miR-206/133b Cluster: A Weapon against Lung Cancer?

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Abstract

Lung cancer is a deadly disease that ends numerous lives around the world. MicroRNAs (miRNAs) are a group of non-coding RNAs involved in a variety of biological processes, such as cell growth, organ development, and tumorigenesis. The miR-206/133b cluster is located on the human chromosome 6p12.2, which is essential for growth and rebuilding of skeletal muscle. The miR-206/133b cluster has been verified to be dysregulated and plays a crucial role in lung cancer. miR-206 and miR-133b participate in lung tumor cell apoptosis, proliferation, migration, invasion, angiogenesis, drug resistance, and cancer treatment. The mechanisms are sophisticated, involving various target genes and molecular pathways, such as MET, EGFR, and the STAT3/HIF-1α/VEGF signal pathway. Hence, in this review, we summarize the role and potential mechanisms of the miR-206/133b cluster in lung cancer.

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During apoptosis, the BCL-2 protein family controls mitochondrial outer membrane permeabilization (MOMP), but the dynamics of this regulation remain controversial. We employed chimeric proteins composed of exogenous BH3 domains inserted into a tBID backbone that can activate the proapoptotic effectors BAX and BAK to permeabilize membranes without being universally sequestered by all antiapoptotic BCL-2 proteins. We thus identified two "modes" whereby prosurvival BCL-2 proteins can block MOMP, by sequestering direct-activator BH3-only proteins ("MODE 1") or by binding active BAX and BAK ("MODE 2"). Notably, we found that MODE 1 sequestration is less efficient and more easily derepressed to promote MOMP than MODE 2. Further, MODE 2 sequestration prevents mitochondrial fusion. We provide a unified model of BCL-2 family function that helps to explain otherwise paradoxical observations relating to MOMP, apoptosis, and mitochondrial dynamics. Copyright © 2011 Elsevier Inc. All rights reserved.

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Myogenic factors that regulate expression of muscle-specific microRNAs.

Prakash Rao, Roshan Kumar, Mina Farkhondeh … (2006)

Since their discovery as key regulators of early animal development, microRNAs now are recognized as widespread regulators of gene expression. Despite their abundance, little is known regarding the regulation of microRNA biogenesis. We show that three highly conserved muscle-specific microRNAs, miR-1, miR-133 and miR-206, are robustly induced during the myoblast-myotube transition, both in primary human myoblasts and in the mouse mesenchymal C2C12 stem cell line. These microRNAs were not induced during osteogenic conversion of C2C12 cells. Moreover, both loci encoding miR-1, miR-1-1, and miR-1-2, and two of the three encoding miR-133, miR-133a-1 and miR-133a-2, are strongly induced during myogenesis. Some of the induced microRNAs are in intergenic regions, whereas two are transcribed in the opposite direction to the nonmuscle-specific gene in which they are embedded. By using CHIP analysis, we demonstrate that the myogenic factors Myogenin and MyoD bind to regions upstream of these microRNAs and, therefore, are likely to regulate their expression. Because miR-1 and miR-206 are predicted to repress similar mRNA targets, our work suggests that induction of these microRNAs is important in regulating the expression of muscle-specific proteins.

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Transcription factor NRF2 regulates miR-1 and miR-206 to drive tumorigenesis.

Sarvesh Kumar, László Boros, Luis Gonzalez … (2013)

The mechanisms by which deregulated nuclear factor erythroid-2-related factor 2 (NRF2) and kelch-like ECH-associated protein 1 (KEAP1) signaling promote cellular proliferation and tumorigenesis are poorly understood. Using an integrated genomics and ¹³C-based targeted tracer fate association (TTFA) study, we found that NRF2 regulates miR-1 and miR-206 to direct carbon flux toward the pentose phosphate pathway (PPP) and the tricarboxylic acid (TCA) cycle, reprogramming glucose metabolism. Sustained activation of NRF2 signaling in cancer cells attenuated miR-1 and miR-206 expression, leading to enhanced expression of PPP genes. Conversely, overexpression of miR-1 and miR-206 decreased the expression of metabolic genes and dramatically impaired NADPH production, ribose synthesis, and in vivo tumor growth in mice. Loss of NRF2 decreased the expression of the redox-sensitive histone deacetylase, HDAC4, resulting in increased expression of miR-1 and miR-206, and not only inhibiting PPP expression and activity but functioning as a regulatory feedback loop that repressed HDAC4 expression. In primary tumor samples, the expression of miR-1 and miR-206 was inversely correlated with PPP gene expression, and increased expression of NRF2-dependent genes was associated with poor prognosis. Our results demonstrate that microRNA-dependent (miRNA-dependent) regulation of the PPP via NRF2 and HDAC4 represents a novel link between miRNA regulation, glucose metabolism, and ROS homeostasis in cancer cells.

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Author and article information

Contributors

Cheng-Cao Sun

De-Jia Li

Journal

Journal ID (nlm-ta): Mol Ther Nucleic Acids

Journal ID (iso-abbrev): Mol Ther Nucleic Acids

Title: Molecular Therapy. Nucleic Acids

Publisher: American Society of Gene & Cell Therapy

ISSN (Electronic): 2162-2531

Publication date PMC-release: 07 June 2017

Publication date Collection: 15 September 2017

Publication date (Electronic): 07 June 2017

Volume: 8

Pages: 442-449

Affiliations

[1 ]Department of Occupational and Environmental Health, School of Public Health, Wuhan University, Wuhan 430071 Hubei, P.R. China

[2 ]Hubei Provincial Key Laboratory for Applied Toxicology (Hubei Provincial Academy for Preventive Medicine), Wuhan 430079 Hubei, P.R. China

[3 ]Wuhan Hospital for the Prevention and Treatment of Occupational Diseases, Wuhan 430022 Hubei, P.R. China

Author notes

[∗ ]Corresponding author: De-Jia Li, No. 115 Donghu Road, Wuchang District, Wuhan, 430071 Hubei, P.R. China. lodjlwhu@ 123456sina.com

[∗∗ ]Corresponding author: Cheng-Cao Sun, No. 115 Donghu Road, Wuchang District, Wuhan, 430071 Hubei, P.R. China. chengcaosun@ 123456whu.edu.cn

[4]

These authors contributed equally to this work.

Article

Publisher ID: S2162-2531(17)30185-3

DOI: 10.1016/j.omtn.2017.06.002

PMC ID: 5542379

PubMed ID: 28918043

SO-VID: 370bbc6f-6b30-4210-aee5-3d47b1c42573

License:

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

miR-206/133b Cluster: A Weapon against Lung Cancer?

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Abstract

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Biomarkers for Inflammatory Lung Disease

Most cited references 64

A unified model of mammalian BCL-2 protein family interactions at the mitochondria.

Myogenic factors that regulate expression of muscle-specific microRNAs.

Transcription factor NRF2 regulates miR-1 and miR-206 to drive tumorigenesis.

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