Related Experiment Video

Updated: Feb 8, 2026

A Sensitive Method to Quantify Senescent Cancer Cells
09:18

A Sensitive Method to Quantify Senescent Cancer Cells

Published on: August 2, 2013

21.3K

miR-30 disrupts senescence and promotes cancer by targeting both p16INK4A and DNA damage pathways

Weijun Su1,2, Lixin Hong3,4, Xin Xu5

  • 1Department of Cancer Biology, Wake Forest Comprehensive Cancer Center, Wake Forest School of Medicine, Winston-Salem, NC, USA.

Oncogene
|June 17, 2018
PubMed

Insights

Overexpressed microRNA-30 (miR-30) disrupts cancer cell senescence, a tumor-suppressing mechanism. By targeting CHD7 and TNRC6A, miR-30 inhibits key tumor suppressors p16INK4A and p53, promoting cancer growth.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Genetics

Background:

  • MicroRNA-30 (miR-30) is frequently overexpressed in human cancers.
  • The precise biological role of miR-30 overexpression in cancer development has remained largely undefined.
  • Oncogene-induced senescence is a critical tumor-suppressing mechanism involving DNA damage responses, p53 activation, and p16INK4A induction.

Purpose of the Study:

  • To elucidate the biological consequences of miR-30 overexpression in cancer.
  • To identify the molecular targets and mechanisms by which miR-30 influences oncogene-induced senescence.
  • To explore the potential of the miR-30 pathway as a diagnostic and therapeutic target in cancer.

Main Methods:

  • Genetic screening to identify miR-30's role in senescence.
  • In vitro cell culture and in vivo mouse models.
  • Analysis of miR-30 targets CHD7 and TNRC6A, and their impact on p16INK4A and p53 pathways.
  • Investigation of DNA damage response RNAs (DDRNAs) and their regulatory mechanisms.

Main Results:

  • miR-30 was found to abrogate oncogene-induced senescence.
  • miR-30 suppresses CHD7, a coactivator essential for p16INK4A induction.
  • miR-30 suppresses TNRC6A, a component required for DNA damage response RNA (DDRNA) function in p53 activation.
  • miR-30 inhibits both p16INK4A and p53, leading to effective disruption of senescence and promotion of cancer.

Conclusions:

  • miR-30 promotes cancer by disrupting the tumor-suppressing mechanism of senescence.
  • The miR-30/CHD7/TNRC6A pathway represents a novel mechanism of oncogenic activity.
  • This pathway offers potential as a diagnostic biomarker and therapeutic target for various human cancers.

More Related Videos

Immunofluorescence Imaging of DNA Damage and Repair Foci in Human Colon Cancer Cells05:18

Immunofluorescence Imaging of DNA Damage and Repair Foci in Human Colon Cancer Cells

Published on: June 9, 2020

11.8K
Visualizing DNA Damage Repair Proteins in Patient-Derived Ovarian Cancer Organoids via Immunofluorescence Assays04:07

Visualizing DNA Damage Repair Proteins in Patient-Derived Ovarian Cancer Organoids via Immunofluorescence Assays

Published on: February 24, 2023

2.3K

Related Concept Videos

DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
3.2K
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
10.1K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
8.9K
DNA-only Transposons02:57

DNA-only Transposons

DNA-only transposons are called autonomous transposons since they code for the enzyme transposase that is required for the transposition mechanism. Insertion of transposons can alter gene functions in multiple ways. They can mutate the gene, alter gene expression by introducing a novel promoter or insulator sequence, introduce new splice sites, and change the mRNA transcripts produced, or remodel chromatin structure.
The donor site from where the transposon is excised is either degraded or...
17.5K
The Eukaryotic Promoter Region02:40

The Eukaryotic Promoter Region

The eukaryotic promoter region is a segment of DNA located upstream of a gene. It contains an RNA polymerase binding site, a transcription start site, and several cis-regulatory sequences.  The proximal promoter region is located in the vicinity of the gene and has cis-regulatory sequences and the core promoter. The core promoter is the binding site for RNA polymerase and is usually located between -35 and +35 nucleotides from the transcription start site. The distal promoter regions are...
18.9K
Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
4.4K