Related Experiment Video

Updated: Oct 1, 2026

Exploring the Pharmacological Action and Molecular Mechanism of Salidroside in Inhibiting MCF-7 Cell Proliferation and Migration
11:13

Exploring the Pharmacological Action and Molecular Mechanism of Salidroside in Inhibiting MCF-7 Cell Proliferation and Migration

Published on: June 9, 2023

ROS, stress-activated kinases and stress signaling in cancer

Moran Benhar1, David Engelberg, Alexander Levitzki

  • 1Department of Biological Chemistry, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem 91904, Israel.

EMBO Reports
|May 7, 2002
PubMed

Insights

Anticancer therapy works best in early stages because stress signaling pathways, involving reactive oxygen species (ROS) and stress-activated protein kinases (SAPKs), promote cancer cell death. In advanced tumors, these pathways are suppressed, leading to treatment resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Anticancer therapies are often effective in early-stage cancers but less so in advanced tumors.
  • The molecular mechanisms driving this differential response remain incompletely understood.
  • Standard anticancer drugs target DNA or the cytoskeleton, primarily affecting dividing cells.

Purpose of the Study:

  • To investigate the role of stress-signaling cascades in mediating anticancer therapy effects.
  • To explore how these signaling pathways change during tumor progression and impact treatment response.
  • To elucidate the molecular basis for acquired resistance to anticancer agents.

Main Methods:

  • Review of recent findings on stress signaling in cancer.
  • Analysis of the role of reactive oxygen species (ROS) and stress-activated protein kinases (SAPKs).
  • Correlation of signaling pathway activity with tumor stage and therapeutic outcomes.

Main Results:

  • Stress-signaling cascades, including ROS and SAPKs, are activated by anticancer agents.
  • These activated pathways are integrated into apoptotic (programmed cell death) pathways in transformed cells.
  • In advanced tumors, ROS and SAPK activity is downregulated, suppressing cell death signaling.

Conclusions:

  • The induction of stress signaling is crucial for the efficacy of anticancer therapy in early-stage disease.
  • Downregulation of ROS and SAPK activity in advanced tumors contributes to therapeutic resistance.
  • Modulating stress-signaling pathways may offer strategies to overcome treatment resistance in advanced cancers.

Related Concept Videos

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...
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...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
Cell Signaling in Plants01:25

Cell Signaling in Plants

Plant cells communicate to coordinate their cycle of growth, flowering and fruiting, and activities in roots, shoots, and leaves in response to the changing environmental conditions. Plant signaling is distinct from animal signaling. Plants primarily utilize enzyme-linked receptors, whereas the largest class of cell-surface receptors in animals are G-protein coupled receptors (GPCRs). Unlike animals, receptor tyrosine kinases are rare in plants. Instead, plants have a diverse class of...
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...