Related Experiment Video

Updated: Apr 17, 2026

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
11:42

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

Published on: April 7, 2017

10.0K

Ionizing radiation-inducible miR-30e promotes glioma cell invasion through EGFR stabilization by directly targeting

Seo-Young Kwak1, Bu-Yeon Kim, Hyun-Joo Ahn

  • 1Division of Radiation Cancer Research, Korea Institute of Radiological and Medical Sciences, Seoul, Korea; Laboratory of Biochemistry, School of Life Sciences and Biotechnology, Korea University, Seoul, Korea.

The FEBS Journal
|February 19, 2015
PubMed

Insights

MicroRNAs (miRNAs) like miR-30e promote cancer cell invasion by increasing matrix metalloproteinase MMP-2 secretion. Targeting miR-30e could potentially reduce invasiveness in glioma radiotherapy.

Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • MicroRNAs (miRNAs) are crucial regulators of gene expression.
  • miR-30e is induced by ionizing radiation.
  • Cellular invasion is a hallmark of cancer progression.

Purpose of the Study:

  • To investigate the role of miR-30e in promoting cellular invasion.
  • To elucidate the molecular mechanisms by which miR-30e enhances invasion.
  • To explore the potential of targeting miR-30e in glioma radiotherapy.

Main Methods:

  • miRNA expression analysis
  • Cellular invasion assays
  • Western blotting
  • 3' UTR reporter assays
  • Gene knockdown and overexpression studies

Main Results:

  • miR-30e enhances cellular invasion by promoting MMP-2 secretion.
  • miR-30e up-regulates epidermal growth factor receptor (EGFR) protein stability.
  • miR-30e down-regulates the E3 ubiquitin ligase CBL-B, a direct target, leading to increased EGFR.
  • Knockdown of CBL-B mimics miR-30e effects; CBL-B overexpression suppresses them.

Conclusions:

  • miR-30e promotes glioma cell invasion through the EGFR/AKT/ERK pathway by down-regulating CBL-B.
  • Targeting miR-30e may be a therapeutic strategy to inhibit radiation-induced invasiveness in glioma.
Keywords:
CBL-BEGFRMMP-2invasionmiR-30e

More Related Videos

Coculture Assays to Study Macrophage and Microglia Stimulation of Glioblastoma Invasion09:23

Coculture Assays to Study Macrophage and Microglia Stimulation of Glioblastoma Invasion

Published on: October 20, 2016

15.0K
Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections05:45

Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections

Published on: July 31, 2017

10.2K

Related Concept Videos

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...
8.5K
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
3.0K
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...
5.5K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
5.1K