Long noncoding ribonucleic acids maternally expressed gene 3 inhibits lung cancer tumor progression through downregulation of MYC
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Published on: December 13, 2018
L Yan-Hua1, L Xiang-Lei1, L Hong1
1Department of Oncology, Huaihe Hospital of Henan University, Kaifeng, China.
Objective:
Long noncoding ribonucleic acids (RNAs) nowadays emerge as important biomarkers or potential therapeutic targets discussed in human cancers. Among them, maternally expressed gene 3 (MEG3) is known to be decreased in a variety of malignancies.
Materials And Methods:
Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was performed to detect the expression of MEG3 in forty pairs of lung cancer (LC) tissues. Overexpression of MEG3 was carried out, and we determined its effect on cell proliferation, apoptosis, and migration evaluated by cell counting kit-8, flow cytometric, and transwell analysis. Messenger RNA and protein expression of MYC were determined by qRT-PCR and western blot, respectively.
Results:
The expression of MEG3 was downregulated in LC tissues. Forced expression of MEG3 led to reduced abilities of cell proliferation and elevated apoptosis rate. It also slightly inhibited cell migration capacity in vitro. In addition, MYC was inhibited by MEG3 overexpression at both transcriptional and translational levels.
Conclusion:
Our findings revealed MEG3 could regulate LC progression and serve as an important target for LC treatment.
Insights
Maternally expressed gene 3 (MEG3) is downregulated in lung cancer (LC). Restoring MEG3 levels inhibits LC cell proliferation, migration, and targets MYC, suggesting its therapeutic potential.
Area of Science:
- Molecular Biology
- Oncology
- Gene Expression
Background:
- Long noncoding RNAs (lncRNAs) are emerging as critical biomarkers and therapeutic targets in human cancers.
- Maternally expressed gene 3 (MEG3) is frequently downregulated in various malignancies, indicating its potential role as a tumor suppressor.
Purpose of the Study:
- To investigate the expression levels of MEG3 in lung cancer (LC) tissues.
- To elucidate the functional role of MEG3 in regulating LC cell proliferation, apoptosis, and migration.
- To explore the relationship between MEG3 and MYC expression in LC.
Main Methods:
- Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) to assess MEG3 expression in 40 paired LC tissues.
- Experimental overexpression of MEG3 to evaluate its impact on cell proliferation, apoptosis, and migration using cell counting kit-8, flow cytometry, and Transwell assays.
- qRT-PCR and Western blot analysis to determine MYC messenger RNA and protein levels.
Main Results:
- MEG3 expression was significantly downregulated in LC tissues compared to normal tissues.
- Forced overexpression of MEG3 suppressed cell proliferation and induced apoptosis in LC cells.
- MEG3 overexpression exhibited a moderate inhibitory effect on cell migration in vitro.
- MEG3 was found to inhibit MYC expression at both the transcriptional and translational levels.
Conclusions:
- The findings demonstrate that MEG3 plays a crucial role in regulating lung cancer progression.
- MEG3 functions as a potential tumor suppressor in lung cancer by inhibiting proliferation, migration, and targeting MYC.
- MEG3 represents a promising therapeutic target for lung cancer treatment.
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