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MicroRNA-21 regulates expression of the PTEN tumor suppressor gene in human hepatocellular cancer.
TLDR
Aberrant expression of miR-21 can contribute to HCC growth and spread by modulating PTEN expression and PTEN-dependent pathways involved in mediating phenotypic characteristics of cancer cells such as cell growth, migration, and invasion.
Essential metabolic, anti-inflammatory, and anti-tumorigenic functions of miR-122 in liver.
TLDR
It is demonstrated that deletion of mouse Mir122 resulted in hepatosteatosis, hepatitis, and the development of tumors resembling HCC, demonstrating critical functions for miR-122 in the maintenance of liver homeostasis and have important therapeutic implications, including the potential utility of mi R-122 delivery for selected patients with HCC and the need for careful monitoring of patients receiving miR -122 inhibition therapy for HCV.
MicroRNA-221/222 Confers Tamoxifen Resistance in Breast Cancer by Targeting p27Kip1*♦
TLDR
This is the first study demonstrating a relationship between miR-221/222 expression and HER2/neu overexpression in primary breast tumors that are generally resistant to tamoxifen therapy, and provides the rationale for the application of altered expression of specific miRNAs as a predictive tamoxIFen-resistant breast cancer marker.
Downregulation of miR‐122 in the rodent and human hepatocellular carcinomas
TLDR
Findings suggest that the downregulation of miR‐122 is associated with hepatocarcinogenesis and could be a potential biomarker for liver cancers.
5-Aza-Deoxycytidine Induces Selective Degradation of DNA Methyltransferase 1 by a Proteasomal Pathway That Requires the KEN Box, Bromo-Adjacent Homology Domain, and Nuclear Localization Signal
TLDR
Results demonstrate a unique mechanism for the selective degradation of DNMT1, the maintenance DNA methyltransferase, by well-known DNA-hypomethylating agents and indicate that covalent bond formation between the enzyme and 5-aza-CdR-incorporated DNA is not essential for enzyme degradation.
A new class of quinoline-based DNA hypomethylating agents reactivates tumor suppressor genes by blocking DNA methyltransferase 1 activity and inducing its degradation.
TLDR
A quinoline-based compound, designated SGI-1027, inhibits the activity of DNMT1, DNMT3A, andDNMT3B as well as competing with S-adenosylmethionine in the methylation reaction and provides a novel class of DNA hypomethylating agents that have the potential for use in epigenetic cancer therapy.
Methylation mediated silencing of MicroRNA-1 gene and its role in hepatocellular carcinogenesis.
TLDR
Up-regulation of several miR-1 targets including FoxP1, MET, and HDAC4 in primary human HCCs and down- regulation of their expression in 5-AzaC-treated HCC cells suggest their role in hepatocarcinogenesis.
TGFβ mediated upregulation of hepatic miR-181b promotes hepatocarcinogenesis by targeting TIMP3
TLDR
Upregulation of miR-181b at early stages of feeding CDAA diet promotes hepatocarcinogenesis and enhanced resistance of HCC cells to the anticancer drug doxorubicin.
Role of microRNA‐155 at early stages of hepatocarcinogenesis induced by choline‐deficient and amino acid–defined diet in C57BL/6 mice
MicroRNAs (miRs) are conserved, small (20‐25 nucleotide) noncoding RNAs that negatively regulate expression of messenger RNAs (mRNAs) at the posttranscriptional level. Aberrant expression of certain
Low levels of miR‐92b/96 induce PRMT5 translation and H3R8/H4R3 methylation in mantle cell lymphoma
TLDR
The studies indicate that aberrant expression of PRMT5 leads to altered epigenetic modification of chromatin, which in turn impacts transcriptional performance of anti‐cancer genes and growth of transformed lymphoid cells.
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