scholarly journals Effective Isolation for Lung Carcinoma Cells Based on Immunomagnetic Separation in a Microfluidic Channel

Biosensors ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 23
Author(s):  
Hien Vu-Dinh ◽  
Hui Feng ◽  
Chun-Ping Jen
Keyword(s):  
Lung Cancer ◽  
Lung Carcinoma ◽  
Magnetic Beads ◽  
A549 Cells ◽  
Microfluidic Channel ◽  
Reference Method ◽  
Immunomagnetic Separation ◽  
Carcinoma Cells ◽  
Isolation System ◽  
Lung Carcinoma Cells

In this paper, we developed an isolation system for A549 human lung carcinoma cells as an effective factor for the early diagnosis of lung cancer. A microfluidic immunomagnetic method was used, in which the combination of immunomagnetic separation and a microfluidic system allowed for increased isolation efficiency with uncomplicated manipulation. In the microfluidic immunomagnetic strategy, A549 cells were combined with aptamer-conjugated carboxylated magnetic beads and then collected in a specified region by applying a magnetic field. The results were recorded using a fluorescence microscope, and the captured targets were then quantified. The isolation efficiency of A549 cells is up to 77.8%. This paper developed a simple working procedure, which is less time consuming, high-throughput, and trustworthy for the isolation of A549 cells. This procedure can be a useful reference method for the development of an effective diagnosis and treatment method for lung cancer in the future.

MiR-32 Suppresses the Development of Lung Cancer via Modulating PI3K/Akt

2021 ◽  
Vol 11 (7) ◽  
pp. 1271-1276
Author(s):  
Qing-Feng Liu ◽  
Ye Zhang ◽  
Lei Deng ◽  
Tao Zhang ◽  
Jian-Ping Xiao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Carcinoma ◽  
Target Gene ◽  
A549 Cells ◽  
Carcinoma Cells ◽  
Lung Carcinoma Cells ◽  
Kaplan Meier ◽  
Primary Lung Carcinoma ◽  
Apoptosis Assay ◽  
The Impact

Our team utilized qRT-PCR for prospecting miR-32 expression level in primary lung carcinoma tissues and cell lines, as well as Kaplan–Meier method for dissecting the relation of miR-32 expression with the prognosis of lung carcinoma. We transfected lung cancer A549 cells with miR-32 mimic/inhibitor and mimic/inhibitor NC, and appraised the influences of miR-32 on the phenotype changes of lung carcinoma cells via MTT assay, wound healing assay and cell apoptosis assay, separately. Then the target gene of miR-32 was predicted via bioinformatics. Finally, Western blotting was adopted for analyzing the impact of alteration of miR-32 expression on the PI3K/Akt axis in A549 cells. In lung carcinoma tissues as well as cells, miR-32 expression is down-regulated, and miR-32 partakes in the progress of lung carcinoma via PI3K/Akt pathway.

scholarly journals An Aptamer-Based Capacitive Sensing Platform for Specific Detection of Lung Carcinoma Cells in the Microfluidic Chip

Biosensors ◽  
2018 ◽  
Vol 8 (4) ◽  
pp. 98 ◽  
Author(s):  
Ngoc-Viet Nguyen ◽  
Chun-Hao Yang ◽  
Chung-Jung Liu ◽  
Chao-Hung Kuo ◽  
Deng-Chyang Wu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Carcinoma ◽  
Early Stage ◽  
A549 Cells ◽  
Microfluidic Channel ◽  
Electrical Impedance Spectroscopy ◽  
Label Free ◽  
Early Stage Lung Cancer ◽  
Sensing Platform ◽  
Label Free Detection

Improvement of methods for reliable and early diagnosis of the cellular diseases is necessary. A biological selectivity probe, such as an aptamer, is one of the candidate recognition layers that can be used to detect important biomolecules. Lung cancer is currently a typical cause of cancer-related deaths. In this work, an electrical sensing platform is built based on amine-terminated aptamer modified-gold electrodes for the specific, label-free detection of a human lung carcinoma cell line (A549). The microdevice, that includes a coplanar electrodes configuration and a simple microfluidic channel on a glass substrate, is fabricated using standard photolithography and cast molding techniques. A procedure of self-assembly onto the gold surface is proposed. Optical microscope observations and electrical impedance spectroscopy measurements confirm that the fabricated microchip can specifically and effectively identify A549 cells. In the experiments, the capacitance element that is dominant in the change of the impedance is calculated at the appropriate frequency for evaluation of the sensitivity of the biosensor. Therefore, a simple, inexpensive, biocompatible, and selective biosensor that has the potential to detect early-stage lung cancer would be developed.

