Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

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,...
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 specific...
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...
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...
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...
Cancer Therapies02:49

Cancer Therapies

Cancer therapies are various modes of treatment, such as surgery, radiation therapy, and chemotherapy that are administered to cancer patients.
However, cancer treatments can pose several challenges, as therapies used to kill cancer cells are generally also toxic to normal cells. Moreover, cancer cells mutate rapidly and can develop resistance to chemical agents or radiation therapy. Besides, all types of cancer cells may not respond to the same therapy. Some cancer cells respond to one...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Identification of a uromodulin fragment for diagnosis of IgA nephropathy.

Rapid communications in mass spectrometry : RCM·2010
Same author

A novel anti-virulence gene revealed by proteomic analysis in Shigella flexneri 2a.

Proteome science·2010
Same author

Delivery of siRNA therapeutics: barriers and carriers.

The AAPS journal·2010
Same author

Effect of Xuefu Zhuyu Capsule (血府逐瘀胶囊) on the symptoms and signs and health-related quality of life in the unstable angina patients with blood-stasis syndrome after percutaneous coronary intervention: A Randomized controlled trial.

Chinese journal of integrative medicine·2010
Same author

Prognostic factors and outcome of 438 Chinese patients with hepatocellular carcinoma underwent partial hepatectomy in a single center.

World journal of surgery·2010
Same author

Proteomic analysis of hydrogen photoproduction in sulfur-deprived Chlamydomonas cells.

Journal of proteome research·2010
Same journal

Effective treatment of human breast tumors by chimeric CCL2 and CCL8 diphtheria toxin cytotoxic peptides.

Cancer biology & therapy·2026
Same journal

<i>NSUN2</i> mediates <i>SALL2</i> m5C methylation to inhibit ferroptosis and promote breast cancer progression.

Cancer biology & therapy·2026
Same journal

Targeting the PI3K/AKT pathway in prostate cancer: the role of PTEN deficiency and biomarker-guided therapy.

Cancer biology & therapy·2026
Same journal

ABHD17C regulates the efficacy of lenvatinib in suppressing hepatocellular carcinoma.

Cancer biology & therapy·2026
Same journal

Advances in SEC61G research: from ER translocon subunit to emerging pan-cancer oncogenic roles.

Cancer biology & therapy·2026
Same journal

Efficacy and safety profiles of CDK4/6 inhibitor in patients with hormone receptor-positive and human epidermal growth factor receptor 2-negative (HR+/HER2-) advanced breast cancer (ABC) from the high-altitude <i>versus</i> low-altitude regions: a multi-center retrospective study.

Cancer biology & therapy·2026
See all related articles

Related Experiment Video

Updated: Jun 28, 2026

Live Imaging to Quantify Cellular Radiosensitivity in Patient-Derived Tumor Organoids
05:39

Live Imaging to Quantify Cellular Radiosensitivity in Patient-Derived Tumor Organoids

Published on: April 5, 2024

Cancer cell killing via ROS: to increase or decrease, that is the question.

Jie Wang1, Jing Yi

  • 1Department of Cell Biology, Key Laboratory of the Education Ministry for Cell Differentiation and Apoptosis, Institutes of Medical Sciences, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Cancer Biology & Therapy
|November 5, 2008
PubMed
Summary
This summary is machine-generated.

Reactive oxygen species (ROS) are crucial in cell signaling and cancer development. Manipulating ROS offers dual therapeutic strategies, either increasing or decreasing ROS levels to combat cancer, with personalized treatment approaches on the horizon.

More Related Videos

Production and Detection of Reactive Oxygen Species (ROS) in Cancers
07:17

Production and Detection of Reactive Oxygen Species (ROS) in Cancers

Published on: November 21, 2011

Related Experiment Videos

Last Updated: Jun 28, 2026

Live Imaging to Quantify Cellular Radiosensitivity in Patient-Derived Tumor Organoids
05:39

Live Imaging to Quantify Cellular Radiosensitivity in Patient-Derived Tumor Organoids

Published on: April 5, 2024

Production and Detection of Reactive Oxygen Species (ROS) in Cancers
07:17

Production and Detection of Reactive Oxygen Species (ROS) in Cancers

Published on: November 21, 2011

Area of Science:

  • Biochemistry
  • Oncology
  • Cell Biology

Background:

  • Reactive oxygen species (ROS) are vital signaling molecules in normal cells but their imbalance is linked to cancer pathogenesis.
  • Elevated ROS levels in cancer cells contribute to initiation, progression, and metastasis, classifying ROS as oncogenic.
  • Paradoxically, ROS generation is a common mechanism in cancer therapies like chemotherapy, radiotherapy, and photodynamic therapy, aiming to induce cancer cell death.

Purpose of the Study:

  • To review current ROS-manipulation strategies for cancer treatment and their underlying mechanisms.
  • To categorize ROS-producing or -eliminating agents and potential drugs.
  • To discuss the paradoxical rationales and concerns of opposing ROS-manipulation strategies.

Main Methods:

  • Literature review of ROS-manipulation strategies in cancer treatment.
  • Categorization of ROS-modulating agents and drugs.
  • Analysis of the dual role of ROS in cancer and therapeutic implications.

Main Results:

  • ROS play a double-edged sword role, implicated in both cancer promotion and therapeutic cell death induction.
  • Both pro-oxidant and antioxidant therapies are being developed, with some showing clinical promise.
  • Selectivity between tumor and non-tumor cells may be achieved by exploiting differences in their redox environments.

Conclusions:

  • Developing a "redox signaling signature" combining cellular parameters is crucial for selecting cancer-specific ROS-elevating or ROS-depleting therapies.
  • Clinical application requires accurate ROS and "redox signaling signature" measurements for predicting treatment efficacy and toxicity.
  • Personalized ROS-manipulation therapy holds promise for optimizing cancer treatment outcomes.