MiR-33a suppresses proliferation of NSCLC cells via targeting METTL3 mRNA

Du, Minjun; Zhang, Yanjiao; Mao, Yousheng; Mou, Juwei; Zhao, Jun; Xue, Qi; Wang, Dali; Huang, Jinfeng; Gao, Shugeng; Gao, Yushun

doi:10.1016/j.bbrc.2016.11.077

Cited by 154 publications

(126 citation statements)

References 29 publications

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“…Epigenetic regulates gene expression from multiple levels, including DNA methylation, RNA regulation, histone modification, and chromosome remodeling [55]. However, up to now, in lung cancers, only FTO and METTL3 have been reported as potential targets for its diagnosis and treatment [31,32]. In this study, except FTO and METTL3, we also found that KIAA1429, HNRNPC, YTHDC2, WTAP, YTHDC1, RBM15, ZC3H13, YTHDF1, YTHDF2, and ALKBH5 had differential expression in LUAD.…”

Section: Discussionsupporting

confidence: 52%

“…As for lung cancer, report has indicated that FTO enhances the expression of myeloid zinc finger 1 (MZF1) by reducing m 6 A levels, thereby promoting the development of lung squamous cell carcinoma (LUSC) [31]. Another evidence points that miR-33a inhibits the proliferation of non-small cell lung cancer (NSCLC) cells by targeting METTL3 mRNA 3'UTR binding sites [32]. Thus, the fully understanding of the pivotal m 6 A RNA methylation regulators is vital for lung cancer treatment.…”

Section: Introductionmentioning

confidence: 99%

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Diagnostic, progressive and prognostic performance of m⁶A methylation RNA regulators in lung adenocarcinoma

Zhuang¹,

Chen²,

Mao³

et al. 2020

Int. J. Biol. Sci.

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Background: N6-methyladenosine (m 6 A) RNA methylation is dynamically and reversibly regulated by methyl-transferases ("writers"), binding proteins ("readers"), and demethylases ("erasers"). The m 6 A is restored to adenosine and thus to achieve demethylation modification. The abnormality of m 6 A epigenetic modification in cancer has been increasingly attended. However, we are rarely aware of its diagnostic, progressive and prognostic performance in lung adenocarcinoma (LUAD). Methods and Results: The expression of 13 widely reported m 6 A RNA regulators in LUAD and normal samples were systematically analyzed. There were 12 m 6 A RNA methylation genes displaying aberrant expressions, and an 11-gene diagnostic score model was finally built (Diagnostic score

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Section: Discussionsupporting

confidence: 52%

Section: Introductionmentioning

confidence: 99%

Diagnostic, progressive and prognostic performance of m⁶A methylation RNA regulators in lung adenocarcinoma

Zhuang¹,

Chen²,

Mao³

et al. 2020

Int. J. Biol. Sci.

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“…and metastasis [12,13]. MiR-33a downregulation has been associated with cancer cell proliferation, mobility and chemotherapy sensitivity in various cancers, including lung cancer [14,15], prostate cancer [16] and BC [17,18], which suggested that it functions as a tumor suppressor. MiR-33a was upregulated after treatment with chidamide in TNBC and suppressed glycolysis by targeting LDHA [19].…”

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confidence: 99%

MiR-33a functions as a tumor suppressor in triple-negative breast cancer by targeting EZH2

et al. 2020

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Background: Increasing reports have confirmed that microRNAs play an important role in breast cancer progression, particularly in triple-negative breast cancer (TNBC). The aim of our study was to investigate the role of miR-33a in TNBC progression.Methods: PCR assays were performed to detect miR-33a and EZH2 expression in TNBC tissues, adjacent nontumor tissues and cell lines. Western blot, CCK8, Transwell, cell colony formation and EdU cell proliferation, cell cycle analysis and luciferase reporter assays were used to determine the regulation of miR-33a/EZH2 in TNBC progression.Results: MiR-33a was significantly downregulated in TNBC tissues and cell lines. MiR-33a overexpression in TNBC cells significantly inhibited cell growth and mobility and induced G1 cell cycle arrest. The luciferase reporter assay revealed that EZH2 is a direct target of miR-33a and that it was upregulated in TNBC tissues and cell lines. There was a negative correlation between miR-33a and EZH2 expression in TNBC tissues. EZH2 knockdown exerted similar inhibitory effects, while ectopic expression of EZH2 showed suppressive effects on malignant behaviors induced by miR-33a overexpression in TNBC cells. Conclusions:These findings revealed that miR-33a is a tumor-suppressive miRNA in TNBC and can inhibit proliferation and mobility and induce G1 cell cycle arrest by directly targeting EZH2.

