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Related Concept Videos

MicroRNAs01:22

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...
MicroRNAs01:22

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...
MicroRNAs01:22

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...
Abnormal Proliferation02:23

Abnormal Proliferation

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...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...

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Tropomodulin 3 Overexpression as a Marker for Platinum Resistance and Immune Infiltration in Ovarian Cancer
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MEG3 noncoding RNA: a tumor suppressor.

Yunli Zhou1, Xun Zhang, Anne Klibanski

  • 1Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street, Bulfinch 457, Boston, Massachusetts 02114, USA. yzhou2@partners.org

Journal of Molecular Endocrinology
|March 7, 2012
PubMed
Summary
This summary is machine-generated.

Maternally expressed gene 3 (MEG3), a long noncoding RNA, is frequently lost in human tumors. Re-expressing MEG3 inhibits cancer cell growth and promotes apoptosis, suggesting its role as a tumor suppressor.

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Published on: December 13, 2018

Area of Science:

  • Genetics
  • Molecular Biology
  • Cancer Research

Background:

  • Maternally expressed gene 3 (MEG3) is an imprinted long noncoding RNA (lncRNA) located at chromosome 14q32.3.
  • MEG3 is expressed in normal tissues but frequently silenced in various human tumors.
  • Loss of MEG3 expression is linked to mechanisms like gene deletion and promoter hypermethylation.

Purpose of the Study:

  • To investigate the role of MEG3 as a potential tumor suppressor.
  • To elucidate the mechanisms by which MEG3 affects tumor cell growth and apoptosis.
  • To explore the impact of MEG3 inactivation on gene expression and physiological processes.

Main Methods:

  • Analysis of MEG3 expression in human tumors and cell lines.
  • Experimental re-expression of MEG3 in cancer cells.
  • Assessment of cell proliferation, apoptosis, and colony formation assays.
  • Investigation of p53 protein accumulation and transcriptional activity.
  • Evaluation of gene expression changes and angiogenesis in mouse models with Meg3 inactivation.

Main Results:

  • Re-expression of MEG3 inhibited tumor cell proliferation and colony formation.
  • MEG3 induced apoptosis, partly through p53 accumulation and regulation of p53 target genes.
  • Maternal deletion of Meg3 in mice caused skeletal defects, perinatal death, and increased angiogenesis in the brain.

Conclusions:

  • MEG3 functions as a novel long noncoding RNA tumor suppressor.
  • Dysregulation of MEG3 contributes to tumorigenesis.
  • MEG3 has critical roles in development and tumor suppression, potentially mediated by the p53 pathway and angiogenesis regulation.