Related Experiment Video

Updated: Feb 24, 2026

Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

35.3K

Molecular Regulation of Cellular Senescence by MicroRNAs: Implications in Cancer and Age-Related Diseases

Mathieu Neault1, Florence Couteau2, Éric Bonneau3

  • 1Chromatin Structure and Cellular Senescence Research Unit, Maisonneuve-Rosemont Hospital Research Centre, Montréal, QC, Canada; Université de Montréal, Montréal, QC, Canada.

International Review of Cell and Molecular Biology
|August 26, 2017
PubMed

Insights

Cellular senescence, a tumor suppressor mechanism, prevents cancer by halting cell growth. MicroRNAs (MiRs) are key regulators, influencing senescence signaling in cancer and aging pathologies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Cellular senescence acts as a crucial tumor suppressor mechanism, inhibiting cancer development and progression.
  • Senescence is triggered by various cellular stresses, leading to stable cell cycle arrest.
  • Cancer cells often inactivate tumor suppressor pathways to bypass senescence and promote uncontrolled proliferation.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which microRNAs (MiRs) regulate cellular senescence.
  • To investigate the reciprocal relationship between cellular senescence and MiR expression.
  • To focus on the role of MiRs in senescence within the context of cancer and aging-related diseases.

Main Methods:

  • Review of molecular mechanisms governing cellular senescence.
  • Analysis of microRNA involvement in senescence signaling pathways.
  • Exploration of MiR expression modulation during senescence.

Main Results:

  • MicroRNAs are identified as critical modulators of cellular senescence.
  • Cellular senescence influences the expression of microRNAs.
  • These interactions play significant roles in cancer progression and age-associated pathologies.

Conclusions:

  • MicroRNAs fine-tune cellular senescence signaling pathways.
  • The senescence response itself impacts MiR expression patterns.
  • Understanding these MiR-senescence interactions is vital for targeting cancer and aging diseases.
Keywords:
AgingCancerCellular senescenceMiRRBp53

More Related Videos

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence13:59

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence

Published on: August 12, 2018

8.6K
Measurement of Protein Turnover Rates in Senescent and Non-Dividing Cultured Cells with Metabolic Labeling and Mass Spectrometry08:52

Measurement of Protein Turnover Rates in Senescent and Non-Dividing Cultured Cells with Metabolic Labeling and Mass Spectrometry

Published on: April 6, 2022

4.1K

Related Concept Videos

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...
4.2K
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...
24.4K
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...
4.9K
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...
4.5K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
5.8K
Mitochondria01:37

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
21.0K