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Preparation and In Vitro Characterization of Magnetized miR-modified Endothelial Cells
Published on: May 2, 2017
The miR-1204 regulates apoptosis in NSCLC cells by targeting DEK
Zhen Qian1, Juan Yang1, Huanhuan Liu1
1College of Life Sciences and Bio-engineering, Beijing Jiaotong University, Beijing 100044, China.
Introduction:
This study endeavors to analyze the effects of miR-1204 on the expression of DEK oncogene in non-small cell lung cancer (NSCLC) cell lines and to study the molecular mechanisms of these effects.
Material And Methods:
The miR-1204 mimics and inhibitors were transfected into the (A549 and SPC) NSCLC cells. Then the mRNA levels, cell viability, apoptosis rate, morphology and caspase activity were determined. The expression of apoptosis-related proteins Bcl-2 and Bax was also analyzed.
Results:
In NSCLC cell lines (A549 and SPC), DEK mRNA levels were down-regulated in miR-1204 overex-pression group. In miR-1204 inhibition group, the expression of DEK mRNA showed an opposite trend. The overexpression of miR-1204 increases the apoptosis rate in NSCLC cells. The Bcl-2 levels in the miR-1204 over-expression group were decreased, while the Bax level was increased. In the miR-1204 inhibition group, expression of Bcl-2 and Bax showed opposite trends. Cell staining revealed cell's morphological changes; the apoptosis in the miR-1204 overexpression group revealed significant morphological features, such as brighter nuclei and nu-clear condensation. Results indicated a typical characteristic of apoptosis in the miR-1204 overexpression group. Caspase-9 and Caspase-3 were involved in the apoptosis pathway, which was mediated by miR-1204 and DEK.
Conclusions:
The miR-1204 induces apoptosis of NSCLC cells by inhibiting the expression of DEK. The mech-anism of apoptosis involves down-regulation of Bcl-2 and up-regulation of Bax expression. Moreover, the apoptosis was mediated by mitochondria-related caspase 9/3 pathway.
Insights
MicroRNA-1204 (miR-1204) induces apoptosis in non-small cell lung cancer (NSCLC) by inhibiting the DEK oncogene. This process involves regulating Bcl-2 and Bax proteins and activating the caspase 9/3 pathway.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related mortality.
- The DEK oncogene plays a role in cancer progression.
- MicroRNAs (miRNAs) are key regulators of gene expression with implications in cancer.
Purpose of the Study:
- To investigate the effect of miR-1204 on DEK oncogene expression in NSCLC.
- To elucidate the molecular mechanisms underlying miR-1204's action in NSCLC cells.
Main Methods:
- Transfection of miR-1204 mimics and inhibitors into NSCLC cell lines (A549 and SPC).
- Analysis of DEK mRNA levels, cell viability, apoptosis rate, cell morphology, and caspase activity.
- Assessment of apoptosis-related proteins Bcl-2 and Bax expression.
Main Results:
- miR-1204 overexpression down-regulated DEK mRNA levels in NSCLC cells.
- miR-1204 overexpression significantly increased apoptosis rates and induced characteristic morphological changes.
- Expression of Bcl-2 was decreased, while Bax expression was increased following miR-1204 overexpression.
- DEK inhibition by miR-1204 involved the mitochondria-related caspase 9/3 pathway.
Conclusions:
- miR-1204 induces apoptosis in NSCLC cells by inhibiting DEK expression.
- The mechanism involves down-regulation of Bcl-2 and up-regulation of Bax.
- Mitochondria-related caspase 9/3 pathway mediates the apoptosis induced by miR-1204 and DEK inhibition.
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