Related Experiment Video

Updated: May 8, 2026

Epigenetic Engineering of K562 Cells: Dual-Vector Episomal Strategy for Stable Targeted DNA Methylation using dCas9-DNMT3A and -HDAC1 Fusion Proteins
09:56

Epigenetic Engineering of K562 Cells: Dual-Vector Episomal Strategy for Stable Targeted DNA Methylation using dCas9-DNMT3A and -HDAC1 Fusion Proteins

Published on: October 31, 2025

The epigenetically-regulated miR-663 targets H-ras in K-562 cells

Yang Yang1, Li-Li Wang, Heng-Xiang Wang

  • 1Department of Haematology and BMT Centre, Chinese PLA General Hospital, Beijing, China; Department of Haematology, Chinese PLA Air Force General Hospital, Beijing, China.

The FEBS Journal
|August 20, 2013
PubMed

Insights

Aberrant methylation of CpG islands in miR-663 is linked to chronic myelogenous leukemia. This microRNA targets H-ras, potentially suppressing cancer cell proliferation and enhancing apoptosis.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Epigenetics

Background:

  • MicroRNA-663 (miR-663) functions as a tumor suppressor.
  • CpG island methylation is a known regulatory mechanism for gene expression.
  • The role of miR-663 dysregulation in cancer, particularly chronic myelogenous leukemia (CML), requires further investigation.

Purpose of the Study:

  • To investigate the aberrant methylation of CpG islands upstream of pre-miR-663 in K-562 cells and CML patient samples.
  • To identify genes targeted by miR-663.
  • To explore the functional impact of miR-663 overexpression on K-562 cell proliferation and apoptosis.

Main Methods:

  • Analysis of CpG island methylation in the pre-miR-663 region.
  • Identification of miR-663 targets using molecular biology techniques.
  • Overexpression of miR-663 in K-562 cells followed by proliferation and apoptosis assays.

Main Results:

  • Aberrant methylation of CpG islands in the upstream region of pre-miR-663 was observed in K-562 cells and white blood cells from CML patients.
  • H-ras was identified as a gene directly targeted by miR-663.
  • Overexpression of miR-663 led to suppressed proliferation of K-562 cells, partly through enhanced apoptosis.

Conclusions:

  • Aberrant CpG island methylation contributes to miR-663 down-regulation in K-562 cells and CML.
  • miR-663 exerts tumor-suppressive functions by targeting oncogenes like H-ras.
  • Restoring miR-663 levels may represent a therapeutic strategy for CML by inhibiting cancer cell growth.
Keywords:
DNA methylationH-rasMiR-663epigeneticsgene expression

More Related Videos

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells09:45

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells

Published on: May 21, 2019

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells11:42

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

Published on: April 7, 2017

Related Concept Videos

The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
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...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
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...