Related Experiment Video

Updated: May 7, 2026

In vitro Organoid Culture of Primary Mouse Colon Tumors
07:33

In vitro Organoid Culture of Primary Mouse Colon Tumors

Published on: May 17, 2013

Impaired DICER1 function promotes stemness and metastasis in colon cancer

M S Iliou1, V da Silva-Diz1, F J Carmona1

  • 1Cancer Epigenetics and Biology Program (PEBC), Bellvitge Biomedical Research Institute (IDIBELL), Barcelona, Spain.

Oncogene
|October 8, 2013
PubMed

Insights

Impaired microRNA (miRNA) processing due to DICER1 defects in colorectal cancer cells enhances tumor stemness and metastasis. This highlights DICER1

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • microRNA (miRNA) expression patterns are altered in human cancers.
  • Defects in miRNA processing machinery can cause these alterations.
  • The impact of these defects on tumor biology is not well understood.

Purpose of the Study:

  • To investigate how impaired DICER1 function affects colorectal cancer cell biology.
  • To determine the consequences of DICER1 defects on tumor initiation and metastasis.

Main Methods:

  • Analysis of colorectal cancer cells with DICER1 impairment.
  • Assessment of tumor stemness features and epithelial-to-mesenchymal transition (EMT).
  • Quantification of specific miRNA levels (miR-34a, miR-126, miR-200 family).
  • Evaluation of tumor initiation and metastatic potential.

Main Results:

  • DICER1 impairment in colorectal cancer cells leads to enriched stemness features and EMT.
  • This is associated with downregulation of key tumor-suppressive miRNAs (miR-34a, miR-126, miR-200 family).
  • DICER1-deficient cells exhibit increased tumor initiation and metastatic capacity.

Conclusions:

  • DICER1 is crucial for maintaining normal miRNA processing in colorectal cancer.
  • Impaired DICER1 function promotes cancer stem cell properties and metastasis.
  • Targeting miRNA biogenesis defects could offer new therapeutic strategies for colorectal cancer.

More Related Videos

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer08:34

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer

Published on: April 13, 2015

Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres06:52

Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres

Published on: July 22, 2020

Related Concept Videos

Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
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 Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
Hedgehog Signaling Pathway02:33

Hedgehog Signaling Pathway

The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...