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 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.

scholarly journals CircZNF652 accelerates the proliferation and migration of primary lung carcinoma cells by downregulating miR-766

2021 ◽  
Vol 20 (11) ◽  
pp. 2255-2260
Author(s):  
Xiaobing Hong ◽  
Yongqing Chen ◽  
Danzhen Zhang
Keyword(s):  
Lung Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Biological Functions ◽  
Mesenchymal Transition ◽  
Lung Carcinoma Cells ◽  
Kaplan Meier ◽  
Primary Lung Carcinoma ◽  
Knockdown Effect ◽  
And Migration

Purpose: To explore the biological functions and molecular mechanism of circZNF652 involvement in primary lung carcinoma.Methods: CircZNF652 levels in primary lung carcinoma cases and controls were determined using quantitative real-time polymerase chain reaction (qRT-PCR). Its prognostic value in primary lung carcinoma was examined by depicting it with Kaplan-Meier curves. The biological functions of circZNF652 in regulating proliferative and migratory capacities in A549 and SPC-A-1 cells were analyzed from the curves. Interaction between circZNF652 and its downstream gene, miR-766, wasassessed, and their co-regulation on primary lung carcinoma was determined by rescue experiments.Results: CircZNF652 was abnormally and significantly upregulated in primary lung carcinoma cases (p< 0.05), resulting in a poor prognosis. The knockdown effect of circZNF652 attenuated the proliferative and migratory capacities of A549 and SPC-A-1 cells, and downregulated epithelial-mesenchymal transition (EMT)-associated genes. CircZNF652 bound and negatively regulated miR-766, a keydownstream gene involved in circZNF652-induced aggravation of primary lung carcinoma.Conclusion: CircZNF652 serves as an oncogene, triggering the aggravation of primary lung carcinoma by negatively regulating miR-766. The results of this study may provide new insights into the treatment of lung carcinoma.

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.

VDAC1 Mediated Anticancer Activity of Gallic Acid in Human Lung Adenocarcinoma A549 Cells

2018 ◽  
Vol 18 (2) ◽  
pp. 255-262 ◽  
Author(s):  
Aikebaier Maimaiti ◽  
Amier Aili ◽  
Hureshitanmu Kuerban ◽  
Xuejun Li
Keyword(s):  
Western Blot ◽  
Cell Viability ◽  
Gallic Acid ◽  
Molecular Mechanisms ◽  
A549 Cells ◽  
Dependent Manner ◽  
Lung Carcinoma Cells ◽  
Induced Apoptosis ◽  
The Impact

Aims: Gallic acid (GA) is generally distributed in a variety of plants and foods, and possesses cell growth-inhibiting activities in cancer cell lines. In the present study, the impact of GA on cell viability, apoptosis induction and possible molecular mechanisms in cultured A549 lung carcinoma cells was investigated. Methods: In vitro experiments showed that treating A549 cells with various concentrations of GA inhibited cell viability and induced apoptosis in a dose-dependent manner. In order to understand the mechanism by which GA inhibits cell viability, comparative proteomic analysis was applied. The changed proteins were identified by Western blot and siRNA methods. Results: Two-dimensional electrophoresis revealed changes that occurred to the cells when treated with or without GA. Four up-regulated protein spots were clearly identified as malate dehydrogenase (MDH), voltagedependent, anion-selective channel protein 1(VDAC1), calreticulin (CRT) and brain acid soluble protein 1(BASP1). VDAC1 in A549 cells was reconfirmed by western blot. Transfection with VDAC1 siRNA significantly increased cell viability after the treatment of GA. Further investigation showed that GA down regulated PI3K/Akt signaling pathways. These data strongly suggest that up-regulation of VDAC1 by GA may play an important role in GA-induced, inhibitory effects on A549 cell viability.

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