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MicroRNAs

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...

MicroRNAs

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MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA ends...

MicroRNAs

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA ends...

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...

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Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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Related Experiment Video

Updated: May 29, 2026

Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library

Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library

Published on: April 6, 2012

Tumor suppressor BRCA1 epigenetically controls oncogenic microRNA-155.

Suhwan Chang¹, Rui-Hong Wang, Keiko Akagi

¹Mouse Cancer Genetics Program, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, Maryland, USA.

Nature Medicine

|September 28, 2011

Summary

This summary is machine-generated.

The BRCA1 tumor suppressor normally represses miR-155, an oncomir. A moderate-risk BRCA1 variant (R1699Q) abrogates this repression, suggesting miR-155 as a therapeutic target for BRCA1-deficient tumors.

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Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library

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Silencing of BRCA2 to Identify Novel BRCA2-regulated Biological Functions in Cultured Human Cells

Silencing of BRCA2 to Identify Novel BRCA2-regulated Biological Functions in Cultured Human Cells

Published on: August 12, 2015

Area of Science:

Molecular Biology
Genetics
Oncology

Background:

BRCA1 is a tumor suppressor primarily known for DNA repair and cell cycle regulation.
Investigating low-penetrant BRCA1 variants can reveal novel physiological functions.
MicroRNA-155 (miR-155) is an oncomir implicated in cancer development.

Purpose of the Study:

To investigate the functional impact of the moderate-risk BRCA1 R1699Q variant.
To explore the relationship between BRCA1 and miR-155 expression.
To elucidate the mechanism of BRCA1-mediated repression of miR-155.

Main Methods:

Studied the BRCA1 R1699Q variant in cell lines.
Assessed DNA damage repair capacity.
Investigated BRCA1's interaction with HDAC2 and its effect on miR-155 promoter.
Performed in vivo tumor cell growth assays with miR-155 overexpression and knockdown.

Main Results:

The BRCA1 R1699Q variant does not impair DNA damage repair.
BRCA1 R1699Q abrogates the repression of miR-155.
BRCA1 epigenetically represses miR-155 via HDAC2-mediated deacetylation of histones on the miR-155 promoter.
miR-155 overexpression accelerates tumor cell growth, while knockdown attenuates it.

Conclusions:

BRCA1 exhibits a novel tumor suppressive function through epigenetic repression of miR-155.
The R1699Q variant disrupts this function, highlighting its oncogenic potential.
miR-155 is a potential therapeutic target for BRCA1-deficient tumors.