higher than 95% while under high-dose concentration ($100{\mu}g/mL$), the survival ratewas still higher than 80%, which suggested Lys@MNPs had limited influence on the viability of A549 cells, with good biocompatibility and and no induction of apoptosis. Moreover, high affinity for cytomembranes, was demonstrated presenting good imaging effects. Conclusion: Lys@MNPs can be regarded as a good MRI negative contrast agents, with promising prospects in biomedicine.

Effects of Vinorelbine on Cisplatin Resistance Reversal in Human Lung Cancer A549/DDP Cells

  • Zhou, Yu-Ting;Li, Kun;Tian, Hui
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.8
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    • pp.4635-4639
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    • 2013
  • Multi-drug resistance (MDR) is an essential aspect of human lung cancer chemotherapy failure. Recent studies have shown that vinorelbine is involved in underlying processes in human tumors, reversing the MDR inseveral types of cancer cells. However, the roles and potential mechanism are not fully clear. In this study, we explored effects of vinorelbine in multi-drug resistance reversal of human lung cancer A549/DDP cells. We found that vinorelbine increased drug sensitivity to cisplatin and intracellular accumulation of rhodamine-123, while decreasing expression of P-glycoprotein (P-gp), multi-drug resistance-associated protein (MRP1) and glutathione-S-transferase ${\pi}$ (GST-${\pi}$) in A549/DDP cells. At the same time, we also established downregulation of p-Akt and decreased transcriptional activation of NF-${\kappa}B$ and twist after vinorelbine treatment. The results indicated that vinorelbine might be used as a potential therapeutic strategy in human lung cancer.

Expression and Function of GSTA1 in Lung Cancer Cells

  • Pan, Xue-Diao;Yang, Zhou-Ping;Tang, Qi-Ling;Peng, Tong;Zhang, Zheng-Bing;Zhou, Si-Gui;Wang, Gui-Xiang;He, Bing;Zang, Lin-Quan
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.20
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    • pp.8631-8635
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    • 2014
  • Glutathione S-transferase A1 (GSTA1) appears to be primarily involved in detoxification processes, but possible roles in lung cancer remain unclear. The objective of this study was to investigate the expression and function of GSTA1 in lung cancer cells. Real-time PCR and Western blotting were performed to assess expression in cancer cell lines and the normal lung cells, then verify the A549 cells line with stable overexpression. Localization of GSTA1 proteins was assessed by cytoimmunofluorescence. Three double-strand DNA oligoRNAs (SiRNAs) were synthesized prior to being transfected into A549 cells with Lipofectamine 2000, and then the most efficient SiRNA was selected. Expression of the GSTA1 gene in the transfected cells was determined by real-time PCR and Western blotting. The viability of the transfected cells were assessed by MTT. Results showed that the mRNA and protein expression of A549 cancer cells was higher than in MRC-5 normal cells. Cytoimmunofluorescence demonstrated GSTA1 localization in the cell cytoplasm and/or membranes. Transfection into A549 cells demonstrated that down-regulated expression could inhibit cell viability. Our data indicated that GSTA1 expression may be a target molecule in early diagnosis and treatment of lung cancer.