Systems Biology of Lung Cancer - Linking Dynamic Properties of Signaling Networks to Migratory Behavior of Lung Carcinoma Cells in Monolayer Culture

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.

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

Journal of Biomaterials and Tissue Engineering ◽

10.1166/jbt.2021.2684 ◽

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.

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Association of eIF3 p170 expression with chemotherapy response of lung cancer and its effects on cisplatin sensitivity in lung carcinoma cells

Cell Biology International ◽

10.1016/j.cellbi.2008.01.141 ◽

2008 ◽

Vol 32 (3) ◽

pp. S32-S32

Author(s):

Jie Shen ◽

Hai Tang Xie ◽

Ji Ye Yin ◽

Hong Hao Zhou ◽

Jing Ting Zhang ◽

...

Keyword(s):

Lung Cancer ◽

Lung Carcinoma ◽

Carcinoma Cells ◽

Chemotherapy Response ◽

Lung Carcinoma Cells ◽

Cisplatin Sensitivity

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

Phytotherapy Research ◽

10.1002/ptr.2784 ◽

2009 ◽

Vol 23 (10) ◽

pp. 1385-1391 ◽

Cited By ~ 31

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

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

Journal of Clinical Oncology ◽

10.1200/jco.2006.24.18_suppl.2568 ◽

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]

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