LNC942 promoting METTL14-mediated m6A methylation in breast cancer cell proliferation and progression

Sun, Tong; Wu, Zhuona; Wang, Xiufang; Wang, Yilin; Hu, Xiaoyun; Qin, Wenyan; Lu, Senxu; Xu, Dong-ping; Wu, Yutong; Chen, Qiuchen; Ding, Xiangyu; Guo, Hao; Li, Yalun; Wang, Yuanhe; Fu, Boshi; Yao, Weifan; Wei, Minjie; Wu, Huizhe

doi:10.1038/s41388-020-1338-9

Cited by 163 publications

(153 citation statements)

References 54 publications

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“…In contrast, METTL14 is highly expressed in acute myeloid leukemia cells and promotes leukemogenesis via m 6 A modification [ 23 ]. Findings from three investigations into METTL14 expression and function in breast cancer are controversial, with one study showing that METTL14 acts as a tumor suppressor [ 24 ], while the other two show that METTL14 promotes cancer growth [ 25 , 26 ].…”

Section: Discussionmentioning

confidence: 99%

“…In one study, significantly decreased METTL14 expression was observed in patients with breast cancer compared with healthy controls, and overexpression of METTL14 inhibited breast cancer cell viability, colony formation, and migration [ 24 ]. Conversely, in another study, significantly upregulated METTL14 expression was observed in breast cancer tissue compared with normal tissue, and METTL14 overexpression enhanced the migration and invasion capacities of breast cancer cells [ 25 ], while other researchers have reported significantly upregulated levels of METTL14 and m 6 A in breast cancer cells and tissues, and the modulation of METTL14 by long noncoding RNA LINC00942 (LNC942) promoted breast cancer initiation and progression [ 26 ]. Thus, further research is needed to better understand the expression and function of METTL14 in breast cancer.…”

Section: Introductionmentioning

confidence: 99%

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Downregulated METTL14 Expression Correlates with Breast Cancer Tumor Grade and Molecular Classification

Dong

Wang

Huang

et al. 2020

BioMed Research International

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It is unclear whether the methyltransferase-like 14 (METTL14) protein promotes or suppresses cancer growth. We examined the association between METTL14 expression, cancer progression, and patient prognosis in a total of 398 breast cancer tissue specimens. Significantly fewer cancer tissue specimens compared with normal breast tissue expressed high levels of METTL14 (52.8% vs. 75.0%). METTL14 expression was negatively associated with tumor grade and positively associated with patient age, estrogen, and progesterone receptor status. High METTL14 expression was more common in luminal A and luminal B tissue (75.9% and 60.8%, respectively), compared with human epidermal growth factor receptor 2- (HER2-) enriched and triple-negative breast cancer (TNBC) samples (38.2% and 18.6%, respectively). In multiple logistic regression analysis, independent predictors of METTL14 expression in breast cancer included higher tumor grade ( odds ratio OR = 0.494 , 95% confidence interval (CI): 0.289–0.844; P = 0.010 ), TNBC subtype ( OR = 0.109 , 95% CI: 0.054–0.222; P < 0.001 ), and HER2-enriched subtype ( OR = 0.298 , 95% CI: 0.156–0.567; P < 0.001 ). No clear relationship was observed between patient prognosis and METTL14 expression. It appears that downregulated METTL14 expression in breast cancer is associated with tumor grade and molecular classification.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Downregulated METTL14 Expression Correlates with Breast Cancer Tumor Grade and Molecular Classification

Dong

Wang

Huang

et al. 2020

BioMed Research International

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“…METTL14 was promoted by LINC00942, enhancing the initiation and progression of breast cancer. 108 Niu et al 109 found that FTO is highly expressed in breast cancer tissues, and the higher the expression, the worse the prognosis of patients. FTO promotes the proliferation and metastasis of breast cancer cells by inhibiting BNIP3.…”

Section: Review Llmentioning

confidence: 99%

RNA m6A Modification in Cancers: Molecular Mechanisms and Potential Clinical Applications

Shi

Dai

et al. 2020

The Innovation

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N 6 -Methyladenosine (m 6 A) RNA modification brings a new dawn for RNA modification researches in recent years. This posttranscriptional RNA modification is dynamic and reversible, and is regulated by methylases (“writers”), demethylases (“erasers”), and proteins that preferentially recognize m 6 A modifications (“readers”). The change of RNA m 6 A modification regulates RNA metabolism in eucaryon, including translation, splicing, exporting, decay, and processing. Thereby the dysregulation of m 6 A may lead to tumorigenesis and progression. Given the tumorigenic role of abnormal m 6 A expression, m 6 A regulators may function as potential clinical therapeutic targets for cancers. In this review, we emphasize on the underlying mechanisms of m 6 A modifications in tumorigenesis and further introduce the potential m 6 A regulators-associated therapeutic targets for tumor therapy.

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“…Recently, studies reported that human methyltransferase like 13 (METTL13) can catalyze dimethylation of eukaryotic elongation factor 1A (eEF1A) lysine 55 (eEF1AK55me2) to promote the protein synthesis in Ras-driven cancers [19,20]. METTL13 was characterized with oncogenicity, as it was involved in various diseases, such as gastric cancer [21], lung cancer [22,23] and breast cancer [24]. METTL13 also functions as a potential inhibitor of apoptosis, for it was found that miR-16 promoted apoptosis of tumor cells by silencing protein synthesis through posttranscriptional regulation [25].…”

Section: Introductionmentioning

confidence: 99%

METTL13 Mediates the Translation of Snail in Head and Neck Squamous Cell Carcinoma

Wang¹,

Li²,

Wan³

et al. 2020

Preprint

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Background: Accumulating evidence supports that Methyltransferase like 13 (METTL13), which is implicated in protein binding and synthesis, act as oncogenic molecule. This study aimed to reveal the potential mechanism of METTL13 in head and neck squamous cell carcinoma (HNSCC) via mediating enhancing translation efficiency of Snail. Methods: The expression of METTL13, Snail and ki67 were detected in patient HNSCC and paired para-carcinoma tissues. Knockdown and ectopic expression experiments were used in HNSCC cells to investigate their effects on tumor cell migration, proliferation and apoptosis. RNA-sequencing, polysome profiling and SUnSET assays were developed to obtain the further mechanism of the interaction among METTL13, Snail and translation.Results: METTL13 was signiﬁcantly upregulated in HNSCC at both mRNA and protein level. Increased METTL13 was negatively associated with clinical prognosis. And METTL13 markedly affected HNSCC cellular phenotypes in vivo and vitro. Further mechanism study revealed that METTL13 could regulate EMT signaling pathway by mediating enhancing translation efficiency of Snail, the key transcription factor in EMT, hence regulating the progression of EMT. Conclusion: Altogether, our study had revealed the clinical signiﬁcance of METTL13 in HNSCC, and providing a potential therapeutic strategy.

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LNC942 promoting METTL14-mediated m6A methylation in breast cancer cell proliferation and progression

Cited by 163 publications

References 54 publications

Downregulated METTL14 Expression Correlates with Breast Cancer Tumor Grade and Molecular Classification

Downregulated METTL14 Expression Correlates with Breast Cancer Tumor Grade and Molecular Classification

RNA m6A Modification in Cancers: Molecular Mechanisms and Potential Clinical Applications

METTL13 Mediates the Translation of Snail in Head and Neck Squamous Cell Carcinoma

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