Related Experiment Video

Updated: Nov 28, 2025

Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

34.4K

Molecular Mechanisms to Target Cellular Senescence in Hepatocellular Carcinoma

Constanze Mittermeier1, Andreas Konopa2, Susanne Muehlich2

  • 1Cancer Science Institute of Singapore, National University of Singapore, Singapore 117599, Singapore.

Cells
|December 1, 2020
PubMed

Insights

Targeting Myocardin-Related Transcription Factors (MRTF-A and -B) induces senescence, halting hepatocellular carcinoma (HCC) growth. This highlights MRTFs as promising drug targets for novel HCC therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Hepatocellular carcinoma (HCC) is a leading cause of cancer mortality.
  • There is a critical need for new HCC therapeutic strategies due to limited drug options.
  • Serum Response Factor (SRF) and its coactivators, MRTF-A and -B, are implicated in HCC development.

Purpose of the Study:

  • To explore the role of MRTF-A and -B in HCC.
  • To investigate the potential of targeting MRTFs for HCC treatment.
  • To highlight senescence as a tumor-suppressive mechanism for therapeutic intervention.

Main Methods:

  • Review of current literature on SRF, MRTFs, and HCC.
  • Analysis of the functional role of senescence in cancer.
  • Focus on MRTFs as potential drug targets.

Main Results:

  • Targeting MRTFs induces oncogene-induced senescence in HCC.
  • Senescence acts as a tumor-suppressive mechanism.
  • MRTF inhibition leads to HCC growth arrest.

Conclusions:

  • MRTF-A and -B are key players in HCC progression.
  • Targeting MRTFs represents a viable therapeutic strategy for HCC.
  • Inducing senescence via MRTF inhibition offers a novel approach to HCC treatment.
Keywords:
DLC1HCCMRTFSRFsenescencesenolytics

More Related Videos

Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity09:32

Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity

Published on: October 17, 2025

176
SA-β-Galactosidase-Based Screening Assay for the Identification of Senotherapeutic Drugs07:39

SA-β-Galactosidase-Based Screening Assay for the Identification of Senotherapeutic Drugs

Published on: June 28, 2019

24.7K

Related Concept Videos

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...
4.1K
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
17.3K
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...
8.2K
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
6.3K
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
6.1K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
5.5K