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“…11 Thus, METTL3 could be a therapeutic target for NSCLC. 12,13 High FTO expression is associated with a low survival LUSC rate. 14 In addition, FTO overexpression has been indicated in various cancers, including LUSC, NSCLC, gastric cancer (GC), cervical carcinoma, pancreatic cancer, and acute myeloid leukemia.…”

Section: Introductionmentioning

confidence: 99%

<p>FTO Facilitates Lung Adenocarcinoma Cell Progression by Activating Cell Migration Through mRNA Demethylation</p>

Ding¹,

Qi²,

Wang³

et al. 2020

OTT

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These authors contributed equally to this workBackground: The fat mass and obesity-associated protein (FTO) was identified as a critical demethylase involved in regulating cellular mRNA stability by removing N6methyladenosine (m6A) residues from mRNA. Emerging evidence has revealed that FTO is deeply implicated in lung cancer. However, knowledge of the function of FTO in lung adenocarcinoma (LUAC) is limited. Methods: FTO and FTO R96Q (R96Q), an FTO missense mutant lacking demethylase activity, were ectopically overexpressed, and FTO was knocked down via siRNA in A549 and H1299 cells. The relationships between FTO with cell characteristics and mRNA m6A levels were explored. Furthermore, RNA sequencing was performed on A549 cells. Results: FTO overexpression enhanced the proliferation, migration, and invasion ability of A549 and H1299 cells, decreased mRNA m6A levels. Interestingly, overexpression of R96Q, blunted the effects of FTO overexpression on cell proliferation and invasion. Through RNA sequencing analysis of A549 cells overexpressing FTO or R96Q and control A594 cells, 45 genes were identified as affected by m6A mRNA demethylation. Most of these genes were related to lung cancer, such as laminin γ2, thrombospondin 1, nerve growth factor inducible, integrin alpha11, and proprotein convertase subtilisin/kexin type 9. Gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses suggested that these genes are fundamental to cancer development processes, such as cell migration and extracellular matrix organization. Conclusion: Our research shows that FTO facilitates LUAC cell progression by activating cell migration through m6A demethylation; however, further research on the mechanism underlying FTO activity in LUAC is necessary.

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MiR-33a suppresses proliferation of NSCLC cells via targeting METTL3 mRNA

Cited by 154 publications

References 29 publications

Diagnostic, progressive and prognostic performance of m⁶A methylation RNA regulators in lung adenocarcinoma

Diagnostic, progressive and prognostic performance of m⁶A methylation RNA regulators in lung adenocarcinoma

MiR-33a functions as a tumor suppressor in triple-negative breast cancer by targeting EZH2

<p>FTO Facilitates Lung Adenocarcinoma Cell Progression by Activating Cell Migration Through mRNA Demethylation</p>

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MiR-33a suppresses proliferation of NSCLC cells via targeting METTL3 mRNA

Cited by 154 publications

References 29 publications

Diagnostic, progressive and prognostic performance of m6A methylation RNA regulators in lung adenocarcinoma

Diagnostic, progressive and prognostic performance of m6A methylation RNA regulators in lung adenocarcinoma

MiR-33a functions as a tumor suppressor in triple-negative breast cancer by targeting EZH2

<p>FTO Facilitates Lung Adenocarcinoma Cell Progression by Activating Cell Migration Through mRNA Demethylation</p>

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Diagnostic, progressive and prognostic performance of m⁶A methylation RNA regulators in lung adenocarcinoma

Diagnostic, progressive and prognostic performance of m⁶A methylation RNA regulators in lung adenocarcinoma