miR-218 suppressed the growth of lung carcinoma by reducing MEF2D expression

Song, Lei; Li, Dan; Zhao, Yongli; Gu, Yue; Zhao, Dan; Li, Xiang; Bai, Xiaoxue; Sun, Ying; Zhang, Xiufang; Sun, Haijie; Wang, Yan; Peng, Liping

doi:10.1007/s13277-015-4038-2

Cited by 29 publications

(26 citation statements)

References 15 publications

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“…Therefore, it was hypothesized that the suppression of MEF2D was responsible, at least in part, for the antitumor effect of miR-30a. In accordance, Song et al (24) demonstrated that the expression of MEF2D is decreased by another miR (miR-218), in lung carcinoma. One possible explanation is that the same miR may have different targets and the same mRNA may be targeted by different miRs in diverse cell types (22,24).…”

Section: Discussionsupporting

confidence: 61%

Absent expression of miR‑30a promotes the growth of lung cancer cells by targeting MEF2D

2018

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Abstract. The microRNA (miR)-30 family has been reported to be aberrantly expressed in several types of cancer. However, its contributions to lung cancer remain to be fully elucidated. Myocyte enhancer factor 2D (MEF2D), an oncogene in liver cancer, has been shown to be aberrantly expressed in lung cancer. In the present study, it was found that MEF2D and miR-30a were inversely correlated in lung cancer samples. Using an online database, it was predicted that miR-30a targeted the 3' untranslated region (UTR) of MEF2D mRNA. The activity of luciferase with MEF2D 3'UTR was suppressed by transfecting cells with miR-30a mimics. The results of western blot analysis showed that the miR-30a mimics also suppressed the MEF2D protein. The miR-30a mimics were able to reduce the growth and colonies of lung cancer cells by suppressing MEF2D. The results of FACS and western blot assays showed that the apoptotic rate was reduced by transfection with the miR-30a mimics. Collectively, the aberrant expression of miR-30a in lung cancer promoted the expression of MEF2D protein. miR-30a inhibited the growth and colony formation of the lung cancer cells by promoting apoptosis.

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Section: Discussionsupporting

confidence: 61%

Absent expression of miR‑30a promotes the growth of lung cancer cells by targeting MEF2D

2018

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“…Altered MEF2 activity serves a role in human diseases and it has recently been implicated in the initiation and progression of various types of cancer in humans (31). Recently, it was reported that MEF2D, one member of MEF2 family, is involved in the progression of several cancer types, including lung carcinoma (27), rhabdomyosarcoma (32), hepatocellular carcinoma (31) and osteosarcoma (25).…”

Section: Discussionmentioning

confidence: 99%

“…miRNA target prediction websites www.microRNA.org and TargetScan (www .targetscan.org) were used to predict the target gene of miR-30a. The 3'-UTR of MEF2D containing the putative binding site of miR-30a was amplified and subcloned into a pGL3 luciferase promoter vector (Promega Corporation, Madison, WI, USA), as described previously (27); the putative binding site was mutated as negative control (MEF2D-Mut). The vector was co-transfected with miR-30a mimic into 293 cells for 48 h. The cells were harvested and relative luciferase activity was detected using a Dual-Luciferase Reporter Assay System (Promega Corporation) according to the manufacturer's protocol.…”

Section: Reverse Transcription-quantitative Polymerase Chain Reactionmentioning

confidence: 99%

Downregulation of miR‑30a is associated with proliferation and invasion via targeting MEF2D in cervical cancer

Zhao

Shu

et al. 2017

Oncol Lett

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Abstract. Accumulating studies have revealed that microRNAs serve crucial roles in cancer development and progression. MicroRNA-30a (miR-30a) has been implicated in various cancer types. However, the role of miR-30a in cervical cancer remains unclear. In the current study, a reverse transcription-quantitative polymerase chain reaction (RT-qPCR) assay revealed that miR-30a was significantly downregulated in cervical cancer tissues compared with adjacent normal tissues, and in the cervical cancer cell lines HeLa, SiHa and Ca-Ski compared with GH329 normal cervical epithelial cells. A functional assay using miR-30a mimic demonstrated that miR-30a could inhibit the growth and invasion of cervical cancer cells. Additionally, bioinformatics-based prediction and luciferase reporter assays indicated that MEF2D is a direct target of miR-30a. Transfection with miR-30a reduced the mRNA expression and protein levels of MEF2D, as determined using RT-qPCR and western blot analyses. Furthermore, MEF2D expression was negatively correlated with that of miR-30a in cervical cancers. Overall, the present study demonstrated that miR-30a functions as a tumor suppressor by targeting MEF2D in cervical cancer, which may provide the basis for a prognostic biomarker or therapeutic strategy for cervical cancer.

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“…Notably, for the first time, we established the link between miR-1244 expression and cisplatin-treated NSCLC cell growth. MEF2D, a member of the myocyte enhancer factor 2 family of transcription factors, has been shown to be expressed in NSCLC cells and to increase the proliferation rate of cells by increasing G2/M transition (14). MEF2D is a target of miR-122 (13).…”

Section: Discussionmentioning

confidence: 99%

“…Its main function is to regulate the survival and differentiation of multiple cell types. Early studies on MEF2 were predominantly limited to its role in muscle and the nervous system (14). However, numerous studies have demonstrated that chromosome translocation in NSCLC may result in abnormally high expression of MEF2D and promote the formation and development of NSCLC (15).…”

Section: Introductionmentioning

confidence: 99%

Effect of miR-1244 on cisplatin-treated non-small cell lung cancer via MEF2D expression

Yang

Zhou

et al. 2017

Oncology Reports

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Abstract. The aim of this study was to investigate the function of miR-1244 in cisplatin-treated non-small cell lung cancer (NSCLC). The results of quantitative PCR analysis revealed that the expression levels of miR-1244 in cisplatin-treated A549 and NCI-H522 human lung cancer cell lines were lower than those in untreated A549 and NCI-H522 cells. Similarly, the expression level of miR-1244 in NSCLC tissue samples from cisplatin-treated patients was also lower than that in non-cisplatin-treated NSCLC patients. Notably, the overall survival times of cisplatin-treated NSCLC patients with high miR-1244 expression were superior to those patients with low miR-1244 expression. We found that overexpression of miR-1244 suppressed cell viability and increased LDH toxicity in cisplatin-treated A549 and NCI-H522 cells. Additionally, overexpression of miR-1244 induced the apoptosis of cisplatin-treated A549 and NCI-H522 cells. Furthermore, overexpression of miR-1244 promoted caspase-3 activity and p53 and Bax protein expression, and suppressed myocyte enhancer factor 2D (MEF2D) and cyclin D1 protein expression in cisplatin-treated A549 and NCI-H522 cells. Small interfering RNA (siRNA) targeting MEF2D suppressed the protein expression of MEF2D, and was able to decrease the proliferation, promote caspase-3 activity, p53 and Bax protein expression and inhibit cyclin D1 protein expression in cisplatin-treated A549 and NCI-H522 cells following the overexpression of miR-1244. In summary, we found that miR-1244 affected cisplatin-treated NSCLC via MEF2D expression.

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miR-218 suppressed the growth of lung carcinoma by reducing MEF2D expression

Cited by 29 publications

References 15 publications

Absent expression of miR‑30a promotes the growth of lung cancer cells by targeting MEF2D

Absent expression of miR‑30a promotes the growth of lung cancer cells by targeting MEF2D

Downregulation of miR‑30a is associated with proliferation and invasion via targeting MEF2D in cervical cancer

Effect of miR-1244 on cisplatin-treated non-small cell lung cancer via MEF2D expression

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