Ocimum sanctuminduces apoptosis in A549 lung cancer cells and suppresses thein vivogrowth of lewis lung carcinoma cells

2009 ◽  
Vol 23 (10) ◽  
pp. 1385-1391 ◽  
Author(s):  
Venkataraman Magesh ◽  
Jang-Choon Lee ◽  
Kwang Seok Ahn ◽  
Hyo-Jung Lee ◽  
Hyo-Jeong Lee ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Carcinoma ◽  
Lewis Lung Carcinoma ◽  
Carcinoma Cells ◽  
Lung Cancer Cells ◽  
Lewis Lung ◽  
Lung Carcinoma Cells ◽  
Lewis Lung Carcinoma Cells ◽  
A549 Lung

Antitumor activity of a synthetic agonist of TLR9 in preclinical lung cancer models

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 2568-2568
Author(s):  
D. Wang ◽  
D. Yu ◽  
E. R. Kandimalla ◽  
S. Agrawal
Keyword(s):  
Lung Cancer ◽  
Antitumor Activity ◽  
Lung Carcinoma ◽  
Chemotherapeutic Agents ◽  
Carcinoma Cells ◽  
Antitumor Effects ◽  
Adaptive Immune ◽  
Lung Carcinoma Cells ◽  
Cancer Models ◽  
Lung Cancer Model

2568 Background: Synthetic agonists of TLR9 induce potent Th1-type innate and adaptive immune responses. In the present study, we have studied antitumor activity of a synthetic agonist of TLR9 referred to as immune modulatory oligonucleotide (IMO) in lung cancer models either alone or in combination with chemotherapeutic agents. Methods: Two different models are evaluated. In one model, mice implanted peritoneally with 3LL-C75 lung carcinoma cells were administered with IMO or PBS once in every two days for six times for evaluating antitumor activity of IMO alone. In a second model, to evaluate combination treatment of IMO with Gemcitabine or cyclophosphamide, mice bearing subcutaneously implanted 3LL tumor were administered with peritumoral injections of IMO and i.p. injections of Gemcitabine or cyclophosphamide. Results and Conclusions: Administration of IMO to mice bearing 3LL-C75 lung carcinoma inhibited tumor growth. Tumor free mice from this study failed to grow tumor when rechallenged with 3LL-C75 lung carcinoma cells, suggesting tumor bearing mice administered with IMO developed memory responses for the same tumor. Further more, naïve mice adoptively transferred with splenocytes obtained from mice that remained tumor free from the above treatment group failed to grow tumor to a rechallenge with 3LL-C75 tumor cells. The co-administration of IMO with chemotherapeutic agents, Gemcitabine and cyclophosphamide resulted in enhanced antitumor effects in 3LL lung cancer model. The present studies show potent antitumor activity of IMO when administered alone and in combination with Gemcitabine and cyclophosphamide in preclinical lung cancer models. [Table: see text]

scholarly journals Regulation of the synthesis and activity of urokinase plasminogen activator in A549 human lung carcinoma cells by transforming growth factor-beta

1988 ◽  
Vol 106 (2) ◽  
pp. 451-459 ◽  
Author(s):  
J Keski-Oja ◽  
F Blasi ◽  
EB Leof ◽  
HL Moses
Keyword(s):  
Growth Factor ◽  
Lung Carcinoma ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Human Lung ◽  
A549 Cells ◽  
Carcinoma Cells ◽  
Tgf Beta ◽  
Lung Carcinoma Cells ◽  
Growth Factor Beta

Transforming growth factor-beta (TGF beta) is a regulator of cellular proliferation which can alter the proteolytic activity of cultured cells by enhancing the secretion of endothelial type plasminogen activator inhibitor and affecting the secretion of plasminogen activators (PAs) in cultured fibroblastic cells. We used the TGF beta-responsive malignant human lung adenocarcinoma cell line A549 to study the relationships between the known TGF beta-induced growth inhibition and the effects of TGF beta on the secretion of PA activity by A549 cells. PA activity was quantitated by caseinolysis assays, and characterized by urokinase mRNA analysis, immunoprecipitation, and zymography assays. PA-inhibitor production was observed in autoradiograms of SDS-polyacrylamide gels and reverse zymography assays. It was found that TGF beta enhanced the production of PA activity by these cells, in accordance with an enhancement of urokinase mRNA levels. A concomitant stimulation of type 1 PA-inhibitor production was also observed in A549 cells in response to TGF beta. In contrast to the observations of A549 cells, TGF beta caused a decrease in the expression of both urokinase and the tissue-type PA mRNA in human embryonic WI-38 lung fibroblasts indicating opposite regulation of the expression of PAs in these cells. The results suggest that TGF beta may play a role in the regulation of the invasive, proteolytically active phenotype of certain lung carcinoma cells.

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