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Mol. Cells 2012; 34(5): 425-432

Published online July 24, 2012

https://doi.org/10.1007/s10059-012-0118-y

© The Korean Society for Molecular and Cellular Biology

BRCA1 and MicroRNAs: Emerging Networks and Potential Therapeutic Targets

Suhwan Chang, and Shyam K. Sharan*

Mouse Cancer Genetics Program, Center for Cancer Research, Frederick National Laboratory for Cancer Research, Frederick, Maryland 21702, USA

Correspondence to : *Correspondence: sharans@mail.nih.gov

Received: April 18, 2012; Revised: June 8, 2012; Accepted: June 15, 2012

Abstract

BRCA1 is a well-known tumor suppressor implicated in familial breast and ovarian cancer. Since its cloning in 1994, numerous studies have established BRCA1’s role in diverse cellular and biochemical processes, such as DNA damage repair, cell cycle control, and transcriptional regulation as well as ubiquitination. In addition, a number of recent studies have functionally linked this tumor suppressor to another important cellular regulator, microRNAs, which are short (19-22 nt) RNAs that were discovered in the nematode in 1993. Soon their presence and function were validated in mammals, and since then, the role of microRNAs has been actively investigated in almost all biological processes, including cancer. In this review, we will describe recent progress in the understanding of the BRCA1 function through microRNAs and the role of microRNAs in regulating BRCA1, with emphasis on the implication of these processes on the development and progression of cancer. We will also discuss the therapeutic potential of microRNA mimics or inhibitors of microRNAs to affect BRCA1 function.

Keywords antagomir, breast cancer, BRCA1, microRNA mimic, microRNAs

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Mol. Cells 2012; 34(5): 425-432

Published online November 30, 2012 https://doi.org/10.1007/s10059-012-0118-y

Copyright © The Korean Society for Molecular and Cellular Biology.

BRCA1 and MicroRNAs: Emerging Networks and Potential Therapeutic Targets

Suhwan Chang, and Shyam K. Sharan*

Mouse Cancer Genetics Program, Center for Cancer Research, Frederick National Laboratory for Cancer Research, Frederick, Maryland 21702, USA

Correspondence to:*Correspondence: sharans@mail.nih.gov

Received: April 18, 2012; Revised: June 8, 2012; Accepted: June 15, 2012

Abstract

BRCA1 is a well-known tumor suppressor implicated in familial breast and ovarian cancer. Since its cloning in 1994, numerous studies have established BRCA1’s role in diverse cellular and biochemical processes, such as DNA damage repair, cell cycle control, and transcriptional regulation as well as ubiquitination. In addition, a number of recent studies have functionally linked this tumor suppressor to another important cellular regulator, microRNAs, which are short (19-22 nt) RNAs that were discovered in the nematode in 1993. Soon their presence and function were validated in mammals, and since then, the role of microRNAs has been actively investigated in almost all biological processes, including cancer. In this review, we will describe recent progress in the understanding of the BRCA1 function through microRNAs and the role of microRNAs in regulating BRCA1, with emphasis on the implication of these processes on the development and progression of cancer. We will also discuss the therapeutic potential of microRNA mimics or inhibitors of microRNAs to affect BRCA1 function.

Keywords: antagomir, breast cancer, BRCA1, microRNA mimic, microRNAs

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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