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.
OBJECTIVE: Long noncoding ribonucleic acids (RNAs) nowadays emerge as important biomarkers or potential therapeutic targets discussed in humancancers. 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.
Authors: Teng Huang; Wei Huang; Hong Lu; Bi-Yun Zhang; Jun Ma; Di Zhao; Yi-Jun Wang; Da-Hai Yu; Xia He Journal: J Transl Med Date: 2018-02-28 Impact factor: 5.531