RETRACTED: miR-639 Expression Is Silenced by DNMT3A-Mediated Hypermethylation and Functions as a Tumor Suppressor in Liver Cancer Cells

Xiao, Jing; Liu, Yankun; Wu, Fuxia; Liu, Ruiyan; Xie, Yongli; Yang, Qian; Li, Yufeng; Liu, Min; Li, Shengping; Tang, Hua

doi:10.1016/j.ymthe.2019.11.021

Cited by 24 publications

(20 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…More and more evidence show that miRNAs play important roles in regulating cancer initiation and development ( Calin and Croce, 2006 ; Moles, 2017 ). Besides, miRNAs are critical for tumorigenesis and have been characterized as oncogenes or tumor suppressors ( Li et al, 2017 ; Xiao et al, 2019 ; Yasukawa et al, 2019 ; Zhang et al, 2019 ; Weidle et al, 2020 ). Yet the role of let-7a-5p in NSCLC has not been completely investigated.…”

Section: Introductionmentioning

confidence: 99%

Tanshinone Inhibits NSCLC by Downregulating AURKA Through Let-7a-5p

et al. 2020

View full text Add to dashboard Cite

Lung cancer is the most deadly malignancy in the last decade, accounting for about 1.6 million deaths every year globally. Tanshinone is the constituent of Salvia miltiorrhiza; it has been found that they influence tumorigenesis. However, the role of tanshinones on lung cancer is still not clear. Let-7a-5p, a short non-coding RNA, is regarded as a suppressor gene in tumorigenesis. Herein, we verified that let-7a-5p is significantly downregulated in non-small-cell lung cancer (NSCLC) tissues and cell lines. Tanshinone suppressed the expression of aurora kinase A (AURKA), inhibited cell proliferation, and arrested cell cycle progression. Our results showed that tanshinones suppressed NSCLC by upregulating the expressions of let-7a-5p via directly targeting AURKA. Besides, the data reveal that the knockdown of AURKA can also inhibit cell proliferation, arrest cell cycle, and promote cell apoptosis. Furthermore, this study demonstrates that AURKA was negatively correlated with let-7a-5p in NSCLC patient tissues. Taken together, our findings suggest that tanshinone inhibits NSCLC by downregulating AURKA through let-7a-5p. Tanshinones and let-7a-5p have the potential to be candidates for drug development of NSCLC. In conclusion, this study revealed that tanshinones with miRNA linking lead to partial mechanism in NSCLC.

show abstract

Section: Introductionmentioning

confidence: 99%

Tanshinone Inhibits NSCLC by Downregulating AURKA Through Let-7a-5p

et al. 2020

View full text Add to dashboard Cite

show abstract

“… 38 In liver cancer, derepressing the expression of ZEB1 through DNMT3A -mediated hypermethylation suppressed miR-639 expression, and finally promoted tumorigenesis of liver cancer and provided new biomarkers for liver cancer. 39 ZEB1 is also involved in regulating tumor resistance. In pancreatic cancer, the sensitivity of ZEB1 knockout cells to gemcitabine increased.…”

Section: Discussionmentioning

confidence: 99%

Screening of Methylation Gene Sites as Prognostic Signature in Lung Adenocarcinoma

Dong

Zengli²,

et al. 2020

Yonsei Med J

View full text Add to dashboard Cite

Purpose: Most lung adenocarcinoma (LUAD) patients are diagnosed at the advanced stage and have poor prognosis. DNA methylation plays an important role in the prognosis prediction of cancers. The objective of this study was to identify new DNA methylation sites as biomarkers for LUAD prognosis. Materials and Methods: We downloaded DNA methylation data from The Cancer Genome Atlas data portal. Cox proportional hazard regression model and random survival forest algorithm were applied to identify the DNA-methylation sites. Methylation of sites were validated in the Gene Expression Omnibus cohorts. Function annotation were done to explore the biological function of DNA methylated sites signature. Results: Six DNA methylation sites were identified as prognosis signature. The signature yielded acceptable discrimination between the high-risk group and low-risk group. The discrimination effect of this DNA methylation signature for the OS was obvious, with a median OS of 21.89 months vs. 17.74 months for high-risk vs. low-risk groups. This prognostic prediction model was validated by the test group and GEO dataset. The predictive survival value was higher for the prognostic prediction model than that for the tumor node metastasis stage. Adjuvant hemotherapy could not affect the prediction of the signature. Functional analysis indicated that these signature genes were involved in protein binding and cytoplasm. Conclusion: We identified the prognostic signature for LUAD by combining six DNA methylation sites. This could service as potential robust and specificity signature in the prognosis prediction of LUAD.

show abstract

“…In fact, DNMT1 is responsible for maintaining methylation patterns after replication [30], whereas DNMT2 is a methyltransferase homologue which mainly methylates aspartic acid cytosine 38 in the tRNA anti-codon loop [31,32]. Recent reports have indicated that DNMT2 can also methylate other RNA molecules and short DNA segments in vitro [33,34]. Moreover, DNMT3A and DNMT3B are responsible for de novo DNA methylation and are particularly crucial in the embryonic development during determining methylation pattern.…”

Section: Dna Methylationmentioning

confidence: 99%

Head and Neck Squamous Cell Carcinoma: Epigenetic Landscape

et al. 2020

View full text Add to dashboard Cite

Head and neck squamous carcinoma (HNSCC) constitutes the sixth most prevalent cancer worldwide. The molecular pathogenesis of HNSCC includes disorders in cell cycle, intercellular signaling, proliferation, squamous cell differentiation and apoptosis. In addition to the genetic mutations, changes in HNSCC are also characterized by the accumulation of epigenetic alterations such as DNA methylation, histone modifications, non-coding RNA activity and RNA methylation. In fact, some of them may promote cancer formation and progression by controlling the gene expression machinery, hence, they could be used as biomarkers in the clinical surveillance of HNSCC or as targets for therapeutic strategies. In this review, we focus on the current knowledge regarding epigenetic modifications observed in HNSCC and its predictive value for cancer development.

show abstract

RETRACTED: miR-639 Expression Is Silenced by DNMT3A-Mediated Hypermethylation and Functions as a Tumor Suppressor in Liver Cancer Cells

Cited by 24 publications

References 43 publications

Tanshinone Inhibits NSCLC by Downregulating AURKA Through Let-7a-5p

Tanshinone Inhibits NSCLC by Downregulating AURKA Through Let-7a-5p

Screening of Methylation Gene Sites as Prognostic Signature in Lung Adenocarcinoma

Head and Neck Squamous Cell Carcinoma: Epigenetic Landscape

Contact Info

Product

Resources

About